Intestinal lipid absorption and transport in type 2 diabetes

Abstract

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.

Dyslipidemia Among Diabetes Mellitus Patients: A Case-Control Study From a Tertiary Care Hospital in South India

“…Similar findings were noted in previous studies from Turkey and India [19,22]. An increase in TC may be due to cholesterol absorption deficiency and higher cholesterol synthesis, especially among obese persons with diabetes, which suggests that diabetes modulates lipid metabolism [23,24].…”

Association of ApoE gene polymorphisms with serum lipid levels and the risk of type 2 diabetes mellitus in the Chinese Han population of central China

“…Our study showed that Apo-B levels are an independent risk factor for T2DM in the elderly Chinese population. Apo-B is a protein present on the surface of some lipoproteins, such as VLDL and LDL, which contain high levels of cholesterol ( Verges, 2022 ). The pancreas and other distal organs, such as the liver, receive lipids (cholesterol and triglycerides) via Apo-B ( Ying et al, 2021 ).…”

Vitamin E (α-Tocopherol) Does Not Ameliorate the Toxic Effect of Bisphenol S on the Metabolic Analytes and Pancreas Histoarchitecture of Diabetic Rats

“…This could be due to the metabolic demands of the sick subjects under experimentation; rats without metabolic alterations do not require nutrients available in the diet beyond those used for homeostatic balance. On the other hand, rats with DM require essential nutrients to compensate for the metabolic state of disease triggered by diabetes, using physiological digestive mechanisms and adaptations to absorb elements in the diet [93][94][95]. For example, studies suggest that in rats, diabetes induced by streptozotocin is connected to a rise in glucose absorption through the small intestinal mucosa [94,95] The observed out-of-range values in the Ctrl group in the serum biochemistry could be associated with a diet rich in fat, possibly produced by the oil used as the vehicle and the high protein in the diet.…”

“…On the other hand, rats with DM require essential nutrients to compensate for the metabolic state of disease triggered by diabetes, using physiological digestive mechanisms and adaptations to absorb elements in the diet [93][94][95]. For example, studies suggest that in rats, diabetes induced by streptozotocin is connected to a rise in glucose absorption through the small intestinal mucosa [94,95] The observed out-of-range values in the Ctrl group in the serum biochemistry could be associated with a diet rich in fat, possibly produced by the oil used as the vehicle and the high protein in the diet. According to dietary recommendations for rodents, a diet with around 14% protein is considered ideal for their organic maintenance [96].…”