Prevalence of the metabolic syndrome in elderly and middle-aged Japanese

AbstractBackground/PurposeDiagnosis and management of the metabolic syndrome (MetS) are beneficial for successful aging. In spite of several criteria for MetS, there is little information on cardiometabolic risk clustering in elderly Japanese. The purpose of this study was, therefore, to determine the relationship between age-associated changes in obesity and metabolic components in the Japanese.MethodsWe analyzed data from the nationwide survey conducted in 2000. Using Adult Treatment Panel III (ATP III) and Japanese diagnostic criteria for MetS, we analyzed 2366 people aged from 40 to 79 years (men, 1425 and women, 941) from the total participants.ResultsThe prevalence of MetS was almost three fold higher by modified ATP III, International Diabetes Federation, and Japanese criteria, in elderly women than in middle-aged women, whereas no difference was found between middle-aged and elderly men by the three criteria. A marked increase in the prevalence of MetS was found by modified ATP III and International Diabetes Federation criteria compared with that by the Japanese criteria in women. Among the risk factors, the prevalence of central obesity and dyslipidemia increased only in women and that of high fasting glucose and high blood pressure increased in both genders with aging. Among the MetS subjects who fulfilled the modified ATP III criteria, more clustering of risk was observed in elderly than in middle-aged subjects, especially in women. Blood pressure increased and triglyceride decreased in both genders, and non-high-density-lipoprotein cholesterol decreased in elderly men. The prevalence of dyslipidemia decreased in elderly men.ConclusionAging is an important factor that affects the metabolic abnormality, and aging of the population would lead to increase in the prevalence of MetS. Therefore, the development of better approaches to the prevention and management of MetS is necessary for successful aging in our society

LECT2 functions as a hepatokine that links obesity to skeletal muscle insulin resistance

Recent articles have reported an association between fatty liver disease and systemic insulin resistance in humans, but the causal relationship remains unclear. The liver may contribute to muscle insulin resistance by releasing secretory proteins called hepatokines. Here we demonstrate that leukocyte cell-derived chemotaxin 2 (LECT2), an energy-sensing hepatokine, is a link between obesity and skeletal muscle insulin resistance. Circulating LECT2 positively correlated with the severity of both obesity and insulin resistance in humans. LECT2 expression was negatively regulated by starvation-sensing kinase adenosine monophosphate-activated protein kinase in H4IIEC hepatocytes. Genetic deletion of LECT2 in mice increased insulin sensitivity in the skeletal muscle. Treatment with recombinant LECT2 protein impaired insulin signaling via phosphorylation of Jun NH2-terminal kinase in C2C12 myocytes. These results demonstrate the involvement of LECT2 in glucose metabolism and suggest that LECT2 may be a therapeutic target for obesity-associated insulin resistance. © 2014 by the American Diabetes Association

Metformin Prevents and Reverses Inflammation in a Non-Diabetic Mouse Model of Nonalcoholic Steatohepatitis

Background: Optimal treatment for nonalcoholic steatohepatitis (NASH) has not yet been established, particularly for individuals without diabetes. We examined the effects of metformin, commonly used to treat patients with type 2 diabetes, on liver pathology in a non-diabetic NASH mouse model. Methodology/Principal Findings: Eight-week-old C57BL/6 mice were fed a methionine- and choline-deficient plus high fat (MCD+HF) diet with or without 0.1% metformin for 8 weeks. Co-administration of metformin significantly decreased fasting plasma glucose levels, but did not affect glucose tolerance or peripheral insulin sensitivity. Metformin ameliorated MCD+HF diet-induced hepatic steatosis, inflammation, and fibrosis. Furthermore, metformin significantly reversed hepatic steatosis and inflammation when administered after the development of experimental NASH. Conclusions/Significance: These histological changes were accompanied by reduced hepatic triglyceride content, suppressed hepatic stellate cell activation, and the downregulation of genes involved in fatty acid metabolism, inflammation, and fibrogenesis. Metformin prevented and reversed steatosis and inflammation of NASH in an experimental non-diabetic model without affecting peripheral insulin resistance. © 2012 Kita et al