Linked Life Data

16901933

Source:http://linkedlifedata.com/resource/pubmed/id/16901933

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-8-11
pubmed:abstractText
In patients with type 2 non-insulin-dependent diabetes mellitus (NIDDM), the biguanide, metformin, exerts its antihyperglycemic effect by improving insulin sensitivity, which is associated with decreased level of circulating free fatty acids (FFA). The flux of FFA and glycerol from adipose tissue to the blood stream primarily depends on the lipolysis of triacylglycerols in the adipocytes. Adipocyte lipolysis is physiologically stimulated by catecholamine hormones. Tumor necrosis factor-alpha (TNF-alpha), a cytokine largely expressed in adipose tissue, stimulates chronic lipolysis, which may be associated with increased systemic FFA and insulin resistance in obesity and NIDDM. In this study, we examined the role of metformin in inhibiting lipolytic action upon various lipolytic stimulations in primary rat adipocytes. Treatment with metformin attenuated TNF-alpha-mediated lipolysis by suppressing phosphorylation of extracellular signal-related kinase 1/2 and reversing the downregulation of perilipin protein in TNF-alpha-stimulated adipocytes. The acute lipolytic response to adrenergic stimulation of isoproterenol was also restricted by metformin. A high concentration of glucose in the adipocyte culture promoted the basal rate of glycerol release and significantly enhanced the lipolytic action stimulated by either TNF-alpha or isoproterenol. Metformin not only inhibits the basal lipolysis simulated by high glucose, but also suppresses the high glucose-enhanced lipolysis response to TNF-alpha or isoproterenol. The antilipolytic action in adipocytes could be the mechanism by which cellular action by metformin reduces systemic FFA concentration and thus improves insulin sensitivity in obese patients and the hyperglycemic conditions of NIDDM.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0952-5041
pubmed:author
pubmed:issnType
Print
pubmed:volume
37
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
175-83
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:16901933-Adipocytes, pubmed-meshheading:16901933-Adrenergic beta-Agonists, pubmed-meshheading:16901933-Animals, pubmed-meshheading:16901933-Carrier Proteins, pubmed-meshheading:16901933-Cells, Cultured, pubmed-meshheading:16901933-Glucose, pubmed-meshheading:16901933-Humans, pubmed-meshheading:16901933-Hypoglycemic Agents, pubmed-meshheading:16901933-Isoproterenol, pubmed-meshheading:16901933-Lipolysis, pubmed-meshheading:16901933-Metformin, pubmed-meshheading:16901933-Mitogen-Activated Protein Kinase 1, pubmed-meshheading:16901933-Mitogen-Activated Protein Kinase 3, pubmed-meshheading:16901933-Phosphoproteins, pubmed-meshheading:16901933-Phosphorylation, pubmed-meshheading:16901933-Rats, pubmed-meshheading:16901933-Rats, Sprague-Dawley, pubmed-meshheading:16901933-Tumor Necrosis Factor-alpha
pubmed:year
2006
pubmed:articleTitle
Metformin reduces lipolysis in primary rat adipocytes stimulated by tumor necrosis factor-alpha or isoproterenol.
pubmed:affiliation
Department of Physiology and Pathophysiology, Peking University Health Science Center, 38 Xueyuan Road, Beijing 100083, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't