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Av. Diabetol. 2006;22(1):19-31

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Metabolic dysregulation in diabetes and HIV-associated insulin resistance: from fatty acids to fat distribution

Revisión - Vol.22 N.1  enero-marzo 2006
J.P.H. van Wijk1, J.W.F. Elte2, M. Castro Cabezas3

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Insulin resistance is one of the most important aspects of the metabolic dysregulation in diabetes and the metabolic syndrome. While most experts agree on the disturbed glucose-insulin axis in insulin resistance, the effects on lipid metabolism have received much less attention. Generally, fasting plasma triglycerides are slightly elevated and HDL cholesterol is diminished in the insulin resistance syndromes. Especially, the postprandial state seems to be one of the most important phases in which all the metabolic dysregulations come together. Postprandial lipemia itself is one of the causes of insulin resistance, and since postprandial lipemia is exaggerated in these syndromes, postprandial studies may be the best situation to investigate insulin resistance. Furthermore, postprandial hyperlipidemia has been closely linked to atherosclerosis making this the major risk factor in insulin resistance. One of the less well studied aspects of postprandial lipemia, which is closely related to insulin resistance, is peripheral fatty acid trapping and adipose tissue distribution. In HIV lipodystrophy, aberrant adipose tissue deposition and impaired peripheral fatty acid trapping are important determinants of many of the metabolic disturbances seen in this disorder. Therefore, HIV lipodystrophy is an interesting model to elucidate the molecular mechanisms regulating fatty acid trapping and adipose tissue distribution. Recent studies have clearly shown that components of the complement system play an important role in lipoprotein metabolism and fatty acid regulation. Especial attention has been drawn to the complement component 3 (C3) which is also a strong predictor of the metabolic syndrome. C3 is synthesized by adipose tissue during lipolysis of triglyceride rich lipoproteins. This process seems to be disturbed in different situations of insulin resistance like the metabolic syndrome, type 2 diabetes and familial combined hyperlipidemia. C3 may be a potential link between inflammation and lipoprotein dysmetabolism. Surprisingly, C3 concentrations are also modulated by several interventions designed to treat the me metabolic syndrome, like statins. Other inflammatory markers like leukocyte count and activation behave similar to C3 concentrations, especially during the postprandial phase. In this overview we will discuss several metabolic aspects of two examples of the insulin resistance syndrome, type 2 diabetes and HIV lipodystrophy.


Correspondencia: M. Castro Cabezas. Internist-endocrinologist/vascular specialist St. Franciscus Gasthuis. 
Center for Diabetes and Vascular Medicine Dpt. Of Internal Medicine. PO Box 10900. 3004 BA Rotterdam The Netherlands

Palabras clave

enfermedad cardiovascular Chylomicrons Fatty acids Triglycerides


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