RGD Reference Report - Effect of diabetes on enzymes involved in rat hepatic corticosterone production. - Rat Genome Database

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Effect of diabetes on enzymes involved in rat hepatic corticosterone production.

Authors: Hyatt, T  Chen, R  Wang, X  Mick, G  McCormick, K 
Citation: Hyatt T, etal., J Diabetes. 2010 Dec;2(4):275-81. doi: 10.1111/j.1753-0407.2010.00087.x.
RGD ID: 6784507
Pubmed: PMID:20923496   (View Abstract at PubMed)
DOI: DOI:10.1111/j.1753-0407.2010.00087.x   (Journal Full-text)

BACKGROUND: Numerous studies have explored the etiologic or permissive role of 11beta-hydroxysteroid dehydrogenase (11beta-HSD1) in obesity and Type 2 diabetes, biochemical conditions often with concurrent hyperinsulinism. In contrast, there are limited data on the effect of insulin deficiency (i.e. Type 1 diabetes) on 11beta-HSD1 or endoplasmic reticulum enzymes that generate the reduced pyridine cofactor NADPH. Thus, the aim of the present study was to examine the effect of insulin-deficient, streptozotozin diabetes on key microsomal enzymes involved in rat hepatic corticosterone production. METHODS: After rats had been rendered diabetic with streptozotocin and some had been treated with insulin (2-6 units, s.c., long-acting insulin once daily) for 7 days, hepatic microsomes were isolated. Serum corticosterone and fructosamine were obtained premortem. Intact microsomes were incubated in vitro and 11beta-HSD1, hexose-6-phosphate dehydrogenase (H6PDH), and isocitrate dehydrogenase (IDH) measured. RESULTS: Although diabetes markedly altered body weight gain and serum protein glycosylation (assessed by fructosamine), there was no significant change in hepatic 11beta-HSD1 reductase activity, with or without insulin treatment. However, serum corticosterone levels were significantly correlated with 11beta-HSD1 reductase activity when all groups were analyzed together (P < 0.05). Untreated diabetes modified (P < 0.01) two hepatic microsomal NADPH-generating enzymes, namely H6PDH and IDH, resulting in a 37% decrease and 14% increase in enzyme levels, respectively. CONCLUSIONS: Consistent with most in vivo studies, chronic insulin deficiency with attendant hyperglycemia does not significantly modify hepatic 11beta-HSD1 reductase activity, but does alter the activity of two microsomal enzymes coupled with pyridine cofactors.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Experimental Diabetes Mellitus  ISOH6pd (Rattus norvegicus)6784507; 6784507 RGD 
Experimental Diabetes Mellitus  IDA 6784507 RGD 

Objects Annotated

Genes (Rattus norvegicus)
H6pd  (hexose-6-phosphate dehydrogenase (glucose 1-dehydrogenase))

Genes (Mus musculus)
H6pd  (hexose-6-phosphate dehydrogenase (glucose 1-dehydrogenase))

Genes (Homo sapiens)
H6PD  (hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase)


Additional Information