👤 Mustafa Ozdemir

Insulin resistance is considered the most important key mechanism in the development of nonalcoholic fatty liver disease (NAFLD). Some studies have reported that hyperinsulinemia decreases the hepatic secretion of apolipoprotein (Apo) B. Chronic hyperinsulinemia in NAFLD may be responsible for the accumulation of triglycerides in hepatocytes. We aimed to investigate whether apolipoproteins are related to histological findings in patients with biopsy-proven NAFLD. We also aimed to evaluate the effects of obesity on apolipoproteins and the pathogenesis of NAFLD. In this cross-sectional study, 91 patients with biopsy-proven NAFLD were included. The control group consisted of 39 healthy subjects who had no history of liver disease or alcohol consumption and were matched for age, gender and smoking. Apoliprotein A1 and Apo B were measured via an immunoturbidimetric method with commercially available OSR6142 Apo A1 and OSR6143 Apo B immunoassay kits on an Olympus AU2700 analyzer. Age, gender, and smoking distribution were similar among nonalcoholic steatohepatitis patients, simple steatosis patients, and controls. The differences in the mean Apo A1 and Apo B levels and the Apo B/A1 ratio among non-alcoholic steatosis, simple steatosis, and control subjects did not reach statistical significance. In addition, patients with obese NAFLD had higher steatosis scores than patients with nonobese NAFLD (p<0.05). Apo A1 and B levels and the B/A1 ratio were not associated with histopathological findings in patients with NAFLD. Fibrosis and ApoB1/A were found to be independent risk factors for metabolic associated fatty liver disease. In addition, obesity increases the grade of hepatic steatosis but does not cause lobular inflammation, ballooning or fibrosis. Show less

Skeletal muscle, a highly complex muscle type in the eukaryotic system, is characterized by different muscle subtypes and functions associated with specific myosin isoforms. As a result, skeletal muscle is the target of numerous diseases, including distal arthrogryposes (DAs). Clinically, DAs are a distinct disorder characterized by variation in the presence of contractures in two or more distal limb joints without neurological issues. DAs are inherited, and up to 40% of patients with this condition have mutations in genes that encode sarcomeric protein, including myosin heavy chains, troponins, and tropomyosin, as well as myosin binding protein-C (MYBPC). Our research group and others are actively studying the specific role of MYBPC in skeletal muscles. The MYBPC family of proteins plays a critical role in the contraction of striated muscles. More specifically, three paralogs of the MYBPC gene exist, and these are named after their predominant expression in slow-skeletal, fast-skeletal, and cardiac muscle as sMyBP-C, fMyBP-C, and cMyBP-C, respectively, and encoded by the MYBPC1, MYBPC2, and MYBPC3 genes, respectively. Although the physiology of various types of skeletal muscle diseases is well defined, the molecular mechanism underlying the pathological regulation of DAs remains to be elucidated. In this review article, we aim to highlight recent discoveries involving the role of skeletal muscle-specific sMyBP-C and fMyBP-C as well as their expression profile, localization in the sarcomere, and potential role(s) in regulating muscle contractility. Thus, this review provides an overall summary of MYBPC skeletal paralogs, their potential roles in skeletal muscle function, and future research directions. Show less