Metformin HCl has curative effect on rebuilding of ventricular diastolic functions in high-fat-diet fed rats

Myocardial lipid accumulation due to diabetes and/or obesity plays a role in the progression of left ventricular diastolic dysfunction. Our aims were to exhibit the correlation between histopathologic stage of the liver and cardiac functions, and to evaluate the effects of metformin HCl and rosiglitazone on myocardial functions. Thirty-two male Sprague-Dawley rats were divided into four groups to exhibit the correlation between histopathologic stage of the liver and cardiac functions and to determine whether metformin HCl and rosiglitazone have effects on cardiac functions. For 20 weeks, one group was fed standard rat basic diet, whereas the other groups were on high-fat-diet. During the last 4 weeks, metformin HCl was given to the third group, rosiglitazone to the fourth group. Histological evaluation of rat livers yielded significantly higher steatosis grade in high-fat-diet group and different fibrosis stages among groups. Also, there was significant correlation between diastolic functions and steatosis grade/fibrosis stage of rat liver. Electrophysiological study of hearts via Langendorff technique showed better coronary perfusion pressures and diastolic functions in standard-diet and metformin HCl groups compared to other groups. Metformin HCl improves LV diastolic dysfunction and coronary perfusion pressures

The presence of MEFV gene mutations in patients with primary osteoarthritis who require surgery

BACKGROUND/AIMS: Chronic arthritis of familial Mediterranean fever (FMF) involves weight-bearing joints and can occur in patients without a history of acute attack. Our aim was to investigate a possible causal relationship between FMF and osteoarthritis in a population in which FMF is quite common. METHODS: Patients with late stage primary osteoarthritis were enrolled, and five MEFV gene mutations were investigated. The frequency of MEFV gene mutations was compared among patients with osteoarthritis and a previous healthy group from our center. RESULTS: One hundred patients with primary osteoarthritis and 100 healthy controls were studied. The frequency of MEFV gene mutations was significantly lower in the osteoarthritis group (9% vs. 19%). M694V was the most frequent mutation (5%) in the osteoarthritis group, whereas in the control group, E148Q was the most common (16%). In subgroup analyses, the mutation frequency of patients with hip osteoarthritis was not different from that of patients with knee osteoarthritis and controls (7.1%, 9.7%, and 19%, respectively). There were no differences among the three groups with respect to MEFV gene mutations other than E148Q (8.1% vs. 3.6%). E148Q was significantly lower in the osteoarthritis group than in the controls (16% vs. 1%), although the mutations did not differ between patients with knee osteoarthritis and controls. CONCLUSIONS: In a population with a high prevalence of MEFV gene mutations, we did not find an increased mutation rate in patients with primary osteoarthritis. Furthermore, we found that some mutations were significantly less frequent in patients with osteoarthritis. Although the number of patients studied was insufficient to claim that E148Q gene mutation protects against osteoarthritis, the potential of this gene merits further investigation.