Inhibitory effects of leptin-related synthetic peptide 116-130 on food intake and body weight gain in female C57BL/6J ob/ob mice may not be mediated by peptide activation of the long isoform of the leptin receptor
Autor: | M C Leinung, Daniel W. Lee, D W White, P Grasso, L A Tartaglia |
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Rok vydání: | 1999 |
Předmět: |
Blood Glucose
Leptin medicine.medical_specialty Endocrinology Diabetes and Metabolism Hypothalamus Mice Obese Peptide Receptors Cell Surface Biology Ligands Transfection Weight Gain Cell Line Mice In vivo Internal medicine Internal Medicine medicine Animals Receptor chemistry.chemical_classification Leptin receptor Homozygote Feeding Behavior Peptide Fragments Recombinant Proteins Mice Inbred C57BL Endocrinology Mechanism of action chemistry COS Cells Receptors Leptin Female medicine.symptom Signal transduction Carrier Proteins hormones hormone substitutes and hormone antagonists Body Temperature Regulation |
Zdroj: | Diabetes. 48(11) |
ISSN: | 0012-1797 |
Popis: | We recently reported that intraperitoneal administration of leptin-related synthetic peptide 116-130 [LEP-(116-130)] resulted in reduced food intake and significant weight loss in homozygous female C57BL/6J ob/ob mice. In this study, we used two in vitro bioassays to show that the interaction of LEP-(116-130) with the long form of the leptin receptor (OB-Rb), the receptor isoform that is predominantly expressed in the hypothalamus, is not required for the observed in vivo effects of the peptide on energy balance. LEP-(116-130) was unable to compete the binding of alkaline phosphatase-leptin fusion protein to OB-R. Moreover, LEP-(116-130) was unable to activate signal transduction by OB-Rb in vitro. In homozygous female C57BLKS/J-m db/db mice that do not express OB-Rb, intraperitoneal administration of LEP-(116-130) reduced body weight gain and blood glucose levels but not food intake, which further supports a mechanism of action that does not require peptide interaction with OB-Rb. |
Databáze: | OpenAIRE |
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