The objective of the study was to determine whether plasma migration inhibitor factor (MIF) concentration and mononuclear cell (MNC) mRNA are elevated in obesity and whether treatment with metformin reduces plasma MIF concentration. Forty obese subjects [body mass index (BMI), 37.5 +/- 4.9 kg/m(2)] and 40 nonobese healthy subjects (BMI, 22.6 +/- 3.4 kg/m(2)) had their plasma MIF, glucose, insulin, free fatty acids (FFAs) and C-reactive protein (CRP) concentrations measured. Sixteen obese patients and 16 nonobese healthy subjects had RNA prepared from MNCs. Eight obese subjects with normal glucose concentration were treated with metformin 1 g (Glucophage XR; 1000 mg twice daily) twice daily for 6 wk. Eight obese subjects were used as controls. Plasma concentration of glucose, insulin, FFAs, and MIF was measured by appropriate assays. mRNA for MIF was measured by real-time PCR. Forty obese subjects had a fasting concentration of MIF of 2.8 +/- 2.0 ng/ml, whereas 40 nonobese subjects had a fasting MIF concentration of 1.2 +/- 0.6 ng/ml (P < 0.001). Plasma MIF concentrations were significantly related to BMI (r = 0.52; P < 0.001). mRNA for MIF was correlated to plasma FFAs (r = 0.40; P < 0.05) and plasma CRP (r = 0.42; P < 0.05) concentrations. Eight obese subjects had their fasting blood samples taken before and after taking a slow-release preparation of metformin at 1, 2, 4, and 6 wk. The mean plasma concentration fell from 2.3 +/- 1.4 to 1.6 +/- 1.2 ng/ml at 6 wk (P < 0.05). Obese subjects not on treatment with metformin showed no change. During the period of treatment with metformin, the body weight did not change and the plasma concentration of glucose, insulin, and FFAs did not alter. We conclude that: 1) plasma MIF concentrations and MIF mRNA expression in the MNCs are elevated in the obese, consistent with a proinflammatory state in obesity; 2) these increases in MIF are related to BMI, FFA concentrations, and CRP; 3) metformin suppresses plasma MIF concentrations in the obese, suggestive of an antiinflammatory effect of this drug; and 4) this action of metformin may contribute to a potential antiatherogenic effect, which may have implications for the reduced cardiovascular mortality observed with metformin therapy in type 2 diabetes mellitus.
High serum insulin and lipoproteins have been reported in pregnancy-induced hypertension. Little is known about the insulin and lipoprotein profile in Indian women. To address this question we compared serum insulin and lipoproteins of women with pregnancy induced hypertension (PIH) and normotensive pregnant women. The serum insulin, triglycerides, total cholesterol and HDL cholesterol of 104 women with PIH were compared with 99 control women. Hypertensive women had significantly higher insulin (53.94 +/- 29.58 versus 37.69 +/- 17.39 pmol/L, p=0.0004) and triglyceride (3.27 +/- 1.2 versus 2.66 +/- 0.6, p=0.0001). There was no significant difference in total cholesterol and HDL cholesterol levels. Insulin levels had a positive correlation with systolic blood pressure (r=0.64) and diastolic blood pressure (r=0.55) in women with PIH. These differences persisted even after adjusting for possible confounding variables such as age, body mass index and the period of gestation. We conclude that elevated serum insulin values or insulin resistance may contribute to the pathogenesis of PIH in Indian women.
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