Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-12-25
pubmed:abstractText
We established a new animal model called SPORTS (Spontaneously-Running Tokushima-Shikoku) rats, which show high-epinephrine (Epi) levels. Recent reports show that Epi activates adenosine monophosphate (AMP)-activated protein kinase (AMPK) in adipocytes. Acetyl-CoA carboxylase (ACC) is the rate-limiting enzyme in fatty acid synthesis, and the enzymatic activity is suppressed when its Ser-79 is phosphorylated by AMPK. The aim of this study was to investigate the in vivo effect of Epi on ACC and abdominal visceral fat accumulation. We divided both 6-week male control and SPORTS rats into two groups, which were fed either normal diet or high fat and sucrose (HFS) diet for 16 weeks. At the end of diet treatment, retroperitoneal fat was collected for western blotting and histological analysis. Food intake was not different among the groups, but SPORTS rats showed significantly lower weight gain than control rats in both diet groups. After 10 weeks of diet treatment, glucose tolerance tests (GTTs) revealed that SPORTS rats had increased insulin sensitivity. Furthermore, SPORTS rats had lower quantities of both abdominal fat and plasma triglyceride (TG). In abdominal fat, elevated ACC Ser-79 phosphorylation was observed in SPORTS rats and suppressed by an antagonist of beta-adrenergic receptor (AR), propranolol, or an inhibitor of AMPK, Compound C. From these results, high level of Epi induced ACC phosphorylation mediated through beta-AR and AMPK signaling pathways in abdominal visceral fat of SPORTS rats, which may contribute to reduce abdominal visceral fat accumulation and increase insulin sensitivity. Our results suggest that beta-AR-regulated ACC activity would be a target for treating lifestyle-related diseases, such as obesity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1930-7381
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
48-54
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:19444233-AMP-Activated Protein Kinases, pubmed-meshheading:19444233-Acetyl-CoA Carboxylase, pubmed-meshheading:19444233-Adrenergic beta-Antagonists, pubmed-meshheading:19444233-Analysis of Variance, pubmed-meshheading:19444233-Animals, pubmed-meshheading:19444233-Blood Glucose, pubmed-meshheading:19444233-Blotting, Western, pubmed-meshheading:19444233-Body Weight, pubmed-meshheading:19444233-Eating, pubmed-meshheading:19444233-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:19444233-Epinephrine, pubmed-meshheading:19444233-Glucose Tolerance Test, pubmed-meshheading:19444233-Insulin, pubmed-meshheading:19444233-Intra-Abdominal Fat, pubmed-meshheading:19444233-Male, pubmed-meshheading:19444233-Obesity, pubmed-meshheading:19444233-Phosphorylation, pubmed-meshheading:19444233-Propranolol, pubmed-meshheading:19444233-Pyrazoles, pubmed-meshheading:19444233-Pyrimidines, pubmed-meshheading:19444233-Rats, pubmed-meshheading:19444233-Receptors, Adrenergic, beta, pubmed-meshheading:19444233-Up-Regulation
pubmed:year
2010
pubmed:articleTitle
Beta-adrenergic-AMPK pathway phosphorylates acetyl-CoA carboxylase in a high-epinephrine rat model, SPORTS.
pubmed:affiliation
Department of Nutrition and Metabolism, Institute of Health Biosciences, the University of Tokushima Graduate School, Tokushima, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't