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 β3-adrenoceptor sensitivity, but not β1 and β2-adrenoceptor sensitivities, differed significantly between the WHR subgroups (p = 0.0001). β3-adrenoceptor sensitivity was also related to the other components of the metabolic syndrome, although a strong covariation between WHR and β3-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 β3-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.
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Abbreviations
- ANOVA:
-
Analysis of variance
- BMI:
-
body mass index
- EC50 :
-
half-maximum agonist concentration
- NEFA:
-
non-esterified fatty acids
- HDL-cholesterol:
-
high density lipoprotein cholesterol
- VLDL:
-
very low density lipoproteins
- WHR:
-
waist-to-hip ratio
References
Bouchard C, Pérusse L (1993) Genetics of obesity. Ann Rev Nutr 13: 337–354
Giacobino J-P (1995) Beta3-adrenoceptor: an update. Eur J Endocrinol 132: 377–385
Lönnqvist F, Thörne A, Nilsell K, Hoffstedt J, Amer P (1995) A pathogenetic role of visceral fat β3-adrenoceptors in obesity. J Clin Invest 95: 1109–1116
Walston J, Silver K, Bogardus C, et al. (1995) Time of onset of non-insulin-dependent diabetes mellitus and genetic variation in the β3-adrenergic-receptor gene. N Engl J Med 333: 343–347
Widén E, Lehto M, Kanninen T, Walston J, Shuldiner AR, Groop LC (1995) Association of a polymorphism in the β3-adrenergic-receptor gene with features of the insulin resistance syndrome in Finns. N Engl J Med 333: 348–351
Clément K, Vaisse C, Manning BSJ, et al. (1995) Genetic variation in the β3-adrenergic receptor and an increased capacity to gain weight in patients with morbid obesity. N Engl J Med 333: 352–354
Kadowaki H, Yasuda K, Iwamoto K, et al. (1995) A mutation in the β3-adrenergic receptor gene is associated with obesity and hyperinsulinemia in Japanese subjects. Biochem Biophys Res Commun 215: 555–560
Birnbaumer M (1995) Mutations and diseases of G protein coupled receptors. J Rec Signal Trans Res 15: 131–160
Fujisawa T, Ikegama H, Yamoto E, et al. (1996) Association of Trp64Arg mutation of the beta3-adrenergic receptor with NIDDM and body-weight gain. Diabetologia 39: 349–352
Granneman JG, Lahners KN, Chaudry A (1991) Molecular cloning and expression of the rat beta3-adrenergic receptor. Mol Pharmacol 40: 895–899
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Hoffstedt, J., Wahrenberg, H., Thörne, A. et al. The metabolic syndrome is related to β3-adrenoceptor sensitivity in visceral adipose tissue. Diabetologia 39, 838–860 (1996). https://doi.org/10.1007/s001250050518
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DOI: https://doi.org/10.1007/s001250050518