Background-The risk of heart failure in type 2 diabetes mellitus is greater than can be accounted for by hypertension and coronary artery disease. Rodent studies indicate that in obesity and type 2 diabetes mellitus, lipid overstorage in cardiac myocytes produces lipotoxic intermediates that cause apoptosis, which leads to heart failure. In humans with diabetes mellitus, cardiac steatosis previously has been demonstrated in explanted hearts of patients with end-stage nonischemic cardiomyopathy. Whether cardiac steatosis precedes the onset of cardiomyopathy in individuals with impaired glucose tolerance or in patients with type 2 diabetes mellitus is unknown. Methods and Results-To represent the progressive stages in the natural history of type 2 diabetes mellitus, we stratified 134 individuals (age 45Ϯ12 years) into 1 of 4 groups: (1) lean normoglycemic (lean), (2) overweight and obese normoglycemic (obese), (3) impaired glucose tolerance, and (4) type 2 diabetes mellitus. Localized 1 H magnetic resonance spectroscopy and cardiac magnetic resonance imaging were used to quantify myocardial triglyceride content and left ventricular function, respectively. Compared with lean subjects, myocardial triglyceride content was 2.3-fold higher in those with impaired glucose tolerance and 2.1-fold higher in those with type 2 diabetes mellitus (PϽ0.05). Left ventricular ejection fraction was normal and comparable across all groups. Conclusions-In humans, impaired glucose tolerance is accompanied by cardiac steatosis, which precedes the onset of type 2 diabetes mellitus and left ventricular systolic dysfunction. Thus, lipid overstorage in human cardiac myocytes is an early manifestation in the pathogenesis of type 2 diabetes mellitus and is evident in the absence of heart failure.

Objective To examine the effect of an exercise and dietary intervention during pregnancy on excessive gestational weight gain (EGWG), dietary habit and physical activity in pregnant women.Design Randomised controlled trial.Setting Community-based study.Population Nondiabetic urban-living pregnant women (<26 weeks of gestation).Methods Participants in the intervention group were provided with community-based group exercise sessions, instructed home exercise and dietary counselling between 20 and 36 weeks of gestation. Participants in both groups received physical activity and food intake surveys at enrolment and 2 months after the enrolment.Main outcome measures Prevalence of EGWG and measures of physical activity and food intakes between the two groups.Results A total of 190 pregnant women, 88 in the control group and 102 in the intervention group, completed the study. Decreased daily intakes of calorie, fat, saturated fat and cholesterol were detected in participants in the intervention group at 2 months after enrolment compared with the control group (P < 0.01). Participants in the intervention group had higher physical activity 2 months after enrolment compared with the control group (P < 0.01). The lifestyle intervention during pregnancy reduced the prevalence of EGWG in the intervention group compared with the control group (P < 0.01) according to the guidelines of the Institute of Medicine. ConclusionThe findings suggest that lifestyle intervention during pregnancy increased physical activity, improved dietary habits and reduced EGWG in urban-living pregnant women.

Obesity is a major risk factor for heart disease. In the face of obesity's growing prevalence, it is important for physicians to be aware of emerging research of novel mechanisms through which adiposity adversely affects the heart. Conventional wisdom suggests that either hemodynamic (that is, increased cardiac output and hypertension) or metabolic (that is, dyslipidemic) derangements associated with obesity may predispose individuals to coronary artery disease and heart failure. The purpose of this review is to highlight a novel mechanism for heart disease in obesity whereby excessive lipid accumulation within the myocardium is directly cardiotoxic and causes left ventricular remodeling and dilated cardiomyopathy. Studies in animal models of obesity reveal that intracellular accumulation of triglyceride renders organs dysfunctional, which leads to several well-recognized clinical syndromes related to obesity (including type 2 diabetes). In these rodent models, excessive lipid accumulation in the myocardium causes left ventricular hypertrophy and nonischemic, dilated cardiomyopathy. Novel magnetic resonance spectroscopy techniques are now available to quantify intracellular lipid content in the myocardium and various other human tissues, which has made it possible to translate these studies into a clinical setting. By using this technology, we have recently begun to study the role of myocardial steatosis in the development of obesity-specific cardiomyopathy in humans. Recent studies in healthy individuals and patients with heart failure reveal that myocardial lipid content increases with the degree of adiposity and may contribute to the adverse structural and functional cardiac adaptations seen in obese persons. These studies parallel the observations in obese animals and provide evidence that myocardial lipid content may be a biomarker and putative therapeutic target for cardiac disease in obese patients.