AI Article Synopsis
- Leptin is a protein produced by fat cells that helps regulate hunger and energy use, with its levels linked to body mass index (BMI) and potential resistance in obese individuals.
- The study investigated how insulin affects leptin signaling by using Huh 7 cells that were genetically modified to express the leptin receptor.
- Results showed that insulin can inhibit leptin's activation of a signaling pathway (STAT3 phosphorylation) in a dose and time-dependent way, while another enzyme's activity (JAK2) remained unaffected.
Article Abstract
Leptin, the 16 kDa protein product of the ob gene, is secreted by adipocytes. The long form leptin receptor (ObRb) is expressed at high levels in the hypothalamus, and regulates appetite and energy expenditure. The fact that serum concentration of leptin is correlated with body mass index (BMI) suggests reduced sensitivity to leptin. Even though hyperinsulinemia and hyperleptinemia could coexist in obese humans, little is known about the interaction of insulin and leptin. In this study, we examined the effect of insulin on leptin signaling using Huh 7 cells transiently transfected with ObRb cDNA. Insulin inhibits leptin-induced STAT3 phosphorylation in a time- and dose-dependent manner without affecting Janus tyrosine kinases (JAKs) JAK2 phosphorylation. Okadaic acid prevents the inhibitory effect of insulin on leptin-induced STAT3 activation.
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| http://dx.doi.org/10.1016/s0303-7207(03)00180-1 | DOI Listing |
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