Abstract
Atherogenic effects of postprandial lipoproteins are supported by many studies comparing patients with advanced clinical signs or early markers of cardiovascular disease with subjects without vascular disease. Postprandial lipoprotein abnormalities are more frequent in individuals with type 2 diabetes and other states of insulin resistance, which could be a major factor accounting for the higher rate of cardiovascular diseases observed in these conditions. In patients with type 2 diabetes multiple abnormalities of lipoproteins of both endogenous and exogenous origin are observed also in the presence of good blood glucose control and normal fasting triglyceridaemia, and a direct role of insulin resistance in the development of postprandial dyslipidaemia has been demonstrated. Clinical and experimental studies have demonstrated that a high fat consumption is associated with impaired insulin sensitivity and may worsen postprandial hypertriglyceridemia in individuals with type 2 diabetes and/or hyperlipidaemia. In addition to the amount of fat also the physical structure of the food in which fat is present is able to influence postprandial lipaemia. Data on the effects of dietary fatty acid (FA) modifications in humans are scarce. These studies have provided some evidence that dietary polyunsaturated FA, particularly those of the n-3 class, induce an attenuated postprandial lipaemic response as compared to saturated FA (SFA) and monounsaturated FA (MUFA); however, the data are often conflicting and their interpretation is, generally, controversial. Very little is known in patients with type 2 diabetes, in whom both insulin sensitivity and postprandial lipaemia are particularly relevant. In a medium term (3 weeks) study in type 2 diabetic patients, a MUFA rich diet did not modify insulin sensitivity as compared to the SFA rich diet. The MUFA diet induced a higher early peak of chylomicrons and a significantly lower postprandial response o f small VLDL after a standard test meal, rich in saturated fat. In conclusion, postprandial lipoprotein abnormalities are a frequent feature of type 2 diabetes and of other conditions clustering with insulin resistance. The total amount of fat, more than the specific type of fatty acid, seems to influence postprandial lipoproteins. Data are needed on long term interventions as well as on the interactions between dietary fat and other food components or physical structure. Keywords: postprandial lipoproteins; metabolism of dietary fat
Highlights
The ingested fat is emulsified with bile acids and phospholipids in the small intestine, it is hydrolysed by pancreatic enzymes to cholesterol, free fatty acids (FFAs) and monoglycerides, which are absorbed from the small intestine into mucosal cells
This study shows that in insulinsensitive subjects the postprandial triglyceride and FFA responses are dependent on the amount of oral fat and are reduced when glucose is added to the fat load
Postprandial lipoprotein abnormalities are a frequent feature of type 2 diabetes and of other conditions clustering with insulin resistance
Summary
The ingested fat is emulsified with bile acids and phospholipids in the small intestine, it is hydrolysed by pancreatic enzymes to cholesterol, free fatty acids (FFAs) and monoglycerides, which are absorbed from the small intestine into mucosal cells. The lipids are re-esterified to form cholesterol esters and triglycerides. These are combined with free cholesterol, several apolipoproteins (ApoA, ApoB48) and phospholipids into chylomicrons, which are secreted into the lymphatic system and, via the thoracic duct, reach the blood. Chylomicrons bind to lipoprotein lipase (LPL) on the luminal surface of the capillary endothelial cells. LPL hydrolyses chylomicron triglycerides producing FFAs, which freely diffuse into cells where they are either oxidized for energy utilization or re-esterified for storage. Chylomicron remnants are cholesteryl ester enriched and maintain their content of ApoB48 and ApoE. Receptors for chylomicron remnants recognize ApoE on the surface of the lipoproteins. M vs 20 controls 61 M vs 40 controls 32 M with AMI vs 10 controls 85 M'/F vs 85 controls 16 M vs 16 controls
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