Document Detail

Downregulation of hepatic glucose-6-phosphatase-α in patients with hepatic steatosis.
MedLine Citation:
PMID:  21593806     Owner:  NLM     Status:  MEDLINE    
Glucose-6-phosphate transporter (G6PT) and microsomal glucose-6-phosphatase-α (G6Pase-α) perform the terminal step in glycogenolysis and gluconeogenesis. Deficiency of these proteins leads to glycogen storage diseases. Partial inhibition of G6Pase in rats results in increased hepatic triglyceride content and de novo lipogenesis leading to hepatic steatosis. Hepatic steatosis represents hepatic manifestation of the metabolic syndrome. We investigated molecular mechanisms that may explain the relationship between fatty liver and G6Pase-α in humans in detail. A total of 27 patients (11 men, 16 women) underwent liver biopsy. Histological diagnosis identified nonfatty liver in seven patients and nonalcoholic fatty liver in 20 patients. We quantified G6Pase-α and G6PT mRNA expression by real-time PCR. Anthropometric measurements and analysis of plasma lipids and liver enzymes were performed. Patients with fatty liver showed no significant differences in age, HOMA(IR) (homeostasis model assessment of insulin resistance), BMI, liver enzymes or waist-to-hip ratio compared to those with nonfatty liver, but total plasma cholesterol levels and liver fat content were higher in patients with fatty liver (P < 0.05). G6Pase-α and G6PT mRNA expressions were significantly downregulated in fatty compared to histologically normal liver (P < 0.05). G6Pase-α and G6PT mRNA expressions correlated positively (R(2) = 0.406 P < 0.05). Both expressions did not correlate with age, BMI, aspartate transaminase, alanine transaminase, alkaline phosphatase, γ-glutamyl transferase, triglycerides or glucose levels. Our data suggest that expression of hepatic G6Pase-α and G6PT are closely interlinked. Downregulation of G6Pase-α in fatty liver might be associated with hepatic fat accumulation and pathogenesis of hepatic steatosis.
Sarah Konopelska; Tina Kienitz; Marcus Quinkler
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Publication Detail:
Type:  Journal Article     Date:  2011-05-19
Journal Detail:
Title:  Obesity (Silver Spring, Md.)     Volume:  19     ISSN:  1930-739X     ISO Abbreviation:  Obesity (Silver Spring)     Publication Date:  2011 Dec 
Date Detail:
Created Date:  2011-11-23     Completed Date:  2012-05-09     Revised Date:  2012-08-13    
Medline Journal Info:
Nlm Unique ID:  101264860     Medline TA:  Obesity (Silver Spring)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2322-6     Citation Subset:  IM    
Department of Clinical Endocrinology, Charité Campus Mitte, Charité University Medicine Berlin, Berlin, Germany.
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MeSH Terms
Adipose Tissue / metabolism*
Antiporters / blood,  genetics,  metabolism*
Cholesterol / blood*
Fatty Liver / etiology,  genetics,  metabolism*
Glucose-6-Phosphatase / genetics,  metabolism*
Liver / metabolism*
Middle Aged
Monosaccharide Transport Proteins / blood,  genetics,  metabolism*
Overweight / complications*,  genetics,  metabolism
RNA, Messenger / metabolism
Real-Time Polymerase Chain Reaction
Reg. No./Substance:
0/Antiporters; 0/Monosaccharide Transport Proteins; 0/RNA, Messenger; 0/glucose 6-phosphate(transporter); 57-88-5/Cholesterol; EC

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