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Molecular regulators of lipid metabolism in the intestine - Underestimated therapeutic targets for obesity?

机译:肥胖症肠道肠道脂质代谢的分子调节剂 - 肥胖症的低估治疗靶标?

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摘要

The incidence of obesity and type 2 diabetes continues to rise across the globe necessitating the need to identify new therapeutic approaches to manage these diseases. In this review, we explore the potential for therapeutic interventions focussed on the intestinal epithelium, by targeting the role of this tissue in lipid uptake, lipid-mediated cross talk and lipid oxidation. We focus initially on ongoing strategies to manage obesity by targeting the essential role of the intestinal epithelium in lipid uptake, and in mediating tissue cross talk to regulate food intake. Subsequently, we explore a previously underestimated capacity of intestinal epithelial cells to oxidize fatty acids. In this context, we describe recent findings which have unveiled a key role for the peroxisome proliferator-activated receptor (PPAR) family of nuclear receptors and histone deacetylases (HDACs) in the regulation of lipid oxidation genes in enterocytes and how targeted genetic manipulation of these factors in enterocytes reduces weight gain, identifying intestinal PPARs and HDACs as potential therapeutic targets in the management of obesity.
机译:肥胖症和2型糖尿病的发病率仍在全球范围内升起,这需要确定新的治疗方法来管理这些疾病。在本综述中,我们探讨治疗干预措施的潜力,其通过靶向该组织在脂质摄取,脂质介导的交谈和脂质氧化中的作用。我们最初关注持续的策略来管理肥胖症,以靶向肠上皮在脂质摄取,并在调解组织交叉谈中来调节食物摄入量。随后,我们探讨了以前低估了肠上皮细胞以氧化脂肪酸的能力。在这种情况下,我们描述了最近对肠细胞脂质氧化基因的调控中的过氧化物酶促增殖物激活的受体(PPAR)系列核受体和组蛋白脱乙酰基酶(HDAC)的关键作用。这些肠细胞的因素减轻了体重增加,鉴定肠道PPAR和HDAC,作为肥胖管理中的潜在治疗目标。

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