| Autor: |
Bennett, Pamela A., Lindell, Kajsa, Karlsson, Cecilia, Robinson, Iain C. A. F., Carlsson, Lena M. S., Carlsson, Björn |
| Předmět: |
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| Zdroj: |
Neuroendocrinology; 1998, Vol. 67 Issue 1, p29-36, 8p, 1 Black and White Photograph, 2 Diagrams, 1 Chart, 2 Graphs |
| Abstrakt: |
Leptin affects body weight and reproduction mainly via receptors in the central nervous system. Different isoforms of the leptin receptor (leptin-R) exist, including a long isoform (leptin-R[sub L] ) with signalling capacity and short isoforms (leptin-R[sub S] ) with unknown function. The aim of this study was to examine leptin-R gene expression in different regions of the brain under conditions with altered body weight, in the female rat, including ovariectomy (OVX), oestradiol (E[sub 2] ) treatment, fasting and a genetic model of obesity (Zucker fa/fa). Leptin-R gene expression was analysed by in situ hybridization using probes recognizing all receptor isoforms (leptin-R) or specifically leptin-R[sub L] . Transcripts recognized by the leptin-R probe were abundant in the choroid plexus (CP), arcuate nucleus (ARC), ventromedial nucleus (VMN), thalamus (TH) and piriform cortex (PC). Leptin-R[sub L] transcripts were detected in the ARC, VMN, TH and PC but not in the CP. Although no sex difference was observed, leptin-R gene expression was reduced by E[sub 2] administration and increased by OVX. Administration of E[sub 2] reduced leptin-R[sub L] gene expression in the ARC and VMN but did not alter the expression in the TH or PC. OVX had no effect on the expression of leptin-R[sub L] mRNA. Fasting also caused a differential regulation of leptin-R mRNAs, with an increase in abundance of leptin-R[sub L] transcripts in the TH despite a decrease in leptin-R in this area. Obese Zucker rats had a similar pattern of expression with an increased expression of leptin-R[sub L] transcripts in all brain areas analysed and a decrease in leptin-R gene expression. These results demonstrate a differential regulation of leptin-R[sub L] and leptin-R[sub S] which could provide a mechanism for regulating access to, and sensitivity of, discrete regions of the brain for circulating leptin. We suggest that fasting and E[sub 2] alter the balance between leptin-R[sub L] and leptin-R[sub S] and that this could increase tissue sensitivity to leptin. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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