Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1996-10-8
pubmed:abstractText
Leptin, the product of the ob gene, is a hormone secreted by adipocytes. Animals with mutations in the ob gene are obese and lose weight when given leptin, but little is known about the physiological role of leptin in humans. Obese subjects have higher concentrations of leptin than lean subjects, the strongest correlation being with percentage body fat. Thus, it appears that obese subjects are resistant to the effects of endogenously secreted leptin. We have also shown that insulin stimulates leptin production, chronically but not acutely, presumably through its trophic effect on adipocytes. Troglitazone is an insulin-sensitizing thiazolidinedione, which improves hepatic and skeletal muscle insulin resistance in NIDDM and obesity. This study was undertaken to investigate the effects of troglitazone on leptin production in vitro and in vivo. In the presence and absence of 100 nmol/l insulin and 10 umol/l troglitazone, 72-h primary cultures of isolated abdominal adipocytes were studied. Insulin led to an almost twofold increase in leptin in vitro, and this increase was completely abolished by coincubation with troglitazone. Incubation with troglitazone alone led to a 40% decrease in leptin production. In obese patients administered troglitazone 200 mg twice daily for 12 weeks, there was no significant change in fasting plasma leptin concentrations, despite a 40-50% reduction in fasting and postmeal plasma insulin concentrations. Troglitazone treatment led to a significant increase in insulin sensitivity, and there was a positive correlation between the change in insulin sensitivity and the change in plasma leptin concentration in these subjects. In conclusion, troglitazone treatment had no net effect on plasma leptin concentrations, possibly because of improvement in insulin sensitivity and reduction in plasma insulin concentrations.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1276-8
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:8772734-Adipocytes, pubmed-meshheading:8772734-Adult, pubmed-meshheading:8772734-Animals, pubmed-meshheading:8772734-Blood Glucose, pubmed-meshheading:8772734-Cells, Cultured, pubmed-meshheading:8772734-Chromans, pubmed-meshheading:8772734-Fasting, pubmed-meshheading:8772734-Female, pubmed-meshheading:8772734-Glucose, pubmed-meshheading:8772734-Humans, pubmed-meshheading:8772734-Hyperinsulinism, pubmed-meshheading:8772734-Hypoglycemic Agents, pubmed-meshheading:8772734-Infusions, Intravenous, pubmed-meshheading:8772734-Insulin, pubmed-meshheading:8772734-Leptin, pubmed-meshheading:8772734-Male, pubmed-meshheading:8772734-Middle Aged, pubmed-meshheading:8772734-Obesity, pubmed-meshheading:8772734-Protein Biosynthesis, pubmed-meshheading:8772734-Proteins, pubmed-meshheading:8772734-Thiazoles, pubmed-meshheading:8772734-Thiazolidinediones
pubmed:year
1996
pubmed:articleTitle
Effect of troglitazone on leptin production. Studies in vitro and in human subjects.
pubmed:affiliation
Department of Medicine, University of California at San Diego, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't