Mutation of IVS2-12A/C > G in combination with 707-714delGAGACTAC in the CYP21 gene is caused by deletion of the C4-CYP21 repeat module with steroid 21-hydroxylase deficiency

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Title:	Mutation of IVS2-12A/C > G in combination with 707-714delGAGACTAC in the CYP21 gene is caused by deletion of the C4-CYP21 repeat module with steroid 21-hydroxylase deficiency
Authors:	Lee, HH;Chang, SF;Tsai, FJ;Tsai, LP;Lin, CY
Contributors:	附設醫院基因醫學部;King Car Food Ind Co Ltd, Yuan Shan Res Inst, Yuan Shan 264, Ilan, Taiwan;Taipei Med Univ, Grad Inst Cell & Mol Biol, Taipei 110, Taiwan;China Med Coll Hosp, Dept Med Genet, Taichung 404, Taiwan;Taipei Municipal Women Childrens Hosp, Dept Pediat, Taipei 100, Taiwan
Date:	2003
Issue Date:	2010-09-24 14:45:49 (UTC+8)
Publisher:	ENDOCRINE SOC
Abstract:	Background Adenosine A1 receptor (A1-AR) activation can lower plasma glucose in diabetic rats lacking insulin. We investigated the change in A1-AR gene expression in diabetic rats. Methods The incorporation of [U-C-14]-glucose into glycogen was carried out to evaluate the effect of N-6-cyclopentyladenosine (CPA) on glucose utilization in vitro. The plasma glucose concentration was assessed by the glucose oxidase method. The mRNA and protein levels of A1-AR in isolated liver were detected by Western blotting analysis and Northern blotting analysis, respectively. Results The effect of CPA, an agonist of A1-AR, on glycogen incorporation in hepatocytes isolated from streptozotocin-induced diabetic rats (STZ-diabetic rats) was more marked than that from the normal rats. However, similar glycogen synthesis was not modified by 12-0-tetradecanoylphorbol-13-acetate (TPA), an activator of protein kinase C, in the isolated hepatocytes from both the normal and the STZ-diabetic rats. A change in response at the receptor level can thus be considered. The mean level of liver mRNA transcripts encoding A1-AR was increased in STZ-diabetic rats to about 250% of that in normal rats. Exogenous insulin at a dose sufficient to normalize the plasma glucose of STZ-diabetic rats reversed the mRNA level of A1-AR in the liver after a four-day treatment. Similar results were also observed in STZ-diabetic rats that received treatment with phlorizin for four days. Moreover, the protein level of A1-AR was higher in the liver of STZ-diabetic rats than that in the normal rats. Similar treatment with exogenous insulin or phlorizin reversed the elevated protein level of A1-AR in the liver of STZ-diabetic rats to near the normal level. Therefore, correction of hyperglycemia in STZ-diabetic rats can reverse the higher gene expression of A1-AR in liver. Conclusions The obtained results suggest that an increase in plasma glucose is responsible for the higher gene expression of A1-AR in the liver of STZ-diabetic rats. Copyright (C) 2003 John Wiley Sons, Ltd.
Relation:	JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM 88(6):2726-2729
Appears in Collections:	[China Medical University Hospital] Jurnal articles

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