title: The metabolic syndrome is related to beta 3-adrenoceptor sensitivity in visceral adipose tissue.
abstract: 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 beta-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 beta-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 beta 3-adrenoceptor sensitivity, but not beta 1-and beta 2-adrenoceptor sensitivities, differed significantly between the WHR subgroups (p = 0.0001). beta 3-adrenoceptor sensitivity was also related to the other components of the metabolic syndrome, although a strong covariation between WHR and beta 3-adrenoceptor sensitivity vs blood pressure and the metabolic parameters was found. The present data provide evidence of a relationship between upperbody obesity and its associated metabolic complications and also, an increased visceral fat beta 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.
authors.affiliation: Department of Medicine, Huddinge University Hospital, Karolinska Institute, Sweden.
authors.forename: J
authors.initials: J
authors.lastname: Hoffstedt
authors.forename: H
authors.initials: H
authors.lastname: Wahrenberg
authors.forename: A
authors.initials: A
authors.lastname: Thörne
authors.forename: F
authors.initials: F
authors.lastname: Lönnqvist
mesh_terms: D000273:Adipose Tissue / Q000737:chemistry / Q000378:metabolism*; D000328:Adult; D000704:Analysis of Variance; D001794:Blood Pressure / Q000502:physiology; D001824:Body Constitution; D008076:Cholesterol, HDL / Q000097:blood; D015331:Cohort Studies; D005260:Female; D018149:Glucose Intolerance / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000378:metabolism; D015228:Hypertriglyceridemia / Q000378:metabolism; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology*; D016014:Linear Models; D008066:Lipolysis; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000378:metabolism; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*; D022702:Receptors, Adrenergic, beta-3; D012680:Sensitivity and Specificity; D012737:Sex Factors; D013577:Syndrome; D014781:Viscera / Q000378:metabolism*
chemical_list: D008076:Cholesterol, HDL; D007328:Insulin; D011943:Receptors, Adrenergic, beta; D022702:Receptors, Adrenergic, beta-3