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The extended postprandial phase in diabetes.

D Owens1

  • 1Department of Diabetes and Endocrinology, Trinity College, The Adelaide and Meath Hospital, Tallaght, Dublin 24, Ireland. daowens@tcd.ie

Biochemical Society Transactions
|September 25, 2003
PubMed
Summary

Diabetes disrupts lipoprotein metabolism, particularly non-esterified fatty acids, accelerating atherosclerosis and cardiovascular disease. This review examines key alterations in lipid pathways contributing to plaque formation in diabetic patients.

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Area of Science:

  • Cardiovascular Medicine
  • Endocrinology
  • Metabolic Syndrome

Background:

  • Atherosclerosis is a significant complication of diabetes, but its underlying mechanisms remain unclear.
  • Metabolic changes during the postprandial phase in diabetes are critical factors in understanding this link.

Purpose of the Study:

  • To examine the metabolic alterations in diabetes that contribute to atherosclerosis.
  • To investigate the role of non-esterified fatty acids and lipoprotein metabolism in diabetic cardiovascular complications.

Main Methods:

  • Review of existing literature on diabetes, lipid metabolism, and atherosclerosis.
  • Examination of metabolic effects of insulin deficiency, focusing on non-esterified fatty acids.
  • Analysis of lipoprotein particle formation, including chylomicrons and low-density lipoproteins.

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Main Results:

  • Insulin deficiency impairs the suppression of non-esterified fatty acids, impacting lipoprotein formation.
  • Alterations in microsomal triacylglycerol transfer protein and apolipoprotein B48 influence intestinally derived lipoproteins.
  • Diabetic patients exhibit modified low-density lipoprotein particles, promoting an atherogenic profile.

Conclusions:

  • The lipoprotein cascade is severely disrupted in diabetes, with abnormal non-esterified fatty acid metabolism being a key issue.
  • These disruptions accelerate cholesterol deposition and plaque instability, contributing to increased cardiovascular disease in diabetes.