International Mammalian Genome Society

The 15th International Mouse Genome Conference (2001)


POSTER 10 - THE IMPORTANCE OF LEPTIN PRODUCTION AND RECEPTION IN MOUSE LINES DIVERGENTLY SELECTED ON FATNESS AFTER INTROGRESSION OF THE  LEPOB AND LEPRDB MUTATIONS

Dr Lutz Bünger
Division of Biological Sciences, ICAPB
The University of Edinburgh
Kings Buildings, West Mains Road
Edinburgh EH9 3JT

Co-Authors: 1)Bünger L, 2)Forsting J, 1)McDonald KL, 3)Horvat S, 4)Speakman JR, 4)Hochscheid S, 5)Baile CA, 1)Hill WG
Institutions: 1)Institute of Cell, Animal and Population Biology, University of Edinburgh, 2)Fachhochschule Lemgo, Liebigstraße, 3)Biotechnical Faculty, Zootechnical Department, University of Ljubljana, 4)Aberdeen Centre for Energy Regulation and Obesity (ACERO), Department of Zoology, University of Aberdeen and Division of Appetite and Energy Balance, Rowett Research Institute, 5)University of Georgia

Divergent selection for over nearly 60 generations produced a fat (F) and a lean line (L), diverging by a factor of over 4 in fat%. To elucidate the importance of leptin in the genetic change produced by this long-term selection on fatness, the two recessive mutations Lepob and Leprdb causing a leptin deficiency and a leptin receptor defect, respectively, were introgressed into both selected mouse lines. After seven backcrosses, an intercross was made to produce all three genotypes at the Lepob or Leprdb locus in the F or L background to examine the line divergence in the absence of leptin and of the leptin receptor. In addition to the total fat content of the body at 106d, plasma leptin, glucose levels, resting metabolic rate, body temperature, and food and water intake were measured. 

Wildtype male mice of the F and L line have about 21% and 5% fat. These values increase dramatically in both lines when the leptin production or leptin reception is knocked-out: F-Lepob/Lepob and F-Leprdb/Leprdb reach 34 and 38%, respectively and the corresponding values for the L line are 37 and 29%.  These results show that the polygenic effects obtained by long-term selection in the L line can not “correct” the knock-out effects of Lepob on leptin production, and only to a minor degree, the effects of Leprdb on leptin reception. This also indicates that the genes responsible for the leanness of the L line most likely act downstream from leptin and/or are dependent on leptin.


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