Background Statins reduce the risk of cardiovascular events in patients with chronic kidney disease (CKD). Although diabetes mellitus (DM) is a reported side effect of statin treatment, some studies have indicated that pitavastatin does not cause DM. The present study investigated the effect of pitavastatin on the fatty acid (FA) content of erythrocyte membranes, which affects the occurrence of DM and cardiovascular diseases. In addition, changes in adiponectin and glycated hemoglobin (HbA1c) levels were evaluated after pitavastatin treatment.
Methods A total of 45 patients were enrolled, 28 of whom completed the study. Over 24 weeks, 16 patients received 2 mg pitavastatin and 12 patients received 10 mg atorvastatin. Dosages were adjusted after 12 weeks if additional lipid control was required. There were 10 and nine patients with DM in the pitavastatin and atorvastatin groups, respectively. Erythrocyte membrane FAs and adiponectin levels were measured using gas chromatography and enzyme-linked immunosorbent assay, respectively.
Results In both groups, saturated FAs, palmitic acid, trans-oleic acid, total cholesterol, and low-density lipoprotein cholesterol levels were significantly lower than those at baseline. The arachidonic acid (AA) content in the erythrocyte membrane increased significantly in the pitavastatin group, but adiponectin levels were unaffected. HbA1c levels decreased in patients treated with pitavastatin. No adverse effects were associated with statin treatment.
Conclusion Pitavastatin treatment in patients with CKD may improve glucose metabolism by altering erythrocyte membrane AA levels. In addition, pitavastatin did not adversely affect glucose control in patients with CKD and DM.
Background Dietary polyunsaturated fatty acids (PUFA) are thought to modify systemic inflammation. The present study aimed to evaluate the relationship between PUFA intake, lung function, and health-related quality of life (HRQoL) in patients with chronic obstructive pulmonary disease (COPD).
Methods In this study, we used the dataset of 6th Korea National Health and Nutrition Examination Survey, in which, a total of 22,948 individuals including 573 participants with a high probability of developing COPD were enrolled. Participants with missing data for the investigated variables were excluded. Linear regression analyses were used to evaluate the association between PUFA intake (omega-3 [N3], omega-6 [N6], and total) with lung function, and HRQoL. HRQoL was determined according to the European Quality of Life-5 Dimensions (EQ-5D). Subgroup analysis of older patients was performed. Age, sex, body mass index, smoking, alcohol, education, residence, total calorie intake, and predicted FEV1% were adjusted in all analyses.
Results Although lung function was not associated with PUFA intake, EQ-5D index was remarkably associated with N3, N6, and total PUFA intake in a dose-dependent manner. This association was more pronounced in elderly COPD patients. Mean levels of N3, N6, and total PUFA intake were significantly higher in patients having better HRQoL with respect to mobility, self-care, and usual activities.
Conclusion Our results suggest that N3, N6, and total PUFA intake are associated with HRQoL in COPD patients. This association may be attributed to mobility, self-care, and usual activities. Further longitudinal study is required to clarify this relationship.
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The incidence of type 2 diabetes mellitus and insulin resistance is growing rapidly. Multiple organs including the liver, skeletal muscle and adipose tissue control insulin sensitivity coordinately, but the mechanism of skeletal muscle insulin resistance has not yet been fully elucidated. However, there is a growing body of evidence that lipotoxicity induced by mitochondrial dysfunction in skeletal muscle is an important mediator of insulin resistance. However, some recent findings suggest that skeletal mitochondrial dysfunction generated by genetic manipulation is not always correlated with insulin resistance in animal models. A high fat diet can provoke insulin resistance despite a coordinate increase in skeletal muscle mitochondria, which implies that mitochondrial dysfunction is not mandatory in insulin resistance. Furthermore, incomplete fatty acid oxidation by excessive nutrition supply compared to mitochondrial demand can induce insulin resistance without preceding impairment of mitochondrial function. Taken together we suggested that skeletal muscle mitochondrial overloading, not mitochondrial dysfunction, plays a pivotal role in insulin resistance.
BACKGROUND The treatment of rheumatoid arthritis still depend on conserve therapy in major. Recent studies report that n-3 polyunsaturated fatty acids(PUFA) could modulate the incidence and progress of arthritis. The purpose of this study was to investigate the effects of n-3 PUFA on the development of collagen-induced arthritis in rats. MATERIALS AND METHODS: Female Louvain rats were used for this experiment. Rats were randomly assigned into either normal(n=8) or collagen-immunized groups, and collagen immunized groups were divided into control(n=8, normal diet) and n-3 PUFA(n=8, 5% n-3 PUFA in diet) groups. One week after feeding n-3 PUFA to rats, they were immunized with type II collagen emulsified in incomplete Freund's adjuvant into tail and back. Development of arthritis was confirmed by x-ray and microscopic examination. RESULTS: Incidence of arthritis at the 5th week after immunization was 38% in control and 0% in n-3 PUFA. Rats with arthritis showed edema in hind paws and inflammation in synovial membrane of the knee joint. Plasma glucose and insulin were not changed by both of immunization and diet. Plasma triglycerides and cholesterol concentrations were decreased by n-3 PUFA. CONCLUSION: n-3 PUFA may prevent or treat collagen-induced arthritis in rats. Further studies are needed for action mechanism of it.