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Metabolic syndrome 

Metabolic syndrome
Chapter:
Metabolic syndrome
Author(s):

Harold E. Lebovitz

DOI:
10.1093/med/9780199235292.003.1362
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date: 19 June 2019

The metabolic syndrome (MetS) has been recognized as a clinical entity for more than 50 years. In 1947, Vague described upper body obesity as a predisposing factor in the development of diabetes mellitus, atherosclerosis, and gout. Reaven, in his 1988 Banting lecture, focused on the importance of insulin resistance and a related cluster of metabolic abnormalities that were associated with an increase in coronary artery disease (1). This cluster included resistance to insulin-stimulated glucose uptake, glucose intolerance, hyperinsulinaemia, increased very-low-density lipoprotein (VLDL) triglyceride, decreased high-density lipoprotein (HDL) cholesterol, and hypertension. He called this cluster ‘syndrome X’, and raised the possibility that resistance to insulin-stimulated glucose uptake and hyperinsulinaemia were involved in the aetiology of the metabolic abnormalities and the clinical diseases associated with them. Obesity and, particularly, visceral obesity have been recognized as a major contributor to the MetS since precise techniques to quantitate regional body composition became available. The MetS was initially thought of as an insulin resistance syndrome, implying that insulin resistance was the underlying unifying abnormality.

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