Leptin receptor expression and suppressor of cytokine signaling transcript levels in high-fat-fed rats

• Published in: Life sciences (1973) Vol. 67; no. 24; pp. 2971 - 2981
• Main Authors: Peiser, Christian, McGregor, Gerard Patrick, Lang, Rudolf Ernst
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 03.11.2000
• Subjects: Adipose Tissue, Brown - metabolism; Animals; Body Weight; Carrier Proteins - genetics; Carrier Proteins - metabolism; Dietary Fats - administration & dosage; DNA Primers - chemistry; Epididymis - metabolism; Epididymis - pathology; High-fat diet; Hypothalamus - metabolism; Leptin - blood; Leptin - pharmacology; Leptin receptor; Male; Proteins - genetics; Proteins - metabolism; Rats; Rats, Wistar; Receptors, Cell Surface; Receptors, Leptin; Repressor Proteins; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger - metabolism; Signal Transduction; Suppressor of cytokine signaling; Suppressor of Cytokine Signaling 3 Protein; Suppressor of Cytokine Signaling Proteins; Transcription Factors; Leptin receptor; Suppressor of cytokine signaling; High-fat diet
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/S0024-3205(00)00884-5

Several lines of evidence suggest that obese individuals have a higher set point for body weight regulation relative to lean subjects. Since obese rodents and humans have high serum levels of leptin, it has been hypothesized that this may be the result of an insensitivity to this weight reducing hormone. In this experiment we assessed whether feeding of a high-fat diet to rats affects leptin receptor (OB-R) transcript levels or induces up-regulation of the suppressors of leptin/cytokine induced signaling, SOCS-3 and PIAS-3. We found that despite a significant weight gain associated with markedly increased circulating leptin levels neither OB-R gene expression nor SOCS-3 or PIAS-3 mRNA levels were significantly altered in the high-fat fed rats. This was in contrast to control experiments where administration of exogenous leptin induced a several-fold increase in SOCS-3. It is concluded that high-caloric food intake per se is not sufficient to provoke suppression of leptin signaling via these factors in animals without genetic predisposition to obesity.