The metabolic syndrome is related to b 3-adrenoceptor sensitivity in visceral adipose tissue |
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Authors: | J. Hoffstedt H. Wahrenberg A. Th?rne F. L?nnqvist |
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Affiliation: | (1) Department of Medicine, and the Research Center at Huddinge University Hospital, Karolinska Institute, Huddinge, Sweden, SE;(2) Department of Surgery, Huddinge University Hospital, Karolinska Institute, Huddinge, Sweden, SE |
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Abstract: | Summary The metabolic syndrome is a well-known risk for the development of cardiovascular disease. In the present study the possible importance of an altered visceral adipocyte β -adrenoceptor function in this syndrome was investigated. In 65 subjects of both sexes undergoing elective surgery for non-malignant disorders, the metabolic syndrome phenotype and the lipolytic sensitivity for various β -adrenoceptor subtype agonists in omental adipocytes were determined. The study group represented a wide range of abdominal adipose tissue distribution (waist-to-hip ratios 0.76–1.13), but was otherwise apparently healthy. The subjects were divided into three subgroups according to their waist-to-hip (WHR) ratios: 1) WHR < 0.92; 2) WHR 0.92–1.04; 3) WHR > 1.04. The subgroups demonstrated significant differences regarding body mass index, sagittal diameter, systolic and diastolic blood pressures, plasma concentrations of glucose, insulin, triglycerides and HDL-cholesterol (p = 0.005–0.0001). Furthermore, in omental adipocytes β 3-adrenoceptor sensitivity, but not β 1- and β 2-adrenoceptor sensitivities, differed significantly between the WHR subgroups (p = 0.0001). β 3-adrenoceptor sensitivity was also related to the other components of the metabolic syndrome, although a strong covariation between WHR and β 3-adrenoceptor sensitivity vs blood pressure and the metabolic parameters was found. The present data provide evidence of a relationship between upper-body obesity and its associated metabolic complications and also, an increased visceral fat β 3-adrenoceptor sensitivity. We suggest that the latter finding results in an augmented release of non-esterified fatty acids from the visceral fat depot to the portal venous system. This may in turn contribute to the development of the metabolic syndrome. [Diabetologia (1996) 39: 838–844] Received: 15 September 1995 and in final revised form: 24 January 1996 |
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Keywords: | Adipocytes β 3-adrenoceptors insulin resistance metabolic syndrome visceral fat. |
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