Potential role of leptin in increase of fatty acid synthase gene expression in chicken liver.
Leptin is reported to have direct effects on lipogenesis in peripheral tissues that are independent of its central effects on food intake and body weight. These experiments have been mainly carried out in rodents (different models of obesity) in which lipogenesis occurs in both adipose tissue and liver. Such effects are unknown in birds in which lipogenesis occurs essentially in the liver. In this study, leptin gene expression and circulating leptin levels were examined in two chicken lines, selected for high (FL) or low (LL) abdominal fat pad size, at different nutritional states (fasted and fed state). In addition, effects of recombinant chicken leptin on liver metabolism were investigated. Hepatic leptin and fatty acid synthase (FAS) gene expression and plasma leptin levels were significantly higher in FL than in LL chickens (P < 0.05). In both lines, fasting significantly reduced hepatic leptin and FAS mRNA levels (P < 0.05). Continuous administration of recombinant chicken leptin (8 microg/kg/h) during 6 h significantly inhibited food intake (51%) and increased leptinemia (23-fold) compared to untreated group. Despite the decrease of food intake, leptin significantly induced the expression of FAS in chicken liver. These changes were accompanied by a significant down-regulation of leptin receptor gene expression, however SREBP-1, the main transcription factor of lipogenic genes, remained unchanged. This result suggests a local potential role of leptin in the regulation of avian hepatic lipogenesis, and explain, at least partly, the metabolic changes evolved during the divergent selection of FL and LL chickens.
Dridi
Sami
S
Laboratory of Physiology and Immunology of Domestic Animals, KU Leuven, 3001 Heverlee, Belgium. sami.dridi@agr.kuleuven.ac.be
Buyse
Johan
J
Decuypere
Eddy
E
Taouis
Mohammed
M
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D015152:Blotting, Northern / Q000662:veterinary; D002645:Chickens / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D005215:Fasting / Q000378:metabolism; D064429:Fatty Acid Synthases / Q000096:biosynthesis* / Q000235:genetics; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects* / Q000502:physiology; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000096:biosynthesis / Q000235:genetics / Q000494:pharmacology* / Q000502:physiology; D050356:Lipid Metabolism / Q000187:drug effects; D008099:Liver / Q000187:drug effects* / Q000201:enzymology* / Q000378:metabolism / Q000502:physiology; D008297:Male; D009752:Nutritional Status / Q000502:physiology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism; D054411:Receptors, Leptin; D011994:Recombinant Proteins / Q000494:pharmacology; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000662:veterinary; D051779:Sterol Regulatory Element Binding Proteins / Q000235:genetics / Q000378:metabolism; D013974:Thyroxine / Q000097:blood; D014280:Triglycerides / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
D001786:Blood Glucose; D007328:Insulin; D020738:Leptin; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D011994:Recombinant Proteins; D051779:Sterol Regulatory Element Binding Proteins; D014280:Triglycerides; D014284:Triiodothyronine; D064429:Fatty Acid Synthases; D013974:Thyroxine