| Popis: |
The existence of mice (ob/ob mice) with a genetic defect causing obesity and type II diabetes has been known since 1950. The mutated ob gene was recently identified and characterized. The gene encodes a 167 amino acid protein that has been given the name leptin, from the greek word leptos, meaning thin. The functionally active hormone, which is synthesised and secreted by adipocytes, is lacking in homozygote ob/ob mice, causing an increase in body fat. Injection of recombinant leptin in ob/ob mice induces loss of fat due to decreased appetite and increased energy expenditure. The ob gene product leptin acts via binding sites in the hypothalamus, where the centre for appetite and satiety is located. Research is now focused on the identification, characterization and cloning of leptin-receptors. Other mice, also with a genetic defect causing obesity and type II diabetes, do not respond to leptin treatment and are therefore suspected to have defective leptin receptors. |
