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Chinese Journal of Endocrinology and Metabolism ; (12): 488-491, 2011.
Artigo em Chinês | WPRIM | ID: wpr-416934

RESUMO

Fourteen neonatal diabetes mellitus(NDM)patients were recruited. 9 patients were treated with glyburide and the other 5 with insulin. ABCC8, KCNJ11, and INS genes were sequenced in 6 of them. Gene mutations were found in 2, 1, and 1 cases in these genes, respectively. One case with 6q24 hypomethylation and another without known mutation were also found. 8 out of 9 patients treated with glyburide reached euglycemia(88.9%). The other 5 patients with insulin therapy either died or lost contact. The results suggest that glyburide therapy is effective in neonatal diabetes mellitus, while insulin therapy may contribute to poor compliance.

2.
Chinese Journal of Endocrinology and Metabolism ; (12)1986.
Artigo em Chinês | WPRIM | ID: wpr-535889

RESUMO

Objective To investigate the effect of human growth hormone antagonist (GHA) on diabetic nephropathy in mice. Methods Thirty nine C57BL male mice were divided into five groups: normal control, diabetic control, two GHA diabetic mice groups, human growth hormone (hGH) diabetic group. Diabetic mice were induced with Streptozotocin. hGH, GHA1 〔del(1 4), G120R, K168A, E174A, C182S, del(186 191) Cys 1〕 and GHA2 〔H21A, G120R, E174A〕, were respectively administered subcutaneously to diabetic mice for eleven weeks, the effects of them on body weight, urinary protein excretion and renal morphology in mice of all groups were observed. Results All diabetic mice showed growth retardation including hGH and GH antagonist groups when comparing with their nondiabetic mice. The results of kidney histology showed a significant increase in glomerular area 〔hGH:(4289?798)?m 2, DM:(4226?894)?m 2,GHA1:(3511?717)?m 2, GHA2:(3428?919)?m 2, Normal control:(3399?573)?m 2〕 and cell proliferation (hGH:37.4?5.5, DM:34.5?6.4, GHA1:31.1?6.5, GHA2:29.2?6.5, Normal control:29.0?6.0) in hGH and DM control groups compared with two GH antagonist groups and normal control group, but the expansion of mesangial area with increased extracellualar matrix existed in all diabetic mice, no significant difference was observed among diabetic groups. No statistical difference was found among diabetic groups in urinary protein excretion. Conclusion hGH may aggravate glomerular hypertrophy and mesangial cell proliferation in diabetic mice, and hGH antagonists are effective in preventing diabetic mice glomerular hypertrophy, mesangial cell proliferation and maintaining integrity of kidney normal morphology in diabetic mice.

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