The effect of gestational diabetes mellitus (GDM) on cardiovascular diseases (CVD) is not assessed within the first 10 years postpartum, regardless of subsequent diabetes. The aim of this study was to determine the risk of CVD events related to GDM within 7 years of postpartum. This nationwide population-based study of deliveries in 2007 and 2008 with a follow-up of 7 years was based on data from the French medico-administrative database. Two groups were formed: women with a history of GDM and women without GDM or previous diabetes. CVD included angina pectoris, myocardial infarction, stroke, heart bypass surgery, coronary angioplasty, carotid endarterectomy and fibrinolysis. Hypertensive disease was assessed separately. Determinants studied included age, obesity, subsequent diabetes mellitus and hypertensive diseases during pregnancy. Adjusted odds ratios for outcomes were calculated using multiple logistic regressions. The hospital database recorded 1,518,990 deliveries in 2007 and 2008. Among these, 62,958 women had a history of GDM. After adjusting for age, DM, obesity and hypertensive disorders in pregnancy, GDM was significantly associated with a higher risk of CVD (adjusted Odds Ratio aOR = 1.25 [1.09–1.43]). Considering each variable in a separate model, GDM was associated with angina pectoris (aOR = 1.68 [1.29–2.20]), myocardial infarction (aOR = 1.92 [1.36–2.71]) and hypertension (aOR = 2.72 [2.58–2.88]) but not with stroke. A history of GDM was identified as a risk factor of CVD, especially coronary vascular diseases, within the 7 years postpartum. A lifestyle changes from postpartum onwards can be recommended and supported.

Objective: Nonalcoholic fatty liver disease (NAFLD) is commonly associated with obesity, metabolic syndrome, and type 2 diabetes. Several studies suggest that NAFLD is independently associated with an increased risk of cardiovascular disease in nondiabetic subjects. In type 2 diabetic subjects, the link between fatty liver and atherosclerosis is less clear. In this study, we set out to determine, whether fatty liver content, evaluated using 1H-magnetic resonance spectroscopy, a very precise imaging technique, was associated with atherosclerosis in people with type 2 diabetes. Research Design and Methods: A total of 101 patients with type 2 diabetes mellitus were included in this study. Liver fat (1H-magnetic resonance spectroscopy) and carotid intima media thickness (IMT) were measured. Results: Sixty-one (60.3%) patients had steatosis (hepatic triglyceride content greater than 5.5%). Liver fat content was correlated with fasting serum triglycerides (r = 0.22; P = 0.02) and alanine aminotransferase (r = 0.42; P = 0.0001). Sixty-eight percent of subjects with severe steatosis (hepatic triglyceride content greater than 15%) had aspartate aminotransferase in the normal range. Age was strongly correlated with IMT (r = 0.37; P = 0.0002). Steatosis did not correlate with IMT (r = −0.03; P = 0.75). There was no significant difference between the two groups (with and without hepatic steatosis) for IMT values. Conclusions: this study suggests that in people with type 2 diabetes, fatty liver is not associated with cardiovascular disease. In a diabetic population, it seems that fatty liver is not a determinant factor associated with carotid IMT. In type 2 diabetic patients, fatty liver is not a determinant factor associated with carotid intima media thickness.

The mechanisms underlying steatosis during hepatitis C virus (HCV) infection are complex and multifactorial. Obesity is a well-recognized risk factor for the development of steatosis in chronic hepatitis C infection. The aim of our study was to investigate the role of adipocytokines in HCV-related steatosis. Therefore, we hypothesized that the endocrine function of adipose tissue could be, in part, responsible for HCV-related steatosis. Seventy-one consecutive untreated chronic hepatitis C patients were studied to assess the effects of adipocytokines, body mass index (BMI), age, and HCV genotype on steatosis. We used ELISA to determine serum adiponectin, leptin, and soluble TNF receptors I and II concentrations. Steatosis was observed in 42 (59.1%) patients. BMI was significantly associated with leptin (r = 0.64; P = 0.0001) and was border significantly associated with adiponectin concentrations (r = -0.22; P = 0.06). In univariate analyses, age, HCV genotype 3, BMI, increased leptin level, increased insulin level, and decreased adiponectin concentration were associated with steatosis. In multivariate analysis, steatosis was significantly associated with low adiponectin concentration, age, HCV genotype 3, and aspartate aminotransferase (ASAT) level, whereas steatosis was not associated with leptin, insulin, and BMI. In chronic HCV patients, hypoadiponectinemia is significantly associated with the development of liver steatosis. The fact that the plasma levels of adiponectin inversely correlate with steatosis in HCV-infected subjects suggests that hypoadiponectinemia may contribute to hepatic steatosis progression and liver injury in this population. One practical implication is that therapy to increase circulating adiponectin concentration, such as overweight reduction or thiazolidinediones, provides the potential to improve steatosis in chronic hepatitis C infection.