Obesity is a well-known risk factor for the development of insulin resistance, type 2 diabetes, dyslipidemia, hypertension, and cardiovascular disease. Rather than the total amount of fat, central distribution of adipose tissue is very important in the pathophysiology of this constellation of abnormalities termed metabolic syndrome. Adipose tissue, regarded only as an energy storage organ until the last decade, is now known as the biggest endocrine organ of the human body. This tissue secretes a number of substances--adipocytokines--with multiple functions in metabolic profile and immunological process. Therefore, excessive fat mass may trigger metabolic and hemostatic disturbances as well as CVD. Adipocytokines may act locally or distally as inflammatory, immune or hormonal signalers. In this review we discuss visceral obesity, the potential mechanisms by which it would be related to insulin resistance, methods for its assessment and focus on the main adipocytokines expressed and secreted by the adipose tissue. Particularly, we review the role of adiponectin, leptin, resistin, angiotensinogen, TNF-alpha, and PAI-1, describing their impact on insulin resistance and cardiovascular risk, based on more recent findings in this area.

Our findings suggest that both metformin and simvastatin have similar beneficial effects on low-grade inflammation, in addition to their classical effects on glucose and lipid metabolism. Moreover, they confirm the importance of treating at-risk individuals even before the precipitation of overt diabetes mellitus or full-blown metabolic syndrome.

BackgroundDouble diabetes (DD) describes both individuals with obesity upon diagnosis of type 1 diabetes and those who have gained weight during follow-up, although cardiovascular risk factors (CVRF) are not well understood in this group. We aim to evaluate the frequency of DD in a real-world type 1 diabetes sample and the interaction of insulin treatment with CVRF.MethodsMulticentre cross-sectional study of 2711 individuals with clinical diagnosis of type 1 diabetes from secondary diabetes centres in 20 Brazilian cities.ResultsPatients with diabetes duration <5 and ≥5 years had similar frequency of overweight (20.4 vs. 25 %) and obesity, (9.8 vs. 6.1 %), p 0.28 for trend. Insulin dose (U/kg/day) was lower in obese individuals compared to normal BMI, with mean (95 % CI) 0.72 (0.62–0.83) vs. 0.88 (0.84–0.92) U/kg/day for diabetes duration <5 years and 0.84 (0.77–0.92) vs. 0.99 (0.97–1.01) U/kg/day for duration ≥5 years. Obese individuals had lower HDL (47.5 vs. 54.4 mg/dL) and higher non-HDL-cholesterol (134.5 vs. 115.2 mg/dL) than lean ones only among those with more than 5 years of diabetes.ConclusionsLower insulin doses in obese individuals point to a role of clinical heterogeneity in insulin deficiency rather than normal progression of type 1 diabetes. Early obesity in type 1 diabetes is associated to lower HDL-cholesterol and higher number of CVRF. These data suggest a broad landscape of pathophysiological phenomena in double diabetes, rather than simple progression of a homogeneous clinical entity.Electronic supplementary materialThe online version of this article (doi:10.1186/s13098-016-0143-7) contains supplementary material, which is available to authorized users.

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In addition to lipid-lowering and cardiovascular protective actions, statins may have beneficial effects on insulin sensitivity. The objective of the present study was to evaluate the effect of simvastatin therapy on insulin resistance and on leptin, adiponectin, and Creactive protein (CRP) levels, as compared to metformin, in overweight pre-diabetic subjects. Forty-one subjects with BMI >25 kg/m 2 and impaired fasting glucose or impaired glucose tolerance were randomized to take simvastatin, 20 mg/day (N = 20) or metformin, 1.7 g/day (N = 21) for 16 weeks. Blood samples for the determination of metabolic, hormonal, and inflammatory parameters were obtained at baseline and after each treatment. After metformin therapy, significant reductions in mean BMI and waist circumference were observed, and after simvastatin treatment LDL and triglyceride levels were significantly reduced. Insulin resistance determined by the homeostasis model assessment decreased only with metformin. Independently of the type of medication, a significant decrease in CRP levels was detected from baseline to the end of the study. CRP showed a mean reduction of 0.12 ± 0.04 mg/dL (P = 0.002) over time. No change in leptin or adiponectin levels was induced by any therapy. The data suggest that a low dose of simvastatin does not affect insulin resistance in overweight pre-diabetic subjects and has no effect on leptin or adiponectin levels. Further studies including a larger sample size, higher doses of statins, and a placebo control group are necessary to confirm the present data.