Document Detail

Exercise enhances insulin and leptin signaling in the cerebral cortex and hypothalamus during dexamethasone-induced stress in diabetic rats.
MedLine Citation:
PMID:  16721034     Owner:  NLM     Status:  MEDLINE    
Exercise and dexamethasone (DEX) are known to have opposite effects on peripheral insulin resistance. However, their effects and mechanism on brain glucose metabolism have been poorly defined. We investigated the modulation of the hypothalamo-pituitary-adrenal (HPA) axis and insulin/leptin signaling associated with glucose utilization in the brains of 90% pancreatectomized diabetic rats, which had been administered two dosages of DEX and exercised for 8 weeks. The data revealed that the administration of a high dose (0.1 mg/kg body weight/day) of DEX (HDEX) attenuated insulin signaling in the cerebral cortex and hypothalamus, whereas exercise potentiated their insulin signaling along with induction of IRS2 expression. In parallel with the modulated signaling, glucose utilization, such as glycogen storage and glycogen synthase activity, was suppressed by DEX in the cortex and hypothalamus, while exercise offset the DEX effects. Despite a decrease in epididymal fat mass, HDEX increased serum leptin levels, possibly due to an activated HPA axis, while exercise suppressed the increment. However, DEX reduced leptin-induced STAT3 phosphorylation in the cortex and hypothalamus, and it increased AMP-activated protein kinase (AMPK) phosphorylation only in the hypothalamus. Exercise reversed the phosphorylation of STAT3 and AMPK which had been modulated by DEX. In conclusion, exercise improves insulin and leptin signaling in the cerebral cortex and hypothalamus of diabetic rats exacerbated with HDEX, contributing to the regulation of body weight and glucose homeostasis.
Sunmin Park; Jin Sun Jang; Dong Wha Jun; Sang Mee Hong
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-05-04
Journal Detail:
Title:  Neuroendocrinology     Volume:  82     ISSN:  0028-3835     ISO Abbreviation:  Neuroendocrinology     Publication Date:  2005  
Date Detail:
Created Date:  2006-05-24     Completed Date:  2006-07-18     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0035665     Medline TA:  Neuroendocrinology     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  282-93     Citation Subset:  IM    
Department of Food and Nutrition, College of Natural Science, Hoseo University, Asan-Si, Korea.
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MeSH Terms
Adrenocorticotropic Hormone / blood
Blood Glucose / analysis,  metabolism
Body Weight / drug effects,  physiology
Cerebral Cortex / physiology*
Corticosterone / blood
Dexamethasone / adverse effects,  pharmacology*
Diabetes Mellitus, Experimental / physiopathology
Dose-Response Relationship, Drug
Eating / drug effects,  physiology
Glucocorticoids / pharmacology*
Glycosylation End Products, Advanced / blood
Hippocampus / physiology
Homeostasis / drug effects,  physiology
Hypothalamo-Hypophyseal System / drug effects,  physiology
Hypothalamus / physiology*
Insulin / blood,  physiology*
Leptin / blood,  physiology*
Phosphorylation / drug effects
Physical Conditioning, Animal / physiology*
Pituitary-Adrenal System / drug effects,  physiology
Protein Kinases / metabolism
Rats, Sprague-Dawley
STAT3 Transcription Factor / metabolism
Signal Transduction / physiology
Stress, Physiological / chemically induced,  physiopathology
Reg. No./Substance:
0/Blood Glucose; 0/Glucocorticoids; 0/Glycosylation End Products, Advanced; 0/Leptin; 0/STAT3 Transcription Factor; 0/Stat3 protein, rat; 11061-68-0/Insulin; 50-02-2/Dexamethasone; 50-22-6/Corticosterone; 9002-60-2/Adrenocorticotropic Hormone; EC 2.7.-/Protein Kinases; EC 2.7.1.-/AMP-activated protein kinase kinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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