Effects of resistin expression on glucose metabolism and hepatic insulin resistance

Autor: Yan Li, Fangping Li, Juan He, Li Yan, Zhao-Fan Luo, Zhi-zhen Li
Rok vydání: 2009
Předmět:
Blood Glucose
Male
medicine.medical_specialty
endocrine system diseases
Endocrinology
Diabetes and Metabolism
Blotting
Western
Genetic Vectors
Gene Expression
AMP-Activated Protein Kinases
Carbohydrate metabolism
Adenoviridae
Mice
Endocrinology
Insulin resistance
AMP-activated protein kinase
Internal medicine
Glucose Intolerance
medicine
Animals
Insulin
Resistin
RNA
Messenger
biology
Reverse Transcriptase Polymerase Chain Reaction
Chemistry
nutritional and metabolic diseases
AMPK
Fasting
Metabolism
medicine.disease
Recombinant Proteins
Enzyme Activation
Mice
Inbred C57BL
Glucose
Liver
Glucose-6-Phosphatase
biology.protein
Decreased glucose tolerance
Phosphoenolpyruvate Carboxykinase (GTP)
Insulin Resistance
Phosphoenolpyruvate carboxykinase
Glycogen
hormones
hormone substitutes
and hormone antagonists
Zdroj: Endocrine. 35:243-251
ISSN: 1559-0100
1355-008X
DOI: 10.1007/s12020-009-9148-4
Popis: In order to observe the effect of increased serum resistin on glucose metabolism, insulin sensitivity, and hepatic insulin resistance (IR), mice were intravenously injected with recombinant adenovirus carrying the resistin gene (Adv-resistin-EGFP). Changes in hepatic glucose metabolism were observed using the Periodic Acid-Schiff method. Hepatic AMP-activated protein kinase (AMPK) activation was assessed by Western blot analysis, and glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK) mRNA expression was determined using real-time RT-PCR. Although no effect on fasting blood glucose was detected, increased fasting insulin levels, decreased glucose tolerance and insulin sensitivity, and reduced hepatic glycogen levels and AMPK activation were seen in the Adv-resistin-EGFP mice. Finally, elevated G6Pase and PEPCK mRNA expression levels were detected upon overexpression of resistin. Resistin may inhibit hepatic AMPK activity, which results in elevated expression of gluconeogenic enzymes thereby affecting glucose metabolism and leading to decreased glycogen storage that contributes to the development of hepatic IR.
Databáze: OpenAIRE
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