| First Author | Pankov IuA | Year | 1996 |
| Journal | Mol Biol (Mosk) | Volume | 30 |
| Issue | 4 | Pages | 743-7 |
| PubMed ID | 8965809 | Mgi Jnum | J:36646 |
| Mgi Id | MGI:84074 | Citation | Pankov IuA (1996) [Obesity gene and the product of expressing its hormone, leptin]. Mol Biol (Mosk) 30(4):743-7 |
| abstractText | Mice homozygous in recessive mutations affecting the obese gene gain excessive weight and develop diabetes mellitus, Positional cloning, exon trapping, and PCR were used to clone and sequence the murine and human ob cDNA. Of 10 organs examined, ob was expressed only in white adipose tissue. The ORF in ob cDNA encodes a protein of 167 residues. The murine and human proteins have 84% homology. Removal of the signal sequence yields a 145-residue polypeptide called leptin, which is secreted into blood and promotes burning of fat in the energy metabolism. Bioactive leptin was produced by gene engineering. Its administration to ob/ob mice reduced the body weight and abolished the diabetic manifestations. Slimming was also observed in healthy animals. Leptin proved effective in both peripheral and central administration (into the lateral ventricle). Using a polyclonal antiserum, leptin was found to be present in human blood as well as in murine blood and adipose tissue, but absent from those of ob/ob mice. On the strength of the data available, Friedman and coworkers have stated that the expression |
