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Regulation of adipose tissue lipolysis by ghrelin is impaired with high-fat diet feeding and is not restored with exercise
Adipocyte ( IF 3.3 ) Pub Date : 2021-07-05 , DOI: 10.1080/21623945.2021.1945787
Barbora Hucik 1 , Andrew J Lovell 1 , Evan M Hoecht 1 , Daniel T Cervone 1 , David M Mutch 1 , David J Dyck 1
Affiliation  

ABSTRACT

Ghrelin is released from the stomach as an anticipatory signal prior to a meal and decreases immediately after. Previous research has shown that both acylated (AG) and unacylated (UnAG) ghrelin blunt adrenoreceptor-stimulated lipolysis in rat white adipose tissue (WAT) ex vivo. We investigated whether acute or chronic consumption of a high fat diet (HFD) impaired the ability of ghrelin to regulate adipose tissue lipolysis, and if this impairment could be restored with exercise. After 5 days (5d) of a HFD, or 6 weeks (6 w) of a HFD (60% kcal from fat) with or without exercise training, inguinal and retroperitoneal WAT was collected from anesthetized rats for adipose tissue organ culture. Samples were treated with 1 μM CL 316,243 (CL; lipolytic control), 1 μM CL+150 ng/ml AG or 1 μM CL+150 ng/ml UnAG. Incubation media and tissue were collected after 2 hours. Colorometric assays were used to determine glycerol and free fatty acid (FFA) concentrations in media. Western blots were used to quantify the protein content of lipolytic enzymes and ghrelin receptors in both depots. CL stimulated lipolysis was evidenced by increases in glycerol (p < 0.0001) and FFA (p < 0.0001) concentrations in media compared to control. AG decreased CL-stimulated glycerol release in inguinal WAT from 5d LFD rats (p = 0.0097). Neither AG nor UnAG blunted lipolysis in adipose tissue from 5d or 6 w HFD-fed rats, and exercise did not restore ghrelin’s anti-lipolytic ability in 6 w HFD-fed rats. Overall, this study demonstrates that HFD consumption impairs ghrelin’s ability to regulate adipose tissue lipolysis.



中文翻译:

ghrelin 对脂肪组织脂肪分解的调节在高脂饮食喂养中受损,并且在运动中无法恢复

摘要

Ghrelin 在餐前作为预期信号从胃中释放出来,并在餐后立即减少。先前的研究表明,离体大鼠白色脂肪组织 (WAT) 中的酰化 (AG) 和未酰化 (UnAG) 生长素释放肽钝化肾上腺素受体刺激的脂解作用. 我们调查了高脂肪饮食 (HFD) 的急性或慢性消耗是否会损害生长素释放肽调节脂肪组织脂肪分解的能力,以及这种损害是否可以通过运动恢复。经过 5 天 (5 天) 的 HFD 或 6 周 (6 w) 的 HFD(60% 来自脂肪的 kcal)有或没有运动训练后,从麻醉大鼠收集腹股沟和腹膜后 WAT 用于脂肪组织器官培养。用 1 μM C​​L 316,243(CL;脂肪分解对照)、1 μM C​​L+150 ng/ml AG 或 1 μM C​​L+150 ng/ml UnAG 处理样品。2小时后收集培养培养基和组织。比色测定法用于确定培养基中的甘油和游离脂肪酸 (FFA) 浓度。Western印迹用于量化两个仓库中脂解酶和生长素释放肽受体的蛋白质含量。与对照相比,培养基中甘油 (p < 0.0001) 和 FFA (p < 0.0001) 浓度的增加证明了 CL 刺激的脂肪分解。AG 降低了 5 天 LFD 大鼠腹股沟 WAT 中 CL 刺激的甘油释放(p = 0.0097)。AG 和 UnAG 均未减弱 5 天或 6 周 HFD 喂养大鼠脂肪组织中的脂肪分解,并且运动并未恢复 6 周 HFD 喂养大鼠的 ghrelin 的抗脂解能力。总体而言,这项研究表明,HFD 消耗会损害生长素释放肽调节脂肪组织脂肪分解的能力。在 6 w HFD 喂养的大鼠中,运动并没有恢复 ghrelin 的抗脂解能力。总体而言,这项研究表明,HFD 消耗会损害生长素释放肽调节脂肪组织脂肪分解的能力。在 6 w HFD 喂养的大鼠中,运动并没有恢复 ghrelin 的抗脂解能力。总体而言,这项研究表明,HFD 消耗会损害生长素释放肽调节脂肪组织脂肪分解的能力。

更新日期:2021-07-06
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