| Research Abstract |
Present study aimed to clarify the functional role of hepatic-portal, leptin sensor in regulation of energy metabolism. Hepatic-portal infusion of leptin at a dose of 1000 μg/rat suppressed 24-h cumulative food intake and increased activity of sympathetic nerve innervating brown adipose tissue (BAT). However, that treatment with small dosage of leptin did not affect food intake nor nerve activity. Administration of leptin into the hepatic-portal vein decreased mRNA expression of sterol regulatory element binding protein and its downstream enzymes related with lipogenesis. Administration of histamine into the third cerebroventricle induced c-fos expressions in the paraventricular nucleus and the arcuate nucleus. In extrahypothalamic regions, c-fos expression was observed in the hippocampus and the amygdala. Intra-peritoneal administration of adiponectin (1.5mg/kg for 7 days) attenuated body weight gain and reduced visceral adiposity in agouti yellow (A^y/a) obese mice. In addition, adiponectin treatment increased mRNA expression of UCP1 mRNA in the BAT. Furthermore, peripheral administration of adiponectin (1.5mg/kg, one shot) increased BAT sympathetic nerve activity accompanied by an increase of body temperature. These above responses were not induced by central application of adiponectin (15μg/kg). In summary, present study indicate that hepatic-portal leptin sensor may regulate lipid metabolism in the liver, but adiponectin may regulate energy metabolism through action of its hepatic-portal sensor.
|
