Abstract
PurposeWe studied effects of diet-induced postmenopausal weight loss on gene expression and activity of proteins involved in lipogenesis and lipolysis in adipose tissue.MethodsFifty-eight postmenopausal women with overweight (BMI 32.5 ± 5.5) were randomized to eat an ad libitum Paleolithic-type diet (PD) aiming for a high intake of protein and unsaturated fatty acids or a prudent control diet (CD) for 24 months. Anthropometry, plasma adipokines, gene expression of proteins involved in fat metabolism in subcutaneous adipose tissue (SAT) and lipoprotein lipase (LPL) activity and mass in SAT were measured at baseline and after 6 months. LPL mass and activity were also measured after 24 months.ResultsThe PD led to improved insulin sensitivity (P < 0.01) and decreased circulating triglycerides (P < 0.001), lipogenesis-related factors, including LPL mRNA (P < 0.05), mass (P < 0.01), and activity (P < 0.001); as well as gene expressions of CD36 (P < 0.05), fatty acid synthase, FAS (P < 0.001) and diglyceride acyltransferase 2, DGAT2 (P < 0.001). The LPL activity (P < 0.05) and gene expression of DGAT2 (P < 0.05) and FAS (P < 0.05) were significantly lowered in the PD group versus the CD group at 6 months and the LPL activity (P < 0.05) remained significantly lowered in the PD group compared to the CD group at 24 months.ConclusionsCompared to the CD, the PD led to a more pronounced reduction of lipogenesis-promoting factors in SAT among postmenopausal women with overweight. This could have mediated the favorable metabolic effects of the PD on triglyceride levels and insulin sensitivity.
Highlights
IntroductionAbdominal obesity, is a major cause of morbidity and mortality
Obesity, abdominal obesity, is a major cause of morbidity and mortality
The orthogonal partial least squares analysis (OPLS) analysis included the following variables: Fat distribution, blood lipids, insulin sensitivity, gene expression and activity levels of key proteins involved in lipogenesis and lipolysis, and adipokines (Fig. 1), at 6 months
Summary
Abdominal obesity, is a major cause of morbidity and mortality. The prevalence of abdominal adiposity increases after menopause and is associated with an increased risk for metabolic disease [1]. Adipose tissue stores energy as triacylglycerols (TGs) in lipid droplets formed through lipogenesis, and fatty acids (FAs) are released from these stored TGs via lipolysis. Both processes are reportedly elevated in insulin-resistant individuals with obesity compared to insulin-sensitive individuals with obesity [2]. Elevated formation of FFAs and DAGs due to increased lipolysis in adipose tissue, may contribute to impaired intracellular insulin signaling, i.e., insulin resistance [2]
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