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  • Emodin and emodin-rich rhubarb inhibits histone deacetylase (HDAC) activity and cardiac myocyte hypertrophy
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2020-01-10
    Levi W. Evans; Abigail Bender; Leah Burnett; Luis Godoy; Yi Shen; Dante Staten; Tong Zhou; Jeffrey E. Angermann; Bradley S. Ferguson

    Pathological cardiac hypertrophy is a classical hallmark of heart failure. At the molecular level, inhibition of histone deacetylase (HDAC) enzymes attenuate pathological cardiac hypertrophy in vitro and in vivo. Emodin is an anthraquinone that has been implicated in cardiac protection. However, it is not known if the cardio-protective actions for emodin are mediated through HDAC-dependent regulation of gene expression. Therefore, we hypothesized that emodin would attenuate pathological cardiac hypertrophy via inhibition of HDACs, and that these actions would be reflected in an emodin-rich food like rhubarb. In this study, we demonstrate that emodin and Turkish rhubarb containing emodin inhibit HDAC activity in vitro, with fast-on, slow-off kinetics. Moreover, we show that emodin increased histone acetylation in cardiomyocytes concomitant to global changes in gene expression; gene expression changes were similar to the well-established pan-HDAC inhibitor trichostatin A (TSA). We additionally present evidence that emodin inhibited phenylephrine (PE) and phorbol myristate acetate (PMA)-induced hypertrophy in neonatal rat ventricular myocytes (NRVMs). Lastly, we demonstrate that the cardioprotective actions of emodin are translated to an angiotensin II (Ang) mouse model of cardiac hypertrophy and fibrosis and are linked to HDAC inhibition. These data suggest that emodin blocked pathological cardiac hypertrophy, in part, by inhibiting HDAC-dependent gene expression changes.

    更新日期:2020-01-11
  • Maize extract rich in ferulic acid and anthocyanins prevents high-fat induced obesity in mice by modulating SIRT1, AMPK, and IL-6 associated metabolic and inflammatory pathways
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2020-01-10
    Diego Luna-Vital; Iván Luzardo-Ocampo; Liceth Cuellar-Nuñez; Guadalupe Loarca-Pina; Elvira Gonzalez de Mejia
    更新日期:2020-01-11
  • 3,3-dimethyl-1-butanol attenuates cardiac remodeling in pressure overload-induced heart failure mice
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2020-01-09
    Guangji Wang; Bin Kong; Wei Shuai; Hui Fu; Xiaobo Jiang; He Huang

    Trimethylamine N-oxide (TMAO) is closely related to cardiovascular diseases (CVD), particularly heart failure (HF). Recent studies shows that 3,3-dimethyl-1-butanol (DMB) can reduce plasma TMAO levels. However, the role of DMB in overload-induced HF is not well-understood. In this research study, we explored the effects and the underlying mechanisms of DMB in overload-induced HF. Aortic banding (AB) surgery was performed in C57BL6/J mice to induce HF and a subset group of mice underwent a sham operation. After surgery, the mice were fed with a normal diet and given water supplemented with or without 1% DMB for 6 weeks. Cardiac function, plasma TMAO level, cardiac hypertrophy and fibrosis, expression of inflammatory, electrophysiological studies and signaling pathway were analyzed at the 6th week after AB surgery. DMB reduced TMAO levels in overload-induced heart failure mice. Adverse cardiac structural remodeling, such as cardiac hypertrophy, fibrosis and inflammation were elevated in overload-induced HF mice. Susceptibility to ventricular arrhythmia also significantly increased in overload-induced HF mice. However, these changes were prevented by DMB treatment. DMB attenuated all of these changes by reducing plasma TMAO levels, hence negatively inhibiting the p65 NF-κB signaling pathway and TGF-β1/Smad3 signaling pathway. DMB plays an important role in attenuating the development of cardiac structural remodeling and electrical remodeling in overload-induced HF mice. This may be attributed to the p65 NF-κB signaling pathway and TGF-β1/Smad3 signaling pathway inhibition.

    更新日期:2020-01-09
  • Impact of caloric restriction on AMPK and endoplasmic reticulum stress in peripheral tissues and circulating peripheral blood mononuclear cells from Zucker rats
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2020-01-09
    Elena Vega-Martín; Raquel González-Blázquez; Francisco J. Manzano-Lista; Miriam Martín-Ramos; Concepción F. García-Prieto; Marta Viana; Miguel A. Rubio; Alfonso L. Calle-Pascual; Lillà Lionetti; Beatriz Somoza; María S. Fernández-Alfonso; Martín Alcalá; Marta Gil-Ortega

    The activation of endoplasmic reticulum (ER) stress and a reduction of AMP-dependent protein kinase (AMPK) phosphorylation have been described in obesity. We hypothesize that a moderate caloric restriction (CR) might contribute to reducing ER stress and increasing AMPK phosphorylation in peripheral tissues from genetically obese Zucker fa/fa rats and in peripheral blood mononuclear cells (PBMCs). Zucker Lean and Zucker fa/fa rats were fed with chow diet either ad libitum (AL) (C, as controls) or 80% of AL (CR) for two weeks, giving rise to four experimental groups: Lean C, Lean CR, fa/fa C and fa/fa CR. CR significantly increased AMPK phosphorylation in the liver, perirenal adipose tissue (PRAT) and PBMCs from fa/fa rats but not in the subcutaneous AT(SCAT), suggesting a reduced response of SCAT to CR. Liver samples of fa/fa rats exhibited an increased mRNA expression of PERK, EIF-2α, XBP-1(s), Chop and caspase 3, that was significantly reduced by CR. PRAT exhibited an overexpression of Edem and PDIA-4 in fa/fa rats, but only PDIA-4 expression was reduced by CR. eIF-2α phosphorylation was significantly increased in all studied tissues from fa/fa rats and reduced by CR. A negative correlation was detected between p-AMPK and p-eIF-2α in the liver, PRAT and PBMCs from fa/fa rats but not in SCAT. This study shows that a moderate CR reduces ER stress and improves AMPK phosphorylation in several peripheral tissues and in circulating PBMCs, suggesting that alterations observed in PBMCs could be a reflect of metabolic alterations associated to obesity.

    更新日期:2020-01-09
  • Maternal malnutrition impacts placental morphology and transporter expression: An origin for poor offspring growth
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2020-01-08
    Kristin L Connor; Mark Kibschull; Elzbieta Matysiak-Zablocki; Tina Tu-Thu Ngoc Nguyen; Stephen G Matthews; Stephen J Lye; Enrrico Bloise

    The placenta promotes fetal growth through nutrient transfer and selective barrier systems. An optimally developed placenta can adapt to changes in the pregnancy environment, buffering the fetus from adverse exposures. We hypothesised that the placenta adapts differently to suboptimal maternal diets, evidenced by changes in placental morphology, developmental markers, and key transport systems. Mice were fed a control diet (CON) during pregnancy, or undernourished (UN) by 30% of control intake from gestational day (GD)5.5–18.5, or fed 60% high fat diet (HF) eight weeks before and during pregnancy. At GD18.5, placental morphometry, development, and transport were assessed. Junctional and labyrinthine areas of UN and HF placentae were smaller than CON by>10%. Fetal blood space area and fetal blood space:fetal weight ratios were reduced in HF vs. CON and UN. Trophoblast giant cell marker Ctsq mRNA expression was lower in UN vs. HF, and expression of glycogen cell markers Cx31.1 and Pcdh12 was lower in HF vs. UN. Efflux transporter Abcb1a mRNA expression was lower in HF vs. UN, and Abcg2 expression was lower in UN vs. HF. mRNA expression of fatty acid binding protein Fabppm was higher in UN vs. CON and HF. mRNA and protein levels of the lipid transporter FAT/CD36 were lower in UN, and FATP4 protein levels were lower in HF vs. UN. UN placentae appear less mature with aberrant transport. HF placentae adapt to excessive nutrient supply. Understanding placental adaptations to common nutritional adversities may reveal mechanisms underlying the developmental origins of later disease.

    更新日期:2020-01-09
  • High ratio of ω-3/ω-6 polyunsaturated fatty acids targets mTORC1 to prevent high fat diet-induced metabolic syndrome and mitochondrial dysfunction in mice
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2020-01-08
    Run Liu; Lei Chen; Yan Wang; Guanfei Zhang; Ying Cheng; Zhihui Feng; Xiaochun Bai; Jiankang Liu
    更新日期:2020-01-09
  • Atherogenic diet-induced bone loss is primarily due to increased osteoclastogenesis in mice
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2020-01-08
    Ok-Joo Sul; Ji-Eun Kim; Ke Ke; Jae-Hee Suh; Hye-Seon Choi
    更新日期:2020-01-09
  • Advanced liver steatosis accompanies an increase in hepatic inflammation, colonic, secondary bile acids and Lactobacillaceae/Lachnospiraceae bacteria in C57BL/6 mice fed a high-fat diet
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2020-01-08
    Huawei Zeng; Kate J. Larson; Wen-Hsing Cheng; Michael R Bukowski; Bryan D. Safratowich; Zhenhua Liu; Reza Hakkak

    Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in Western countries, and the gut-liver axis is implicated in liver disease pathogenesis. We hypothesize that advanced liver steatosis accompanies an increase in hepatic inflammation, colonic secondary bile acids (BAs) and secondary BA-producing bacteria in mice fed a high-fat (HF) diet model of obesity. Four-week old male C57BL/6 mice were fed an HF (45% energy) or a low-fat (LF) (10% energy) diet for 21 weeks. At the end of the study, body weight and body fat percentage in the HF group were 0.23- and 0.41- fold greater than those in the LF group, respectively. Similarly, the HF group exhibited an increase in hepatic lipid droplets, inflammatory cell infiltration, inducible nitric oxide synthase, and hepatocellular ballooning (but without hepatic Mallory bodies) which are key histological features of advanced hepatic steatosis. Furthermore, RNA sequencing, qPCR and immunohistological methods found that nicotinamide n-methyltransferase and selenoprotein P, two inflammation-related hepatic genes, were upregulated in the HF group. Consistent with the hepatic inflammation, the levels of proinflammatory plasma-cytokines (TNF-α and IL6), colonic secondary BAs (LCA, DCA) and secondary BA producing bacteria (e, g., lactobacillaceae/Lachnospiraceae) were at least 0.5-fold greater in the HF group compared with the LF group. Taken together, the data demonstrate that advanced liver-steatosis is concurrent with an elevated level of hepatic inflammation, colonic secondary bile acids and their associated bacteria in mice fed an HF diet. These data suggest a potential gut-liver crosstalk at the stage of advanced liver-steatosis.

    更新日期:2020-01-09
  • Moderate intake of BCAA-rich protein improves glucose homeostasis in high-fat fed mice
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2020-01-08
    Aline Rissetti Roquetto; Carolina Soares Moura; Valfredo de Almeida Santos-Junior; Paulo Otávio Sammarco Oliveira; Karla Idelça Aires Machado; Gessika Cristina Borges Castro Carvalho; Eder Müller Risso; Jaime Amaya-Farfan

    Notwithstanding the fact that dietary branched-chain amino acids (BCAA) have been considered to be a cause of insulin resistance (IR), evidence indicates that BCAA-rich whey proteins (WP) do not lead to IR in animals consuming high-fat (HF) diets and may instead improve glucose homeostasis. To address the role of BCAA-rich WP as dietary protein in IR and inflammatory response, we fed C57BL/6 J mice either high-fat (HF) or low-fat (LF) diets formulated with moderate-protein levels (13% w/w) of either WP or hydrolyzed WP (WPH), and compared them with casein (CAS) as a reference. The muscle and plasma free amino acid profiles, inflammatory parameters, and glycemic homeostasis were examined. While the LF/CAS diet promoted the rise in triglycerides and inflammatory parameters, the HF/CAS induced typical IR responses and impaired biochemical parameters. No differences in plasma BCAAs were detected, but the HF/WPH diet led to a two-fold increase in gastrocnemius muscle free amino acids, including BCAAs. In general, ingestion of WPH was effective at averting or attenuating the damage caused by both the LF and HF diets. No high concentrations of BCAAs in the plasma or signs of IR were found in those mice fed a HF-diet along with the hydrolyzed whey proteins. It is concluded that consumption of BCAA-rich whey proteins, especially WPH, does not result in the development of IR.

    更新日期:2020-01-09
  • Perinatal exposure of rats to a maternal diet with varying protein quantity and quality affects the risk of overweight in female adult offspring
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2020-01-08
    Gabrielle Carlin; Catherine Chaumontet; François Blachier; Pierre Barbillon; Nicolas Darcel; Corine Delteil; Eline M. van der Beek; Andrea Kodde; Bert J.M. van de Heijning; Daniel Tomé; Anne-Marie Davila

    The maternal protein diet during the perinatal period can program the health of adult offspring. This study in rats evaluated the effects of protein quantity and quality in the maternal diet during gestation and lactation on weight and adiposity in female offspring. Six groups of dams were fed a high-protein (HP; 47% protein) or normal protein (NP; 19% protein) isocaloric diet during gestation (G) using either cow's milk (M), pea (P) or turkey (T) proteins. During lactation, all dams received the NP diet (protein source unchanged). From post-natal day (PND) 28 until PND70, female pups (n=8) from the dam milk groups were exposed to either an NP milk diet (NPMW), or to DSS. All other pups were only exposed to DSS. The DSS design was a choice between five food cups containing HPM, HPP, HPT, carbohydrates or lipids. The weights and food intakes of the animals were recorded throughout the study and samples from offspring were collected on PND70. During the lactation and post-weaning periods, body weight was lower in the pea and turkey groups (NPG and HPG) versus the milk group (P<.0001). DSS groups increased their total energy and fat intakes compared to the NPMW group (P<.0001). In all HPG groups, total adipose tissue was increased (P=.03) associated with higher fasting plasma leptin (P<.05). These results suggest that the maternal protein source impacted offspring body weight and that protein excess during gestation, irrespective of its source, increased the risk of adiposity development in female adult offspring.

    更新日期:2020-01-09
  • Impaired glucose transport in inguinal adipocytes after short-term high-sucrose feeding in mice
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2020-01-08
    Claes Fryklund; Madelene Borg; Tobias Svensson; Sara Schumacher; Florentina Negoita; Björn Morén; Karin G Stenkula

    Diets enriched in sucrose severely impair metabolic regulation and are associated with obesity, insulin resistance and glucose intolerance. In the current study, we investigated the effect of 4 weeks high-sucrose diet (HSD)-feeding in C57BL6/J mice, with specific focus on adipocyte function. Mice fed HSD had slightly increased adipose tissue mass but displayed similar hepatic triglycerides, glucose- and insulin levels, and glucose clearance capacity as chow-fed mice. Interestingly, we found adipose depot-specific differences, where both the non- and insulin stimulated glucose transport was markedly impaired in primary adipocytes isolated from the inguinal fat depot from HSD-fed mice. This was accompanied by decreased protein levels of both GLUT4 and AS160. A similar, but much less pronounced trend was observed in the retroperitoneal depot. In contrast both GLUT4 expression and insulin-stimulated glucose uptake were preserved in adipocytes isolated from epididymal adipose tissue with HSD. Further, we found a slight shift in cell size distribution towards larger cells with HSD, and a significant decrease of ACC and PGC-1α expression in the inguinal adipose tissue depot. Moreover, fructose alone was sufficient to decrease GLUT4 expression in cultured, mature adipocytes. Altogether, we demonstrate that short-term HSD-feeding has deleterious impact on insulin response and glucose transport in the inguinal adipose tissue depot, specifically. These changes occur before the onset of systemic glucose dysmetabolism, and therefore could provide a mechanistic link to overall impaired energy metabolism reported after prolonged HSD feeding, alone or in combination with HFD.

    更新日期:2020-01-09
  • Curcumin supplementation improves heat stress-induced cardiac injury of mice: Physiological and molecular mechanisms
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2020-01-08
    Yong Chen; Weijian Jiang; Xin Liu; Yuechao Du; Liang Liu; Jose M. Ordovas; Chao-Qiang Lai; Lirong Shen

    Heat stress (HS) causes serious physiological dysfunction associated with cardiovascular diseases. Curcumin (CUR) may increase animal survival and lifespan under HS. However, its effects and mechanism on mammal are underexplored. The goal of this study was to examine the protective effect of CUR on the cardiac health of mice exposed to HS. Mice were divided into six groups (n=8 per group): no-heat treatment (NHT), heat treatment (HT), aspirin, CUR 50 mg/kg.day, CUR 100 mg/kg.day and CUR 200 mg/kg.day. After administration for 4 weeks, except for NHT, other groups were exposed once to HS at 41 °C for 20 min. After HS treatment, the physiological related indexes of blood pressure, rectal temperature and heart rate were measured. Serum biochemical indexes, the levels of cardiac troponin I (cTn-I) in serum and angiotensin II (Ang II) in cardiomyocytes were analyzed. Furthermore, the mRNA and proteins levels of angiotensin receptor 1 (AT1), 78-kDa glucose-regulated protein (GRP78), C/EBP homologous protein (CHOP) and B-cell lymphoma 2 (Bcl-2) were measured. Our results indicated that CUR supplementation could alleviate HS-induced physiological disorders and the increasing of cTn-I and Ang II. The expression of AT1 gene in HT group was significantly higher than that of CUR groups, indicating the cardio-protective effects of CUR. Moreover, the levels of GRP78 and CHOP proteins in the HT group were significantly higher than those of CUR groups, indicating that CUR supplementation reversed the endoplasmic reticulum HS-mediated apoptosis. In summary, CUR supplementation alleviates physiological stress and cardiac damage caused by HS.

    更新日期:2020-01-08
  • Lycopene attenuates body weight gain through induction of browning via regulation of peroxisome proliferator-activated receptor γ in high-fat diet-induced obese mice
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2020-01-07
    Ruyuan Zhu; Junping Wei; Haixia Liu; Chenyue Liu; Lili Wang; Beibei Chen; Lin Li; Qiangqiang Jia; Yimiao Tian; Rui Li; Dandan Zhao; Fangfang Mo; Yu Li; Sihua Gao; Xiang-Dong Wang; Dongwei Zhang

    Lycopene (LYC), one of the major carotenoids in tomatoes, has been preclinically and clinically used to obesity and type 2 diabetes management. However, whether its ability to counter body weight gain is mediated through induction of brown-like adipocyte phenotype in white adipose tissues (WAT) remains largely unknown. Activation of peroxisome proliferator-activated receptor γ (PPARγ) serves the brown-like phenotype conversion and energy expenditure. Here, we show that LYC treatment promotes glucose consumption and improves insulin sensitivity, as well as fosters white adipocytes browning through upregulating mRNA and protein expression levels of PPARγ, uncoupling protein 1, PPARγ coactivator-1α and PR domain-containing 16 in the differentiated 3 T3-L1 adipocytes and primary adipocytes, as well as in the WAT of HFD exposed obese mice. In addition, LYC treatment attenuates body weight gain and improves serum lipid profiles as well as promotes BAT activation in obese mice. Moreover, PPARγ is induced with LYC intervention in mitochondria respiration and browning in white adipocytes and tissues. Taken together, these results suggest that LYC counteracts obesity and improves glucose and lipid metabolism through induction of the browning via up-regulation of PPARγ, which offers a new perspective of this compound to combat obesity and obesity-related disorders.

    更新日期:2020-01-07
  • Maternal diets enriched in olive oil regulate lipid metabolism and levels of PPARs and their coactivators in the fetal liver in a rat model of gestational diabetes mellitus
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2020-01-07
    Daiana Fornes; Dalmiro Gomez Ribot; Florencia Heinecke; Sabrina Lorena Roberti; Evangelina Capobianco; Alicia Jawerbaum

    In a rat model of gestational diabetes mellitus (GDM) programmed in the offspring of neonatal streptozotocin-induced (nSTZ) diabetic rats, lipids are accumulated in the fetal liver in a sex-dependent way. Here, we evaluated whether maternal diets enriched in olive oil in rats that will develop GDM ameliorate lipid metabolic impairments in the fetal livers. Pregnant offspring of control and nSTZ diabetic rats (F0) were fed a 6% olive oil-supplemented diet throughout the F1 gestation. We evaluated maternal metabolic parameters as well as lipid content, expression of lipid metabolizing enzymes and protein expression of PLIN2, PPARs and PPAR coactivators in the fetal livers. The offspring of nSTZ diabetic rats developed GDM regardless of the maternal treatment. Hypertriglyceridemia in GDM rats was prevented by the olive oil-enriched maternal treatment. In the livers of male fetuses of GDM rats, the maternal olive oil-supplemented diet prevented lipid overaccumulation and prevented the increase in PPARγ and PPARδ levels. In the livers of female fetuses of GDM rats, the maternal olive oil supplementation prevented the increase in PPARδ levels and the reduction in PGC1α levels, but did not prevent the reduced lipid content. Control and GDM rats showed a reduction of lipid metabolic enzymes in the fetal livers, which was associated with reduced levels of the PPAR coactivators PGC-1α and SRC-1 in males and of SRC-1 in females. These results suggest powerful effects of a maternal olive oil-supplemented diet in the fetal liver, possibly providing benefits in the fetuses and offspring from GDM rats.

    更新日期:2020-01-07
  • The anthocyanins in black currants regulate postprandial hyperglycaemia primarily by inhibiting α-glucosidase while other phenolics modulate salivary α-amylase, glucose uptake and sugar transporters
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-12-26
    Sisir Kumar Barik; Wendy R Russell; Kim M Moar; Morven Cruickshank; Lorraine Scobbie; Gary Duncan; Nigel Hoggard
    更新日期:2019-12-27
  • Myricetin inhibits Endometriosis growth through Cyclin E1 Downregulation In Vitro and In Vivo
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-12-23
    Sunwoo Park; Gwonhwa Song; Whasun Lim

    Endometriosis is a benign gynecological condition prevalent among reproductive-aged women. Although active research and studies have been carried out to discover new drugs, surgery and hormone therapy are still the gold standard for endometriosis treatment. Nowadays, various flavonoids are considered long-term supplements for different diseases. Myricetin, a flavonol, has anti-proliferative, anti- or pro-oxidant, and anti-cancer effects in gynecological diseases. Here, we reveal for the first time, to our knowledge, the anti-growth effects of myricetin in endometriosis. Myricetin inhibited cell proliferation and cell cycle progression of human VK2/E6E7 and End1/E6E7 cells and induced apoptosis, with the loss of mitochondrial membrane potential (MMP) and accumulation of reactive oxygen species (ROS) and calcium ions. Additionally, myricetin decreased the activation of AKT and ERK1/2 proteins, whereas it induced p38 activation in both cell lines. Moreover, myricetin decreased lesion size in the endometriosis mouse model via Ccne1 inhibition. Thus, myricetin has anti-proliferative effects on endometriosis through cell cycle regulation.

    更新日期:2019-12-23
  • Carbohydrate-restricted diet alters the gut microbiota, promotes senescence, and shortens the lifespan in senescence-accelerated prone mice
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-12-20
    Chaoqi He; Qiming Wu; Nao Hayashi; Fumika Nakano; Eriko Nakatsukasa; Tsuyoshi Tsuduki

    This study examined the effects of a carbohydrate-restricted diet on aging, brain function, intestinal bacteria, and the life span to determine long-term carbohydrate-restriction effects on the aging process in senescence-accelerated prone mice (SAMP8). Three-week-old (wk) male SAMP8 were divided into 3 groups after a wk. of preliminary feeding. One group was given a controlled diet, while the others fed on high-fat and carbohydrate-restricted diets, respectively. The mice in each group were further divided into 2 subgroups, of which one was the longevity measurement group. The other groups fed ad libitum until the mice were 50-wk-old. Before the test period termination, passive avoidance test evaluated the learning and memory abilities. Following the test period, serum and various mice organs were obtained and submitted for analysis. The carbohydrate-restricted diet group exhibited significant decrease in the survival rate as compared to the other 2 diet groups. The passive avoidance test revealed a remarkable decrease in the learning and memory ability of carbohydrate-restricted diet group as compared to the control-diet group. Measurement of lipid peroxide level in tissues displayed a marked increase in the brain and spleen of carbohydrate-restricted diet group than the control-diet and high-fat diet groups. Furthermore, notable serum IL-6 and IL-1β level (inflammation indicators) elevations, decrease in Enterobacteria (with anti-inflammatory action) and increase in inflammation inducing Enterobacteria, lowering of short-chain fatty acids levels in cecum was observed in the carbohydrate-restricted diet group. Hence, carbohydrate-restricted diet was revealed to promote aging and shortening of life in senescence-accelerated prone mice.

    更新日期:2019-12-20
  • Green tea polyphenols decrease weight gain, ameliorate alteration of gut microbiota, and mitigate intestinal inflammation in Canines with high-fat-diet-induced obesity
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-12-20
    Yu Li; Sajid Ur Rahman; Yingying Huang; Yafei Zhang; Pengfei Ming; Lei Zhu; Xiaoyan Chu; Jinchun Li; Shibin Feng; Xichun Wang; Jinjie Wu
    更新日期:2019-12-20
  • The nonalcoholic fatty liver disease-like phenotype and lowered serum VLDL are associated with decreased expression and DNA hypermethylation of hepatic ApoB in male offspring of ApoE deficient mothers fed a with Western diet
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-12-19
    Hsiao-Chien Chen; Yi-Zhen Chen; Chih-Hong Wang; Fu-Jung Lin

    Increasing evidence indicates that the intra-uterine environment has consequences for later life. However, the mechanisms of this fetal programming remain unclear. We aimed to investigate the impact of diet-induced maternal hypercholesterolemia on the predisposition of offspring to nonalcoholic fatty liver diseases (NAFLD) and metabolic diseases and its underlying mechanisms. Female apolipoprotein (Apo) E-deficient mice were fed a control diet (CD) or high fat/high cholesterol Western-type diet (WD) before and throughout pregnancy and lactation, and their offspring were weaned onto a CD postnatally. Strikingly, male offspring of WD-fed dams developed glucose intolerance and decreased peripheral insulin sensitivity and exhibited hepatic steatosis. Hepatic steatosis could be attributed, at least in part, to increased hepatic lipogenesis in E18.5 embryos and decreased serum VLDL levels in adulthood. In addition, males born to WD-fed dams had lower serum ApoB levels and hepatic ApoB gene expression compared with males born to CD-fed dams. DNA methylation analysis revealed increased methylation of CpG dinucleotides on the promoter region of the ApoB genes in the livers of male offspring of WD-fed dams. Our findings suggest that maternal WD intake can exacerbate the development of NAFLD in male offspring potentially by affecting ApoB gene expression through epigenetic alterations.

    更新日期:2019-12-19
  • Ferulic acid maintains the self-renewal capacity of embryo stem cells and adipose-derived mesenchymal stem cells in high fat diet-induced obese mice
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-12-19
    Jinkyung Cho; Eunmi Park

    Self-renewal is required for embryo stem cells (ESCs) and adipose-derived mesenchymal stem cells (ADMSCs). This study examined the ability of ferulic acid in mouse ESCs and ADMSCs, in a high fat diet-induced mouse model. Initially, five natural compounds of ferulic acid, xanthohumol, curcumin, ascorbic acid, and quercetin were screened in ESCs using an alkaline phosphate +(AP+) assay, as a self-renewal biomarker. A ferulic acid treatment was the highest AP+ staining in hop-hit screening compounds. Also a ferulic acid increased Nanog mRNA levels in ESCs. The in vivo effects of ferulic acid were next examined in an obese mouse model. C57BL/6 J male mice were fed either a high fat diet (HFD) or control diet with ferulic acid (5 g/kg diet) for eight weeks. Ferulic acid exhibited weight loss and improved glucose homeostasis, lipid profiling, and hepatic steatosis in a HFD-induced mouse model. Next, ADMSCs (Sca-1+CD45−), a hallmark of fat stem cells, were then isolated and quantified from mouse abdominal adipose tissue. A HFD decreased the Sca-1+CD45− cell population of ADMSCs, but HFD-induced obese mice given ferulic acid showed an increased the Sca-1+CD45− cell population of ADMSCs. Moreover, ferulic acid enhanced NANOG mRNA levels in human ADMSCs and its related gene mRNA expression. Overall, this study suggests that ferulic acid preserves self-renewal in ESCs, and contributes to ADMSCs self-renewal and effective weight control in obesity.

    更新日期:2019-12-19
  • Identification of a pro-elongation effect of diallyl disulfide, a major organosulfur compound in garlic oil, on microglial process
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-12-17
    Xing Xu; Peili Hu; Yaoying Ma; Lijuan Tong; Dan Wang; Yue Wu; Zhuo Chen; Chao Huang

    Microglia are the innate immune cells in the nervous system. In the resting state, they display a ramified morphology, while upon disease stimulation their processes would be retracted, along with pro-inflammatory cytokine overproduction. Reversing microglial process retraction may help reduce pro-inflammatory cytokine production and restore microglia's ability to scan surrounding environments, rendering brain function regulation to be more effective. We found that diallyl disulfide (DADS), a major organosulfur compound in garlic oil, administered at different doses and time points, promoted microglial process elongation in both cultured systems and prefrontal cortexes in mice in a reversible manner. Lipopolysaccharide (LPS), a classical activator of microglia, did not affect this pro-elongation effect of DADS at conditions in vitro and in vivo. Functional studies revealed that DADS pre-treatment attenuated LPS-induced decreases in levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) mRNA as well as LPS-induced increases in levels of IL-10 and CD206 mRNA in both cultured microglia and prefrontal cortexes in mice. Protein kinase B (Akt) inhibition attenuated the pro-elongation effect of DADS on microglial process and blocked the regulatory effects of DADS on LPS-induced inflammatory responses in both cultured microglia and prefrontal cortexes in mice. In an in vivo model of neuroinflammation, DADS pre-treatment prevented LPS-induced retraction of microglial process in the prefrontal cortex in mice, and attenuated LPS-induced increase in immobility time in the tail suspension test and forced swim test. These results indicate that DADS induces an Akt-dependent elongation of microglia process, along with the induction of an anti-inflammatory phenotype.

    更新日期:2019-12-18
  • Kefir ameliorates hypertension via gut-brain mechanism in spontaneously hypertensive rats
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-12-12
    Mirian de Almeida Silva; Francesca Elisabeth Mowry; Sarah Christine Peaden; Tadeu Uggere Andrade; Vinicia Campana Biancardi

    Hypertension is associated with gut dysbiosis and dysregulation of the gut-brain axis, and previous work has shown that probiotic treatments exert beneficial cardiovascular effects in humans and animal models of hypertension. Coupled with the evidence of elevated sympathetic outflow and chronic inflammation in hypertension, we hypothesized that both peripherally- and centrally-mediated mechanisms underlie the antihypertensive effects of kefir, a probiotic obtained from the fermentation of milk by kefir grains. Eight-week-old spontaneously hypertensive rats (SHRs) were treated by oral gavage with either a vehicle or kefir (0.3 mL/100 g/day; 9 weeks; SHR-Kefir), and age-matched with vehicle-treated Wistar Kyoto rats (WKY). Long-term kefir treatment attenuated mean arterial pressure elevations in SHR-Kefir relative to vehicle-treated SHRs. Peripherally, SHRs exhibited differences in the wall of the jejunum (fewer Paneth cells per crypt of Lieberkϋhn and increased tunica muscularis thickness) and higher serum lipopolysaccharide levels compared to WKY, alterations which were reversed in SHR-Kefir. Centrally, kefir treatment reduced IL-6 and TNF-α protein densities, and abolished the microglial activation observed in the hypothalamic paraventricular nucleus and rostral ventrolateral medulla of SHRs. Taken together, our findings indicate that the antihypertensive effects of long-term kefir treatment occur, at least in part, through improved structural and functional integrity of the intestinal wall and protection against neuroinflammation within cardioregulatory nuclei.

    更新日期:2019-12-13
  • Severe magnesium deficiency compromises systemic bone mineral density and aggravates inflammatory bone resorption
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-11-26
    Marina Montosa Belluci, Rafael Scaf de Molon, Carlos Rossa Jr, Sotirios Tetradis, Gabriela Giro, Paulo Sergio Cerri, Elcio Marcantonio Jr, Silvana Regina Peres Orrico

    We sought to evaluate the effects of magnesium (Mg) intake deficiency on bone metabolism in rats with induced periodontal disease (PD). Holtzman rats were randomly divided into two groups: Control — animals fed a standard diet and test — animals fed a diet with 90% Mg deficiency. After 60 days on the diets, all animals received ligature on the lower left first molars to induce PD. Animals were euthanized after 30 days following ligature placement. Blood and urine were collected for determination of serum concentrations of Mg, calcium, osteocalcin (OCN), alkaline phosphatase and parathyroid hormone (PTH) by enzyme-linked immunosorbent assay, and the urinary concentration of deoxypyridinoline (DPD). Systemic bone mineral density (BMD), bone volume and architectural bone parameters were evaluated by micro-CT in L4 lumbar vertebrae and mandible. Tartrate-resistant acid phosphatase staining and immunohistochemical (IHC) analysis of inducible nitric oxide synthase (iNOS), Runt-related transcription factor 2 (RUNX2), CD86, CD80, proliferating cell nuclear antigen, vascular endothelial growth factor, OCN and osteopontin were investigated. Reverse-transcription polymerase chain reaction was employed to assess mRNA expression of receptor-activator of nuclear factor-kB ligand, osteoprotegerin (OPG) and interleukin (IL)-6. Mg deficiency was associated with higher concentrations of PTH and DPD, and significant decrease on both systemic and mandibular BMD, as well as greater severity of alveolar and trabecular bone loss. Significant increase in osteoclasts was observed in the test group with PD. IHC analysis showed significant increase in the expression of iNOS and decreased expression of OCN and RUNX2. Increased IL-6 mRNA and decreased OPG mRNA expressions were evidenced in the test group with PD. Mg deficiency caused systemic effects indicative of altered bone metabolism in the vertebrae and affected both immune and stromal cells, aggravating inflammatory bone resorption in the ligature-induced model of periodontitis.

    更新日期:2019-12-11
  • Genetic ablation of tumor necrosis factor-alpha attenuates the promoted colonic Wnt signaling in high fat diet-induced obese mice
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-11-23
    Chi Guo, Susan J. Kim, Armina-Lyn M. Frederick, Jinchao Li, Yu Jin, Huawei Zeng, Joel B. Mason, Zhenhua Liu
    更新日期:2019-12-11
  • Dietary compound glycyrrhetinic acid suppresses tumor angiogenesis and growth by modulating antiangiogenic and proapoptotic pathways in vitro and in vivo
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-11-09
    Jingjing Li, Fan Tang, Renkai Li, Zhejie Chen, Simon Ming-Yuen Lee, Chaomei Fu, Jinming Zhang, George Pak-Heng Leung
    更新日期:2019-12-11
  • Oral flavonoid fisetin treatment protects against prolonged high-fat-diet-induced cardiac dysfunction by regulation of multicombined signaling
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-11-25
    Lin-Feng Hu, Jing Feng, Xianling Dai, Yan Sun, Mingxin Xiong, Lili Lai, Shaoyu Zhong, Chao Yi, Geng Chen, Huanhuan Li, Qiufeng Yang, Qin Kuang, Tingting Long, Jianxia Zhan, Tingting Tang, Chenxu Ge, Jun Tan, Minxuan Xu

    Excess high-fat diet (HFD) intake predisposes the occurrence of obesity-associated heart injury, but the mechanism is elusive. Fisetin (FIS), as a natural flavonoid, has potential activities to alleviate obesity-induced metabolic syndrome. However, the underlying molecular mechanisms of FIS against HFD-induced cardiac injury remain unclear. The present study was to explore the protective effects of FIS on cardiac dysfunction in HFD-fed mice. We found that FIS alleviated HFD-triggered metabolic disorder by reducing body weight, fasting blood glucose and insulin levels, and insulin resistance. Moreover, FIS supplements significantly alleviated dyslipidemia in both mouse hearts and cardiomyocytes stimulated by metabolic stress. FIS treatment abolished HFD-induced inflammatory response in heart tissues through suppressing TNF receptor-1/TNF receptor-associated factor-2 (Tnfr-1/Traf-2) signaling. Furthermore, FIS induced a strong reduction in the expression of fibrosis-related genes, contributing to the inhibition of fibrosis by inactivating transforming growth factor (Tgf)-β1/Smads/Erk1/2 signaling. Collectively, these results demonstrated that FIS could be a promising therapeutic strategy for the treatment of obesity-associated cardiac injury.

    更新日期:2019-12-11
  • Adipose monocyte chemotactic protein-1 deficiency reduces high-fat diet-enhanced mammary tumorigenesis in MMTV-PyMT mice
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-11-29
    Sneha Sundaram, Lin Yan

    Monocyte chemotactic protein-1 (MCP-1) is an adipokine with demonstrated carcinogenic potential. However, there is a lack of evidence whether adipose-produced MCP-1 contributes to breast cancer. We tested the hypothesis that adipose-produced MCP-1 contributes to mammary tumorigenesis in this study. In a breast cancer model of mouse mammary tumor virus-polyomavirus middle T-antigen (MMTV-PyMT), mice with or without adipose MCP-1 knockout [designated as Mcp-1−/− or wild-type (WT)] were fed the standard AIN93G diet (16% of energy from soybean oil) or a high-fat diet (HFD, 45% of energy from soybean oil). Adipose MCP-1 knockout reduced Mcp-1 expression in adipose tissue and concentrations of MCP-1 in plasma. Mcp-1−/− mice fed the HFD had less body fat than their WT counterparts. Adipose MCP-1 knockout attenuated HFD-enhanced mammary tumorigenesis, evidenced by lower mammary tumor volume. Furthermore, Mcp-1−/− mice, regardless of diet, had a longer tumor latency and less tumor weight than WT mice. When fed the HFD, Mcp-1−/− mice, compared to WT mice, exhibited lower concentrations of insulin, leptin, resistin, vascular endothelial growth factor and hepatic growth factor in plasma. In summary, adipose MCP-1 deficiency attenuated HFD-enhanced MMTV-PyMT mammary tumorigenesis. This attenuation can be attributed to less body adiposity, improvement in insulin sensitivity and down-regulation in protumorigenic inflammation cytokines and angiogenic factors in Mcp-1−/− mice. It concludes that adipose-produced MCP-1 contributes to mammary tumorigenesis in the MMTV-PyMT mouse model.

    更新日期:2019-12-11
  • Polyphenol-rich green tea extract induces thermogenesis in mice by a mechanism dependent on adiponectin signaling
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-12-11
    Anaysa Paola Bolin, Celso Pereira Batista Sousa Filho, Marcelo Paradiso Marinovic, Alice Cristina Rodrigues, Rosemari Otton

    Adiponectin is downregulated in obesity negatively impacting the thermogenesis and impairing white fat browning. Despite the notable effects of green tea (GT) extract in the enhancement of thermogenesis, if its effects are being mediated by adiponectin has been scarcely explored. For this purpose, we investigated the role of adiponectin in the thermogenic actions of GT extract by using an adiponectin-knockout mice model. Male wild-type (WT) and knockout (AdipoKO) C57Bl/6 mice (3 months) were divided into 6 groups: mice fed a standard diet + gavage with water (SD WT, and SD AdipoKO), high-fat diet (HFD) + gavage with water (HFD WT, and HFD AdipoKO), and HFD + gavage with 500 mg/Kg of body weight (BW) of GT extract (HFD + GT WT, and HFD + GT AdipoKO). After 20 weeks of experimentation, mice were euthanized and adipose tissue was properly removed. Our findings indicate that treatment with GT extract reversed complications of obesity in WT mice by decreasing final BW gain, adiposity index, adipocyte size and insulin resistance (IR). However, the action of the GT extract was not effective in reversing those markers in the AdipoKO mice, although GT acts independently in the reversal of IR. GT-treatment induced enhancement in energy expenditure (EE), BAT thermogenesis, and promoted browning phenotype in the subcutaneous WAT (scWAT). On the other hand, the thermogenic program was markedly impaired in BAT and scWAT of AdipoKO mice. Our outcomes unveiled adiponectin as a key direct signal for GT extract inducing adaptive thermogenesis and browning in scWAT.

    更新日期:2019-12-11
  • High-refined carbohydrate diet consumption induces neuroinflammation and anxiety-like behavior in mice
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-12-11
    Julia A.S. Gomes, Josiane F. Silva, Grazielle C. Silva, Giovanni F. Gomes, Antonio C.P. de Oliveira, Virginia L. Soares, Marina C. Oliveira, Adaliene V.M. Ferreira, Daniele C Aguiar

    Consumption of poor nutrients diets is associated with fat tissue expansion and with a central and peripheral low-grade inflammation. In this sense, the microglial cells in the central nervous system are activated and release pro-inflammatory cytokines that up-regulate the inducible nitric oxide synthase (iNOS), promoting Nitric Oxide (NO) production. The excess of NO has been proposed to facilitate anxious states in humans and rodents. We evaluated whether consumption of a high-refined carbohydrate-containing diet (HC) in mice induced anxiety-like behavior in the Novelty Suppressed Feeding Test (NFST) trough facilitation of NO, in the prefrontal cortex (PFC) and hippocampus (HIP). We also verified if HC diet induces activation of microglial cells, alterations in cytokine and leptin levels in such regions. Male BALB/c mice received a standard diet or a HC diet for 3 days or 12 weeks. The chronic consumption of HC diet, but not acute, induced an anxiogenic-like effect in the NSF test and an increase in the nitrite levels in the PFC and HIP. The preferential iNOS inhibitor, aminoguanidine (50 mg/kg, i.p), attenuated such effects. Moreover, microglial cells in the HIP and PFC were activated after chronic consumption of HC diet. Finally, the expression of iNOS in the PFC and TNF, IL6 and leptin levels in HIP were higher in chronically HC fed mice. Taken together, our data reinforce the notion that diets containing high-refined carbohydrate facilitate anxiety-like behavior, mainly after a long period of consumption. The mechanisms involve, at least in part, the augmentation of neuroinflammatory processes in brain areas responsible for anxiety control.

    更新日期:2019-12-11
  • miR-222 is involved in the regulation of genistein on skeletal muscle fiber type
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-12-11
    Mailin Gan, Linyuan Shen, Lin Liu, Zhixian Guo, Shujie Wang, Lei Chen, Ting Zheng, Yuan Fan, Ya Tan, Dongmei Jiang, Xuewei Li, Shunhua Zhang, Li Zhu
    更新日期:2019-12-11
  • Treatment with cinnamaldehyde reduces the visceral adiposity and regulates lipid metabolism, autophagy and endoplasmic reticulum stress in the liver of a rat model of early obesity
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-12-11
    Jessika Geisebel Oliveira Neto, Silvia Karl Boechat, Juliana Santos Romão, Carmen Cabanelas Pazos-Moura, Karen Jesus Oliveira
    更新日期:2019-12-11
  • Resveratrol regulates muscle fiber type conversion via miR-22-3p and AMPK/SIRT1/PGC-1α pathway
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-11-27
    Wanxue Wen, Xiaoling Chen, Zhiqing Huang, Daiwen Chen, Hong Chen, Yuheng Luo, Jun He, Ping Zheng, Jie Yu, Bing Yu

    This study investigated the effects of resveratrol and miR-22-3p on muscle fiber type conversion in mouse C2C12 myotubes. Here we showed that resveratrol significantly increased the protein level of slow myosin heavy chain (MyHC) and the activities of succinic dehydrogenase and malate dehydrogenase, as well as markedly decreased the protein level of fast MyHC and the activity of lactate dehydrogenase. Immunofluorescence staining showed that resveratrol remarkably upregulated the number of slow MyHC-positive myotubes and downregulated the number of fast MyHC-positive myotubes, suggesting that resveratrol promoted muscle fiber type conversion from fast-twitch to slow-twitch in C2C12 myotubes. We also showed that miR-22-3p had an opposite function on muscle fiber type conversion and resveratrol was able to repress the expression of miR-22-3p. Furthermore, AMP-activated protein kinase (AMPK) inhibitor Compound C and miR-22-3p mimics could attenuate and eliminate muscle fiber type conversion from fast-twitch to slow-twitch cause by resveratrol, respectively. Together, we provided the first evidence that resveratrol promotes muscle fiber type conversion from fast-twitch to slow-twitch via miR-22-3p and AMPK/SIRT1/PGC-1α pathway in C2C12 myotubes.

    更新日期:2019-12-11
  • Decreased placental folate transporter expression and activity in first and second trimester in obese mothers
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-11-25
    Rebecca H. Jessel, Fredrick J. Rosario, Yi-Yung Chen, Kathryn Erickson, Stephanie B. Teal, Anita Kramer, Eleanor Cotton, Sarah Ryan, Thomas Jansson, Theresa L. Powell

    Obese women have a ~two-fold higher risk to deliver an infant with neural tube defects (NTDs) despite folate supplementation. Placental transfer of folate is mediated by folate receptor alpha (FR-α), proton coupled folate transporter (PCFT), and reduced folate carrier (RFC). Decreased placental transport may contribute to NTDs in obese women. Serum folate levels were measured and placental tissue was collected from 13 women with normal BMI (21.9±1.9) and 11 obese women (33.1±2.8) undergoing elective termination at 8–22 weeks of gestation. The syncytiotrophoblast microvillous plasma membranes (MVM) were isolated using homogenization, magnesium precipitation, and differential centrifugation. MVM expression of FR-α, PCFT and RFC was determined by western blot. Folate transport capacity was assessed using radiolabeled methyl-tetrahydrofolate and rapid filtration techniques. Differences in expression and transport capacity were adjusted for gestational age and maternal age in multivariable regression models. P<.05 was considered statistically significant. Serum folate levels were not significantly different between groups. Placental MVM folate transporter expression did not change with gestational age. MVM RFC (−19%) and FR-α (−17%) expression was significantly reduced in placentas from obese women (P<.05). MVM folate transporter activity was reduced by−52% (P<.05) in obese women. These differences remained after adjustment for gestational age. There was no difference in mTOR signaling between groups. In conclusion, RFC and FR alpha expression and transporter activity in the placental MVM is significantly reduced in obese women in early pregnancy. These results may explain the higher incidence of NTDs in infants of obese women with adequate serum folate.

    更新日期:2019-12-11
  • Effects of (−) - epicatechin on the time course of the expression of perilipins in a diet-induced model of non-alcoholic steatohepatitis
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-11-23
    Isabel Hidalgo, Nayelli Nájera, Eduardo Meaney, Javier Pérez-Durán, Yolotzin Valdespino-Vazquez, Francisco Villarreal, Guillermo Ceballos

    The existing treatments for non-alcoholic steatohepatitis (NASH) are not completely effective. The need for new alternatives without adverse effects and low cost, such as the flavonoid: (−) - epicatechin (EC), which has beneficial effects on lipids metabolism and cardiovascular diseases, arises. The objective of this work was to analyze EC effects in the NASH induced by a Paigen type diet (PD). Mice were administered with: 1) normal chow and water, 2) PD + fructose 30% and 3) PD + fructose 30% + EC[1 mg / kg] per gavage during 9 weeks. At the end of each treatment, serum was collected for analysis of the biochemical profile and liver enzymes. The liver was collected for microscopic analysis and for the evaluation of the relative expression of Plin2, Plin3, CD36, adiponectin and UCP2. Results shown that EC reduced weight gain, decreased TG, LDL-c, TG / HDL and the activity of liver enzymes (ALT and ALP) suggesting lower liver damage. The microscopic analysis showed less “balonization” of the hepatocyte, small drops of lipids, less accumulation of collagen and infiltration of inflammatory cells as compared to non-treated group. Finally, a decrease in the expression of Plin 2 was observed. While CD36 decreased, adiponectin and UCP2 increased. In conclusion, EC improves the biochemical profile, the microscopic characteristics and protein expression. Therefore, it may be a possible therapeutic approach for NASH since it prevents the progression of the hepatic and metabolic damage induced by high-fat diets.

    更新日期:2019-12-11
  • Apple polyphenols induce browning of white adipose tissue
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-11-23
    Yuki Tamura, Shigeto Tomiya, Junya Takegaki, Karina Kouzaki, Arata Tsutaki, Koichi Nakazato

    We and others have shown that apple polyphenols decrease adipose tissue mass. To better understand the underlying mechanisms and to expand clinical applicability, we herein examine whether apple polyphenols induce adipose thermogenic adaptations (browning) and prevent diet-induced obesity and related insulin resistance. In mice fed a standard diet, daily apple polyphenol consumption induced thermogenic adaptations in inguinal white adipose tissue (iWAT), based on increases in the expression of brown/beige adipocyte selective genes (Ucp1, Cidea, Tbx1, Cd137) and protein content of uncoupling protein 1 and mitochondrial oxidative phosphorylation enzymes. Among the upstream regulatory factors of browning, fibroblast growth factor 21 (FGF21) and peroxisome proliferator-activated receptor gamma coactivator 1 α (PGC-1α) levels were concomitantly up-regulated by apple polyphenols. In the primary cell culture experiment, the results did not support a direct action of apple polyphenols on beige adipogenesis. Instead, apple polyphenols increased tyrosine hydroxylase (a rate-limiting enzyme of catecholamine synthesis) in iWAT, which activates the adipocyte thermogenic program possibly via intra-tissue cellular communications. In high-fat fed mice, apple polyphenols induced beige adipocyte development in iWAT, reduced fat accumulation, and increased glucose disposal rates in the glucose and insulin tolerance tests. Taken together, dietary administration of apple polyphenols induced beige adipocyte development in iWAT possibly via activation/induction of the peripheral catecholamine synthesis-FGF21-PGC-1α cascade. Results from diet-induced obese mice indicate that apple polyphenols have therapeutic potential for obesity and related metabolic disorders.

    更新日期:2019-12-11
  • trans, trans-2,4-decadienal, a lipid peroxidation product, induces inflammatory responses via Hsp90- or 14–3-3ζ-dependent mechanisms
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-11-13
    Yuxin Wang, Devon A. Dattmore, Weicang Wang, Georg Pohnert, Stefanie Wolfram, Jianan Zhang, Ran Yang, Eric A. Decker, Kin Sing Stephen Lee, Guodong Zhang
    更新日期:2019-12-11
  • Dietary genistein supplementation improves intestinal mucosal barrier function in Escherichia coli O78-challenged broilers
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-11-09
    Ming Zhang, Jiao Kou, Yujun Wu, Mengmeng Wang, Xiumin Zhou, Ying Yang, Zhenlong Wu

    Genistein has multiple biological activities in both humans and animals. However, a protective effect of genistein on Escherichia coli (E. coli)-induced intestinal mucosal barrier dysfunction remains unknown. In the present study, a total of 288 1-day-old male Arbor Acre broilers fed a corn-soybean basal diet unsupplemented or supplemented with 20 mg genistein/kg diet were subjected to E. coli serotype O78 (108 cfu per bird) infection or equal volume of sodium chloride at 19 days of age. Sera and tissue samples were collected 2 day after E. coli infection. Growth performance, index of immune-related organs, mortality rate at 7 day post E. coli challenge, intestinal barrier permeability, protein level of inflammatory cytokines, sIgA, tight junction protein, and mRNA of apoptotic genes in jejunum were determined. The results showed that E. coli challenge led to a reduced average daily gain, a decreased thymus index, and bursal index in broilers, an increase of fluorescein isothiocyanate (FITC)-dextran in serum, and a decreased sIgA in jejunum. These effects were reversed by genistein administration. Western blot results showed that E. coli infection led to increased protein level of claudin-1 and zonula occludens (ZO)-1, which was markedly abolished by genistein. Moreover, E. coli infection-resulted increase of TNF-α and IL-6, and enhanced apoptosis were abrogated by genistein in jujunum of broilers. In conclusion, the results indicate that genistein supplementation improves intestinal mucosal barrier function which is associated with a regulatory effect on tight junction proteins, sIgA, apoptosis, and secretion of inflammatory cytokines in jejunum of E. coli-challenged broilers.

    更新日期:2019-12-11
  • Micronutrients in autoimmune diseases: Possible therapeutic benefits of zinc and vitamin D
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-10-30
    Inga Wessels, Lothar Rink

    A functional immune system is essential for healthy life. This is achieved by the coordinate activation and interaction of different immune cells. One should be aware that activation of the immune response is as important as its de-activation when the pathogens are cleared, as otherwise host tissue can be damaged up to life-threatening levels. Autoimmune diseases (AID) represent a phenomenon of immune cells attacking host cells and tissue. 5 – 8% of the world´s population are currently affected by 80 – 100 AID. In recent years, the incidence has been constantly increasing reaching alarmingly high numbers particularly for type 1 diabetes mellitus, crohn’s disease, rheumatoid arthritis, sjogren’s syndrome and multiple sclerosis. This indicates a higher societal burden of AID for the future. This article provides an overview of general concepts of triggers and underlying mechanisms leading to self-destruction. Lately, several original concepts of disease etiology were revised and there is a variety of hypotheses on triggers, underlying mechanisms and preventive actions. This article concentrates on the importance of nutrition, especially zinc and vitamin D, for balancing the immune function. Homespun nutritional remedies seem to re-enter today’s therapeutic strategies. Current treatment approaches are largely symptomatic or suppress the immune system. However, recent studies reveal significant benefits of nutrition-related therapeutic approaches including prevention and treatment of established disease, which offers a cost-efficient and trigger-unspecific alternative addressing balancing rather than suppression of the immune system. Zinc and vitamin D are currently the best studied and most promising candidates for therapeutic intervention.

    更新日期:2019-12-11
  • Resveratrol attenuates doxorubicin-induced cardiotoxicity in rats by up-regulation of vascular endothelial growth factor B
    J. Nutr. Biochem. (IF 4.49) Pub Date : 2019-02-08
    Wencong Tian, Lei Yang, Yuansheng Liu, Jianxiang He, Liang Yang, Qiong Zhang, Fei Liu, Jing Li, Jie Liu, Shoichiro Sumi, Yanna Shen, Zhi Qi

    Doxorubicin (DOX) is a broad spectrum antitumor agent. However, its clinical utility is limited due to the well-known cardiotoxicity. Resveratrol (RSV) has been reported to exert cardioprotective effect in some cardiovascular diseases. In this study, we aimed to determine the effect of RSV on DOX-induced cardiotoxicity, and further explore the underlying mechanism in this process.Male Sprague-Dawley (SD) rats were randomly divided into four groups: CON, DOX, RSV, or DOX+RSV group (10 rats in each group). DOX treatment significantly decreased cardiac function, and increased the release of serum lactate dehydrogenase (LDH) and creatine kinase isoenzyme (CK-MB) in rat serum. Increased cell death and apoptosis of cardiomyocytes were also observed in DOX group in comparison with CON group. DOX treatment dramatically down-regulated expression of VEGF-B either in vivo or in vitro. In contrast, the combination of RSV and DOX markedly attenuated DOX-induced cardiotoxicity with the up-regulation of VEGF-B. Inhibition of VEGF-B by small interfering RNA (siRNA) abolished the protective effects of RSV on DOX-treated cardiomyocytes.Consequently,our findings indicated that RSV attenuates DOX-induced cardiotoxicity through up-regulation of VEGF-B.

    更新日期:2019-12-11
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