The results suggest that during brief-intensity exercise, as the glycogen content of type IIA fibres is reduced earlier than that of type I fibres, bag2 fibres are most important early in this type of exercise.
Objective: 17 Alpha-hydroxylase/17,20-lyase deficiency (17OHD) is a form of congenital adrenal hyperplasia caused by homozygous or compound heterozygous mutations in the CYP17A1 gene. Impaired activities of 17 alphahydroxylase and 17,20-lyase typically induce hypertension, hypokalemia, and amenorrhea, with the vast majority of patients with 17OHD are diagnosed in adolescence.Methods: We present a case of 17OHD diagnosed at the age of 50 with complete endocrinologic investigations and genetic analysis.Results: The patient had hypokalemia and a low cortisol level. Her dehydroepiandrosterone sulfate (DHEA-S) and androstenedione levels were undetectable, although her adrenocorticotropic hormone (ACTH) level was elevated. She had markedly elevated pregnenolone, progesterone, deoxycorticosterone, and corticosterone levels. In addition, her plasma renin activity and plasma aldosterone concentration were suppressed and elevated, respectively.Rapid ACTH stimulation increased the hormones upstream of 17 alpha-hydroxylase, and overnight 1-mg dexamethasone suppressed them. The patient was thus diagnosed with 17OHD. Genetic testing confirmed the diagnosis, revealing 2 distinct mutations in the CYP17A1 gene, c985_987delTACinsAA and R416C, which have been previously reported.Conclusion: The present case is a mild form of 17OHD that had gone undiagnosed until the age of 50. The R416C genotype seems to relate to a mild phenotype. Mild 17OHD may remain undiagnosed or be misdiagnosed as primary aldosteronism or idiopathic hyperaldosteronism.
We studied the effects of exercise on muscle mitochondria, and lipid and glycogen content in nonalcoholic steatohepatitis (NASH) model rats. Male Sprague-Dawley rats were randomly separated into 3 groups: the control group was fed standard chow; the NASH group was fed a methioninecholine-deficient high-fat diet (MCD); the NASH-exercise group was fed the MCD and exercised three times a week. Exercise training consisted of continuous running for thirty minutes at a 13 m/min, 6˚ slope on a motor-driven rodent treadmill for 6 weeks. Mitochondria content in NASH group decreased in the both fiber types compared with those of the control group. As compared between the NASH and NASH-exercise groups, however, exercise not only promoted significant improvements in liver fibrosis and cirrhosis and triglyceride (TG) content but also increased mitochondria content in type I muscle fiber in particular. These data suggest that exercise improved hepatic steatosis in NASH model rats and can prevent the progression of NASH.
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