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Total Postprandial Hepatic Non-Esterified and Dietary Fatty Acid Uptake is Increased and Insufficiently Curbed by Adipose Tissue Fatty Acid Trapping in Prediabetes with Overweight
Diabetes ( IF 6.2 ) Pub Date : 2022-06-24 , DOI: 10.2337/db21-1097
Run Zhou Ye 1 , Émilie Montastier 1 , Christophe Noll 1 , Frédérique Frisch 1 , Mélanie Fortin 1 , Lucie Bouffard 1 , Serge Phoenix 2 , Brigitte Guérin 2 , Éric E Turcotte 2 , André C Carpentier 1
Affiliation  

Excessive lean tissue uptake of fatty acids (FA) is important in the development of insulin resistance and may be caused by impaired dietary FA (DFA) storage and/or increased non-esterified FA (NEFA) flux from adipose tissue intracellular lipolysis. Cardiac and hepatic total postprandial FA uptake of NEFA+DFA has, however, never been reported in prediabetes with overweight. Twenty-one individuals with impaired glucose tolerance (IGT) and 19 participants with normal glucose tolerance (NGT) and normal fasting glucose underwent postprandial studies with whole-body positron emission tomography/computed tomography (PET/CT) with oral [18F]-fluoro-thia-heptadecanoic acid and dynamic PET/CT with intravenous [11C]-palmitate. Hepatic (96 [range 39-213]mmol/6h vs. 75 [23-145]mmol/6h, P=0.05), but not cardiac (11 [range 4-24]mmol/6h vs. 7 [2-20]mmol/6h, P=0.1) uptake of most sources of postprandial FA (NEFA+DFA uptake) integrated over 6 hours was higher in IGT vs. NGT. DFA accounted for lower fractions of total cardiac (19 [5-47]% vs. 25 [10-40]%, P=0.08) and hepatic (22 [6-50]% vs. 29 [15-52]%, P=0.04) uptake in IGT vs. NGT. Increased adipose tissue DFA trapping predicted lower hepatic DFA uptake, and was associated with higher total cardiac fatty acid uptake. Hence, enhanced adipose tissue DFA trapping in the face of increased postprandial NEFA flux is insufficient to fully curb increased postprandial lean organ FA uptake in prediabetes with overweight (ClinicalTrials.gov; NCT02808182).

中文翻译:

超重前驱糖尿病患者的餐后肝脏非酯化脂肪酸和膳食脂肪酸总摄取量增加,但脂肪组织脂肪酸捕获不能充分抑制

过多的瘦组织摄取脂肪酸 (FA) 在胰岛素抵抗的发展中很重要,可能是由膳食 FA (DFA) 储存受损和/或脂肪组织细胞内脂肪分解引起的非酯化 FA (NEFA) 通量增加引起的。然而,NEFA + DFA 的心脏和肝脏餐后总 FA 摄取从未在超重的糖尿病前期中被报道过。21 名葡萄糖耐量受损 (IGT) 患者和 19 名葡萄糖耐量正常 (NGT) 且空腹血糖正常的参与者接受了餐后全身正电子发射断层扫描/计算机断层扫描 (PET/CT) 研究,并使用口服 [18F]-fluoro -硫杂-十七烷酸和动态 PET/CT 静脉注射 [11C]-棕榈酸酯。肝脏(96 [范围 39-213] 毫摩尔/6 小时对比 75 [23-145] 毫摩尔/6 小时,P=0.05),但不是心脏(11 [范围 4-24] 毫摩尔/6 小时对比 7 [2-20] ]mmol/6h,P=0。1) 与 NGT 相比,IGT 在 6 小时内整合的大多数餐后 FA 来源的摄取(NEFA+DFA 摄取)更高。DFA 占总心脏(19 [5-47]% 对 25 [10-40]%,P=0.08)和肝脏(22 [6-50]% 对 29 [15-52]%, P=0.04) IGT 与 NGT 的摄取。增加的脂肪组织 DFA 捕获预示着较低的肝脏 DFA 摄取,并且与较高的总心脏脂肪酸摄取有关。因此,在餐后 NEFA 通量增加的情况下,增强的脂肪组织 DFA 捕获不足以完全抑制超重前驱糖尿病患者餐后瘦器官 FA 摄取的增加(ClinicalTrials.gov;NCT02808182)。08) 和肝脏(22 [6-50]% 对比 29 [15-52]%,P=0.04)摄取 IGT 对比 NGT。增加的脂肪组织 DFA 捕获预示着较低的肝脏 DFA 摄取,并且与较高的总心脏脂肪酸摄取有关。因此,在餐后 NEFA 通量增加的情况下,增强的脂肪组织 DFA 捕获不足以完全抑制超重前驱糖尿病患者餐后瘦器官 FA 摄取的增加(ClinicalTrials.gov;NCT02808182)。08) 和肝脏(22 [6-50]% 对比 29 [15-52]%,P=0.04)摄取 IGT 对比 NGT。增加的脂肪组织 DFA 捕获预示着较低的肝脏 DFA 摄取,并且与较高的总心脏脂肪酸摄取有关。因此,在餐后 NEFA 通量增加的情况下,增强的脂肪组织 DFA 捕获不足以完全抑制超重前驱糖尿病患者餐后瘦器官 FA 摄取的增加(ClinicalTrials.gov;NCT02808182)。
更新日期:2022-06-24
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