No abstract

Despite decades of research, obesity and diabetes remain major health problems in the USA and worldwide. Among the many complications associated with diabetes is an increased risk of cardiovascular diseases, including myocardial infarction and heart failure. Recently, microRNAs have emerged as important players in heart disease and energy regulation. However, little work has investigated the role of microRNAs in cardiac energy regulation. Both human and animal studies have reported a significant increase in circulating free fatty acids and triacylglycerol, increased cardiac reliance on fatty acid oxidation, and subsequent decrease in glucose oxidation which all contributes to insulin resistance and lipotoxicity seen in obesity and diabetes. Importantly, MED13 was initially identified as a negative regulator of lipid accumulation in Drosophilia. Various metabolic genes were downregulated in MED13 transgenic heart, including sterol regulatory element-binding protein. Moreover, miR-33 and miR-122 have recently revealed as key regulators of lipid metabolism. In this review, we will focus on the role of microRNAs in regulation of cardiac and total body energy metabolism. We will also discuss the pharmacological and non-pharmacological interventions that target microRNAs for the treatment of obesity and diabetes.

Fasting levels of cholesterol, triglycerides, uric acid, fructosamine and glycosylated hemoglobin were measured in normal and in Type II diabetic subjects before the beginning and at the end of the Muslim month of fasting (Ramadan). In normal subjects, there was a significant increase (P<0.01) in triglycerides and uric acid levels as a result of Ramadan fasting. In diabetic patients, triglyceride levels decreased significantly (P<0.05), while uric acid levels showed a significant increase (P<0.01) as a result of the same type of fasting. There were no significant differences in cholesterol, fructosamine and glycosylated hemoglobin levels before and after fasting in either group. These findings suggest that although this type of fasting is effective in causing considerable changes in certain blood biochemical parameters in normal and diabetic subjects, it has no effect on the glycemic control of either normal or Type II diabetic subjects.

Objective. To examine the relationship of handgrip strength with forearm blood flow (BF) and vascular resistance (VR) in rheumatoid arthritis (RA) patients. Methods. Forearm BF at rest (RBF) and after upper arm occlusion (RHBF), and handgrip strength were examined in 78 individuals (RA = 42 and controls (CT) = 36). Subsequently, VR at rest (RVR) and after occlusion (RHVR) were calculated. Results. The patients' RBF (P = 0.02) and RHBF (P = 0.0001) were less, whereas RVR (P = 0.002) and RHVR (P = 0.0001) were greater as compared to the CTs. Similarly, handgrip strength was lower in the RAs (P = 0.0001). Finally, handgrip strength was directly associated with RBF (r = 0.43; P = 0.0001), and RHBF (r = 0.5; P = 0.0001), and inversely related to RVR (r = −0.3; P = 0.009) and RHVR (r = −0.3; P = 0.007). Conclusion. The present study uniquely identifies an association between regional measures of forearm blood flow and handgrip strength in patients and healthy control. In addition, this study confirms the presence of vascular and muscle dysfunction in patients with rheumatoid arthritis, as evidenced by lower forearm blood flow indices, at rest and following occlusion, and lower handgrip strength as compared to healthy individuals.

Basal thyroid function was assessed by serum thyroxine, tri-iodothyronine and thyroid-stimulating hormone levels in 90 patients 2-10 years old with beta-thalassaemia major. Based on measured serum ferritin levels, patients were classified into two groups: group (I) which included 63 patients with ferritin concentrations ranging from 300 to 7000 ng/ml (mild iron overload) and group (II) which included 27 patients with ferritin concentrations higher than 7000 ng/ml (severe iron overload). The results of thyroid function in both groups were compared with those of 50 control subjects. In group (I), the mean concentrations of all measured hormones were not significantly different from those of the controls. In group (II), the mean concentrations of thyroxine and tri-iodothyronine decreased by 29 and 35 per cent (P < 0.05), respectively, and the mean concentration of thyroid-stimulating hormone showed a 2.6-fold increase (P < 0.01) in comparison with those of the controls. The data clearly demonstrate the occurrence of impaired thyroid function and its possible association with iron overload in a considerable proportion of transfusion-dependent beta-thalassaemic patients.