Postprandial hyperlipidaemia is an important feature of diabetic dyslipidaemia and plays an important role in the development of cardiovascular disease in individuals with type 2 diabetes. Postprandial hyperlipidaemia in type 2 diabetes is secondary to increased chylomicron production by the enterocytes and delayed catabolism of chylomicrons and chylomicron remnants. Insulin and some intestinal hormones (e.g. glucagon-like peptide-1 [GLP-1]) influence intestinal lipid metabolism. In individuals with type 2 diabetes, insulin resistance and possibly reduced GLP-1 secretion are involved in the pathophysiology of postprandial hyperlipidaemia. Several factors are involved in the overproduction of chylomicrons: (1) increased expression of microsomal triglyceride transfer protein, which is a key enzyme in chylomicron synthesis; (2) higher stability and availability of apolipoprotein B-48; and (3) increased de novo lipogenesis. Individuals with type 2 diabetes present with disorders of cholesterol metabolism in the enterocytes with reduced absorption and increased synthesis. The increased production of chylomicrons in type 2 diabetes is also associated with a reduction in their catabolism, mostly because of a reduction in activity of lipoprotein lipase. Modification of the microbiota, which is observed in type 2 diabetes, may also generate disorders of intestinal lipid metabolism, but human data remain limited. Some glucose-lowering treatments significantly influence intestinal lipid absorption and transport. Postprandial hyperlipidaemia is reduced by metformin, pioglitazone, alpha-glucosidase inhibitors, dipeptidyl peptidase 4 inhibitors and GLP-1 agonists. The most pronounced effect is observed with GLP-1 agonists, which reduce chylomicron production significantly in individuals with type 2 diabetes and have a direct effect on the intestine by reducing the expression of genes involved in intestinal lipoprotein metabolism. The effect of sodium–glucose cotransporter 2 inhibitors on intestinal lipid metabolism needs to be clarified.

Graphical abstract

中文翻译：

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2型糖尿病的肠道脂质吸收和转运

餐后高脂血症是糖尿病血脂异常的一个重要特征，在 2 型糖尿病患者心血管疾病的发生发展中起重要作用。2 型糖尿病的餐后高脂血症继发于肠细胞产生的乳糜微粒增加以及乳糜微粒和乳糜微粒残余物的分解代谢延迟。胰岛素和一些肠道激素（例如胰高血糖素样肽-1 [GLP-1]）影响肠道脂质代谢。在 2 型糖尿病患者中，胰岛素抵抗和可能减少的 GLP-1 分泌与餐后高脂血症的病理生理有关。几个因素与乳糜微粒的过量产生有关：（1）微粒体甘油三酯转移蛋白的表达增加，这是乳糜微粒合成的关键酶；(2)载脂蛋白B-48的稳定性和可用性更高；(3) 增加从头脂肪生成。患有 2 型糖尿病的个体在肠细胞中存在胆固醇代谢紊乱，吸收减少和合成增加。2 型糖尿病中乳糜微粒产生的增加也与其分解代谢的减少有关，这主要是因为脂蛋白脂肪酶的活性降低。在 2 型糖尿病中观察到的微生物群的改变也可能导致肠道脂质代谢紊乱，但人类数据仍然有限。一些降糖治疗显着影响肠道脂质吸收和转运。二甲双胍、吡格列酮、α-葡萄糖苷酶抑制剂、二肽基肽酶 4 抑制剂和 GLP-1 激动剂可降低餐后高脂血症。使用 GLP-1 激动剂观察到最显着的效果，它显着减少 2 型糖尿病患者的乳糜微粒产生，并通过减少参与肠道脂蛋白代谢的基因的表达对肠道产生直接影响。钠-葡萄糖协同转运蛋白 2 抑制剂对肠道脂质代谢的影响需要阐明。

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