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胰岛素通过控制甘油代谢和增加脂肪生成来控制三酰甘油合成。

Insulin Controls Triacylglycerol Synthesis through Control of Glycerol Metabolism and Despite Increased Lipogenesis.

机构信息

Department of Biochemistry and Molecular Biomedicine, Faculty of Biology, University of Barcelona, 08028 Barcelona, Spain.

Faculty of Medicine, Universidad Nacional del Centro del Perú, 12006 Huancayo, Perú.

出版信息

Nutrients. 2019 Feb 28;11(3):513. doi: 10.3390/nu11030513.

DOI:10.3390/nu11030513
PMID:30823376
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6470968/
Abstract

Under normoxic conditions, adipocytes in primary culture convert huge amounts of glucose to lactate and glycerol. This "wasting" of glucose may help to diminish hyperglycemia. Given the importance of insulin in the metabolism, we have studied how it affects adipocyte response to varying glucose levels, and whether the high basal conversion of glucose to 3-carbon fragments is affected by insulin. Rat fat cells were incubated for 24 h in the presence or absence of 175 nM insulin and 3.5, 7, or 14 mM glucose; half of the wells contained C-glucose. We analyzed glucose label fate, medium metabolites, and the expression of key genes controlling glucose and lipid metabolism. Insulin increased both glucose uptake and the flow of carbon through glycolysis and lipogenesis. Lactate excretion was related to medium glucose levels, which agrees with the purported role of disposing excess (circulating) glucose. When medium glucose was low, most basal glycerol came from lipolysis, but when glucose was high, release of glycerol via breakup of glycerol-3P was predominant. Although insulin promotes lipogenesis, it also limited the synthesis of glycerol-3P from glucose and its incorporation into acyl-glycerols. We assume that this is a mechanism of adipose tissue defense to avoid crippling fat accumulation which has not yet been described.

摘要

在常氧条件下,原代培养的脂肪细胞将大量的葡萄糖转化为乳酸和甘油。这种“浪费”葡萄糖的行为可能有助于降低高血糖。鉴于胰岛素在代谢中的重要性,我们研究了它如何影响脂肪细胞对不同葡萄糖水平的反应,以及胰岛素是否会影响葡萄糖向 3 碳片段的高基础转化率。将大鼠脂肪细胞在存在或不存在 175 nM 胰岛素以及 3.5、7 或 14 mM 葡萄糖的情况下孵育 24 小时;一半的孔含有 C-葡萄糖。我们分析了葡萄糖标记物的命运、培养基代谢物以及控制葡萄糖和脂质代谢的关键基因的表达。胰岛素增加了葡萄糖摄取和通过糖酵解和脂肪生成的碳通量。乳酸排泄与培养基葡萄糖水平有关,这与处理多余(循环)葡萄糖的作用一致。当培养基葡萄糖较低时,大多数基础甘油来自脂肪分解,但当葡萄糖较高时,通过甘油-3P 的分解释放甘油占主导地位。尽管胰岛素促进脂肪生成,但它也限制了葡萄糖合成甘油-3P 及其掺入酰基甘油。我们假设这是脂肪组织防御的一种机制,以避免尚未描述的破坏性脂肪积累。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/6470968/959743d0d4cc/nutrients-11-00513-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/6470968/aa2e948ab933/nutrients-11-00513-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/6470968/e2f9b9c7922e/nutrients-11-00513-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/6470968/6819b4563710/nutrients-11-00513-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/6470968/959743d0d4cc/nutrients-11-00513-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/6470968/aa2e948ab933/nutrients-11-00513-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/6470968/add71f9a469f/nutrients-11-00513-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/6470968/558a2638d06d/nutrients-11-00513-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/6470968/e2f9b9c7922e/nutrients-11-00513-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/6470968/6819b4563710/nutrients-11-00513-g005.jpg
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