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Propionic acid and butyric acid inhibit lipolysis and de novo lipogenesis and increase insulin-stimulated glucose uptake in primary rat adipocytes

机译:丙酸和丁酸抑制脂肪分解和新生脂肪形成并增加胰岛素刺激的原代大鼠脂肪细胞的葡萄糖摄取

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摘要

Fermentation of dietary fibers by colonic microbiota generates short-chain fatty acids (SCFAs), e.g., propionic acid and butyric acid, which have been described to have “anti-obesity properties” by ameliorating fasting glycaemia, body weight and insulin tolerance in animal models. In the present study, we therefore investigate if propionic acid and butyric acid have effects on lipolysis, de novo lipogenesis and glucose uptake in primary rat adipocytes. We show that both propionic acid and butyric acid inhibit isoproterenol- and adenosine deaminase-stimulated lipolysis as well as isoproterenol-stimulated lipolysis in the presence of a phosphodiesterase (PDE3) inhibitor. In addition, we show that propionic acid and butyric acid inhibit basal and insulin-stimulated de novo lipogenesis, which is associated with increased phosphorylation and thus inhibition of acetyl CoA carboxylase, a rate-limiting enzyme in fatty acid synthesis. Furthermore, we show that propionic acid and butyric acid increase insulin-stimulated glucose uptake. To conclude, our study shows that SCFAs have effects on fat storage and mobilization as well as glucose uptake in rat primary adipocytes. Thus, the SCFAs might contribute to healthier adipocytes and subsequently also to improved energy metabolism with for example less circulating free fatty acids, which is beneficial in the context of obesity and type 2 diabetes.
机译:结肠微生物群对膳食纤维的发酵会产生短链脂肪酸(SCFA),例如丙酸和丁酸,在动物模型中通过改善空腹血糖,体重和胰岛素耐受性,这些脂肪酸被描述为具有“抗肥胖特性” 。因此,在本研究中,我们因此调查丙酸和丁酸是否对原代大鼠脂肪细胞中的脂肪分解,新生脂肪形成和葡萄糖摄取有影响。我们显示丙酸和丁酸在磷酸二酯酶(PDE3)抑制剂的存在下均抑制异丙肾上腺素和腺苷脱氨酶刺激的脂解以及异丙肾上腺素刺激的脂解。此外,我们显示丙酸和丁酸抑制基础和胰岛素刺激的从头脂肪生成,这与磷酸化增加有关,从而抑制了乙酰辅酶A羧化酶(一种脂肪酸合成中的限速酶)。此外,我们表明丙酸和丁酸增加胰岛素刺激的葡萄糖摄取。总而言之,我们的研究表明SCFA对大鼠原代脂肪细胞中的脂肪存储和动员以及葡萄糖摄取具有影响。因此,SCFA可能有助于更健康的脂肪细胞,并随后也以例如更少的循环游离脂肪酸促进能量代谢,这在肥胖症和2型糖尿病的背景下是有益的。

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