Spontaneous mutation in the db gene results in obesity and diabetes in CD-1 outbred mice

被引:15
作者
Brown, JA
Chua, SC
Liu, SM
Andrews, MT
Vandenbergh, JG [1 ]
机构
[1] N Carolina State Univ, Dept Zool, Raleigh, NC 27695 USA
[2] N Carolina State Univ, Dept Genet, Raleigh, NC 27695 USA
[3] Columbia Univ, New York, NY 10032 USA
关键词
leptin; phenotype; mouse; insulin;
D O I
10.1152/ajpregu.2000.278.2.R320
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Five allelic mutants of the diabetes (db) gene have been previously described in mice and rats causing obesity, infertility, and varying degrees of diabetes. We have identified a new, spontaneous mutation resulting in obesity and diabetes in a colony of CD-1 outbred mice, Mus musculus domesticus. Genetic complementation studies indicated that the new mutation was an allele of the diabetes locus. Sequence analysis of cDNA fragments showed a deletion of one G residue located in exon 12 of the leptin receptor gene. The mutation, Lepr(db-NCSU), results in a frameshift and reduces Lepr transcript levels 10-fold. Mutant mice drank up to four times more water and were up to two times heavier than wild-type mice. Blood glucose and plasma insulin and leptin concentrations were sexually dimorphic among affected mice, suggesting an effect of sex steroids. Mortality of affected males was 100% by 5 mo, whereas affected females survived up to 10 mo of age.
引用
收藏
页码:R320 / R330
页数:11
相关论文
共 36 条
[1]   Role of leptin in the neuroendocrine response to fasting [J].
Ahima, RS ;
Prabakaran, D ;
Mantzoros, C ;
Qu, DQ ;
Lowell, B ;
MaratosFlier, E ;
Flier, JS .
NATURE, 1996, 382 (6588) :250-252
[2]   DESCRIPTION OF A NEW MODEL OF GENETIC OBESITY - THE DBPAS MOUSE [J].
AUBERT, R ;
HERZOG, J ;
CAMUS, MC ;
GUENET, JL ;
LEMONNIER, D .
JOURNAL OF NUTRITION, 1985, 115 (03) :327-333
[3]  
Ausubel FM., 1994, Curr. Protoc. Mol. Biol
[4]   Development of a novel polygenic model of NIDDM in mice heterozygous for IR and IRS-1 null alleles [J].
Bruning, JC ;
Winnay, J ;
BonnerWeir, S ;
Taylor, SI ;
Accili, D ;
Kahn, CR .
CELL, 1997, 88 (04) :561-572
[5]   Correction of the sterility defect in homozygous obese female mice by treatment with the human recombinant leptin [J].
Chehab, FE ;
Lim, ME ;
Lu, RH .
NATURE GENETICS, 1996, 12 (03) :318-320
[6]   Evidence that the diabetes gene encodes the leptin receptor: Identification of a mutation in the leptin receptor gene in db/db mice [J].
Chen, H ;
Charlat, O ;
Tartaglia, LA ;
Woolf, EA ;
Weng, X ;
Ellis, SJ ;
Lakey, ND ;
Culpepper, J ;
Moore, KJ ;
Breitbart, RE ;
Duyk, GM ;
Tepper, RI ;
Morgenstern, JP .
CELL, 1996, 84 (03) :491-495
[7]   Leptin is a metabolic gate for the onset of puberty in the female rat [J].
Cheung, CC ;
Thornton, JE ;
Kuijper, JL ;
Weigle, DS ;
Clifton, DK ;
Steiner, RA .
ENDOCRINOLOGY, 1997, 138 (02) :855-858
[8]   SINGLE-STEP METHOD OF RNA ISOLATION BY ACID GUANIDINIUM THIOCYANATE PHENOL CHLOROFORM EXTRACTION [J].
CHOMCZYNSKI, P ;
SACCHI, N .
ANALYTICAL BIOCHEMISTRY, 1987, 162 (01) :156-159
[9]   Monogenic models of obesity [J].
Chua Jr. S.C. .
Behavior Genetics, 1997, 27 (4) :277-284
[10]   Fine structure of the murine leptin receptor gene: Splice site suppression is required to form two alternatively spliced transcripts [J].
Chua, SC ;
Koutras, IK ;
Han, L ;
Liu, SM ;
Kay, J ;
Young, SJ ;
Chung, WK ;
Leibel, RL .
GENOMICS, 1997, 45 (02) :264-270