Showing papers by "Changqin Liu published in 2010"

Metabolic disorders in newly diagnosed young adult female patients with simple virilizing 21-hydroxylase deficiency

Abstract: Classical congenital adrenal hyperplasia (CAH) is characterized by the defects in cortisol and aldosterone secretion, and accompanied with adrenal hyperandrogenism. It is likely that the impaired adrenocortical function and intermittent treatment-related hypercortisolism may predispose patients to the development of metabolic syndrome in adulthood. Our aim was to assess the impact of hyperandrogenism on metabolic profiles in CAH women without glucocorticosteroid treatment. We evaluated the clinical characteristics and metabolic profiles in 30 untreated Chinese female adults with simple virilizing congenital adrenal hyperplasia (SV-CAH). Mutation analysis was performed by sequencing the entire 21-hydroxylase gene (CYP21A2). As compared with the controls, CAH patients had higher BMI (BMI, 21.5±2.1 vs. 20.0±1.8 kg/m2, P<0.05), higher 2 h post-load plasma glucose levels (6. 35±1.74 vs. 5. 35±1.17 mmol/l, P<0.05), higher serum triglycerides (TG) (1.12±0.64 vs. 0.63±0.15 mmol/l, P<0.01), and lower high-density lipoprotein cholesterol (HDL-c) (1.30±0.39 vs. 1.67±0.29 mmol/l, P<0.01). Moreover, CAH patients had higher fasting insulin and homeostasis model assessment of insulin resistance (HOMA-IR) (1.81±0.99 vs. 1.24±0.50, P<0.05), while ΔIns30/ΔGlu30 showed no statistically significant difference in two groups. In addition, a marked reduction of serum adiponectin levels were observed in CAH patients (7.0±3.3 vs. 13.2±4.8 μg/ml, P<0.001), however, serum CRP levels were not different between patients and the controls. Further regression analysis showed that higher serum testosterone concentrations were associated with metabolic disorder indexes and reduction of serum adiponectin. Our study demonstrates that untreated CAH patients are prone to have metabolic disorders in association with elevated serum testosterone levels and reduced insulin insensitivity.

Immediate But Not Long-Term Administration of Nicardipine Inhibits Tolbutamide-Induced Insulin Secretion From Rat Pancreatic beta Cells

Abstract: OBJECTIVES Calcium channel blockers alter glucose homeostasis, but sufficient data regarding this effect in healthy animals have not been provided. We test the effect of nicardipine on beta cell function in healthy rats. METHODS Islets from Sprague-Dawley rats were coincubated with nicardipine, tolbutamide, or their combination for 1 hour. Insulin secretion was measured by radioimmunoassay. The rats were given nicardipine, tolbutamide, or their combination by intravenous injection. Intravenous glucose tolerance tests were performed after the first drug administration and 4 weeks later. Pancreata were excised for assessment of insulin content and immunohistochemical staining in the end. RESULTS Nicardipine markedly inhibited not only the insulin secretion by islets per se but also that enhanced by tolbutamide in vitro. Blood glucose was reduced by tolbutamide in vivo but elevated by nicardipine abruptly in parallel with retarded insulin secretion. Long-term administration of nicardipine altered neither fasting blood glucose level nor fasting serum insulin level, whereas pancreatic insulin content was unmodified despite that nicardipine caused shrunken islets with weak immunoreactivity of beta cells by immunohistochemistry. CONCLUSIONS In healthy rats, immediate administration of nicardipine inhibits insulin secretion of beta cells both in vitro and in vivo but does not exert a deleterious effect in vivo after long-term treatment.