Postprandial dyslipidemia: an atherogenic disorder common in patients with diabetes mellitus
Section snippets
Lipoprotein metabolism and physiology
The major neutral lipids transported through the bloodstream—esterified cholesterol and triglycerides—are insoluble in aqueous solutions and, therefore, must be protected from plasma by a coating of both hydrophobic and hydrophilic amphipathic molecules. Lipoproteins are macromolecular complexes that provide protection in carrying various lipids and proteins in plasma.6 Several major classes of lipoproteins have been defined by their physical-chemical characteristics: (1) chylomicrons; (2)
Postprandial lipoprotein metabolism
Under normal conditions, both postprandial plasma levels of triglycerides and the conversion of VLDL particles to LDL are controlled by a dynamic metabolic process involving the enzymes lipoprotein lipase and hepatic lipase.8 Lipoprotein lipase converts lipoprotein triglyceride into free fatty acids, monoglycerides, and diglycerides, thus permitting the uptake of fatty acids by peripheral tissues. Hepatic lipase removes triglycerides and phospholipids from chylomicron remnants and VLDL
Abnormal postprandial lipoprotein metabolism in diabetes
Patients with type 1 diabetes mellitus with very good glycemic control can have normal postprandial lipid levels. However, as glycemic control worsens because of inadequate insulin, lipoprotein lipase activity decreases, and postprandial hyperlipidemia can result. In patients with type 2 diabetes, the underlying insulin resistance can be associated with mild reductions in lipoprotein lipase, but overproduction of VLDL is a major problem. Increased VLDL competes with chylomicrons for lipoprotein
Therapy for lipoprotein disorders
Because the diabetic patient with no evidence of atherosclerosis carries a risk for a subsequent cardiovascular event that is comparable to the risk for persons without diabetes with known cardiovascular disease, diabetic hyperlipidemia should be treated aggressively.3 According to the National Cholesterol Education Program (NCEP), the goal of lipoprotein therapy for adults with <2 cardiovascular risk factors is an LDL cholesterol level <160 mg/dL; for patients with ≥2 risk factors, an LDL
Conclusion
The increased risk of coronary artery disease that is now well documented for patients with diabetes mellitus is attributable in part to the lipoprotein abnormalities associated with diabetes. Physicians have gained a better understanding of the specific disorders of lipoprotein metabolism that are common in this population, based on 2 pieces of evidence: (1) that postprandial triglyceride-rich lipoproteins are atherogenic and (2) that the disordered metabolism of VLDL and/or chylomicrons may
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Mean postprandial triglyceride concentration is an independent risk factor for carotid atherosclerosis in patients with type 2 diabetes
2014, Clinica Chimica ActaCitation Excerpt :Insulin resistance induces and exaggerates these abnormalities and promotes the formation of sd-LDLs [6,24–26]. In addition, high TRLs in the postprandial state may also contribute to proatherosclerotic and prothrombotic processes, including inflammation, oxidative stress, and endothelial dysfunction [20,24,25]. The mean-PTG concentration has some advantages over other markers related to TRLs, such as sd-LDL, apo CIII, and RLP-C. For example, the sd-LDL concentration is higher in patients with diabetes than in healthy subjects.
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2012, Endocrinologia y NutricionCitation Excerpt :In the capillaries of the adipose and muscular tissues, the kilomicrons interact with lipase lipoprotein (LPL) and its nucleus (that contain triglycerides) is hydrolyzed.47 The products of the hydrolysed triglycerides – the free fatty acids – through lipase lipoprotein (LPL) can be stored in the adipocytes or used by the muscular cells as a source of energy.47 Post-prandial lipemia has been suggested as a risk factor for coronary heart disease.44
A review of the putative causal mechanisms associated with lower macular pigment in diabetes mellitus
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