Since pGDM exhibit many features of the Cardio-metabolic Gentiopicrin Syndrome, including hyperglycemia and hyperinsulinemia we hypothesized that cardiac steatosis might present an early sign of cardiac vulnerability and can be detected in these women with impaired glucose tolerance and early diabetes. Therefore, the aim of this study was to investigate myocardial lipid content and cardiac function and its relations to other features of the Cardio-metabolic Syndrome, such as fatty liver, insulin insensitivity and altered insulin secretion in women with prior gestational diabetes, when compared to healthy controls. The current study aimed to assess whether women with prior gestational diabetes – at different stages of glucose intolerance – already exhibit features of incident cardiac steatosis, predisposing them for the development of cardiomyopathy. According to our data, neither myocardial lipid content nor left ventricular function differed between pGDM and healthy controls. In addition, none of the groups showed evidence of cardiac steatosis or cardiac dysfunction, indicating that metabolic disturbances might not influence cardiac morbidity in this relatively young female population. In contrast to prior investigations in 10-Gingerol patients with diabetes, we could not detect a link between MYCL and diastolic function, assessed by the E/A-ratio. Our results are also in contrast to a prior investigation, which reported increased MYCL in women with diabetes. However, in both studies male patients were over-represented and, moreover, the study populations were about 10�C15 years older than ours. Assuming that the development of cardiomyopathy in patients with diabetes may take years and furthermore be accelerated by the co-existence of arterial hypertension and coronary artery disease, our study population might be too young to detect cardiac abnormalities. In addition, myocardial lipid content was independent of medication intake and not associated with insulin sensitivity, described by OGIS. This is in line with our prior studies, in which we also could not find a link between insulin resistance and myocardial lipid accumulation in healthy women. Furthermore, we have previously shown that combined hyperglycemia and hyperinsulinemia increase myocardial lipid content in both, healthy men and women, and that myocardial lipid accumulation tightly relates to hyperinsulinemia. However, MYCL was not associated with insulin sensitivity, calculated by the M-value during the clamp, and its increase comparable between male and female subjects. In contrast to our findings, another group has described a link between insulin resistance and cardiac steatosis in sedentary, obese women; subsequently we assume that this might be related to increased adiposity in those women with a mean BMI of 33 kg/m2. This assumption is supported by our data, which showed a positive correlation between BMI and MYCL in the CON- and NGT-group, both with normal glucose tolerance. Thus, the co-existence of obesity might accelerate myocardial lipid accumulation due to increased endogenous fatty acids and insulin supply, at least in women without disturbed glucose metabolism.