Author(s): Karelis AD, Faraj M, Bastard JP, StPierre DH, Brochu M,
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Abstract OBJECTIVE: The purpose of this study was to investigate the inflammatory state in obese women displaying the "metabolically healthy but obese" (MHO) phenotype. DESIGN: We examined the metabolic characteristics of 88 obese, sedentary postmenopausal women. Subjects were classified as MHO or as "at risk" based on the upper and lower quartiles of insulin sensitivity as measured by the hyperinsulinemic-euglycemic clamp technique. Thereafter, we determined 1) body composition, 2) body fat distribution, 3) plasma lipid and lipoprotein levels, 4) glucose homeostasis, 5) resting blood pressure, 6) peak oxygen consumption, and 7) inflammation markers as potential modulators of differences in the coronary risk profile. RESULTS: Twenty-two MHO women displayed high insulin sensitivity (15.35 +/- 2.3 mg/min.kg fat-free mass), and 22 at risk subjects with low insulin sensitivity (7.98 +/- 1.4 mg/min.kg fat-free mass) were identified. Despite comparable total body fatness between groups (47.7 +/- 4.8 vs. 45.5 +/- 4.4\%; not significant), MHO individuals had significantly lower levels of visceral fat, fasting insulin, plasma triglycerides, high-sensitivity C-reactive protein (CRP), and alpha-1 antitrypsin levels and higher levels of high-density lipoprotein cholesterol than at risk individuals (P < 0.05). Stepwise regression analysis showed that CRP, fasting triglycerides, and the lean body mass index explained 19.5, 8.5, and 4.0\%, respectively, of the variance observed in glucose disposal (total r(2) = 0.320; P < 0.001). CONCLUSION: Results of the present study indicate that postmenopausal women displaying the MHO phenotype also have a favorable inflammation profile as shown by lower CRP and alpha-1 antitrypsin levels compared with insulin-resistant women. This suggests that a lower inflammation state, as attested by low CRP levels, could play a role in the protective profile of the MHO individual, and this may be associated metabolically to a lower risk for cardiovascular disease.
This article was published in J Clin Endocrinol Metab
and referenced in Journal of Metabolic Syndrome