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Impaired subcutaneous adipocyte lipogenesis is associated with systemic insulin resistance and increased apolipoprotein B/AI ratio in men and women
Author(s) -
Hoffstedt J.,
Förster D.,
Löfgren P.
Publication year - 2007
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.2007.01811.x
Subject(s) - lipogenesis , medicine , endocrinology , insulin resistance , adipocyte , insulin , body mass index , apolipoprotein b , metabolic syndrome , obesity , adipose tissue , cholesterol
. Objectives. To study the association between subcutaneous fat cell lipogenesis and components of the metabolic syndrome (systemic insulin resistance, dyslipidaemia and hypertension). Design and setting. A university hospital‐based cross‐sectional study of 383 subjects (303 women and 80 men) with a wide range of BMI (18–53 kg m −2 ). Results. Strong negative correlations between in vitro fat cell lipogenesis (basal and after maximal insulin stimulation) and HOMA‐IR were present in both genders ( r = −0.42 to −0.56, P < 0.0001 and r = −0.37 to −0.44, P < 0.001, for women and men respectively). Insulin sensitivity measured using the insulin tolerance test (K ITT ) was also correlated with adipocyte lipogenesis ( r = 0.47–0.57, P < 0.0001, women, r = 0.52–0.70, P < 0.001, men). Plasma apolipoprotein B/AI‐ratio negatively associated with fat cell lipogenesis in women ( r = −0.41 to−0.51, P < 0.0001,) and men ( r = −0.49 to −0.55, P < 0.0001). The negative relationship of fat cell lipogenesis with blood pressure was significant in women ( r = −0.27 to −0.28, P < 0.0002,) but not in men ( P = 0.08–0.09). All correlations remained significant after adjusting for differences in fat cell volume, body mass index, waist‐ to hip‐ ratio or age ( P < 0.01). Conclusions. Subcutaneous adipocyte lipogenesis is negatively associated with systemic insulin resistance, plasma apolipoprotein B/AI‐ratio and blood pressure supporting the view that impaired fat cell function per se may contribute to the development of the metabolic syndrome.