scholarly journals Identification of an obesity quantitative trait locus on mouse chromosome 2 and evidence of linkage to body fat and insulin on the human homologous region 20q.

1997 ◽  
Vol 100 (5) ◽  
pp. 1240-1247 ◽  
Author(s):  
A V Lembertas ◽  
L Pérusse ◽  
Y C Chagnon ◽  
J S Fisler ◽  
C H Warden ◽  
...  
1999 ◽  
Vol 19 (2) ◽  
pp. 549-561 ◽  
Author(s):  
Kristin Demarest ◽  
James McCaughran ◽  
Elham Mahjubi ◽  
Laura Cipp ◽  
Robert Hitzemann

2001 ◽  
Vol 7 (2) ◽  
pp. 171-177 ◽  
Author(s):  
SERGEI N. ORLOV ◽  
JULIE DUTIL ◽  
PAVEL HAMET ◽  
ALAN Y. DENG

Both linkage and use of congenic strains have shown that a chromosome region near the gene for the Na-K-ATPase α1-subunit ( Atp1a1) contained a quantitative trait locus (QTL) for blood pressure (BP). Currently, two congenic strains, designated S.M5 and S.M6, were made by replacing a segment of the Dahl salt-sensitive SS/Jr (S) rat by the homologous region of the Milan normotensive rat (MNS). In S.M5, the gene for Atp1a1 is from the MNS strain; whereas in S.M6, Atp1a1 is from the S strain. The baseline activity of the α1-Na-K-ATPase and its stoichiometry were evaluated by an assay of ouabain-sensitive inwardly and outwardly directed 86Rb and 22Na fluxes in erythrocytes. The two congenic strains showed a similar BP, but both had a BP lower than that of S rats ( P < 0.0001). Neither the α1-Na-K-ATPase activity nor its stoichiometry was affected by the substitution of the Atp1a1 alleles of S by those of MNS. Thus the BP-lowering effects observed in S.M5 and S.M6 could not be attributed to the α1-Na-K-ATPase activity or its stoichiometry. Atp1a1 is not supported as a candidate to be a BP QTL.


1997 ◽  
Vol 15 (3) ◽  
pp. 273-276 ◽  
Author(s):  
Anthony G. Comuzzie ◽  
James E. Hixson ◽  
Laura Almasy ◽  
Braxton D. Mitchell ◽  
Michael C. Mahaney ◽  
...  

2009 ◽  
Vol 38 (2) ◽  
pp. 226-232 ◽  
Author(s):  
Heike Vogel ◽  
Matthias Nestler ◽  
Franz Rüschendorf ◽  
Marcel-Dominique Block ◽  
Sina Tischer ◽  
...  

New Zealand obese (NZO) mice present a metabolic syndrome of obesity, insulin resistance, and diabetes. To identify chromosomal segments associated with these traits, we intercrossed NZO mice with the lean and diabetes-resistant C57BL/6J (B6) strain. Obesity and hyperglycemia in the (NZO×B6)F2 intercross population were predominantly due to a broad quantitative trait locus (QTL) on chromosome 1 ( Nob3; logarithm of the odds score 16.1, 16.0, 4.0 for body weight, body fat, and blood glucose, respectively), producing a difference between genotypes of 12.7 or 5.2 g of body weight and 12.0 or 4.0 g of body fat in females or males, respectively. In addition, significant QTL on chromosomes 3 and 13 and suggestive QTL on chromosomes 4, 6, 9, 12, 14, and 19 contributed to the obese phenotype. Distal chromosome 5 was significantly linked with plasma cholesterol (LOD score 10.7). Introgression of two segments of Nob3 into B6 confirmed the adipogenic effect of the QTL and suggested the presence of at least one causal gene. Haplotype mapping reduced the critical region of the distal part of the QTL to 31 Mbp containing the potential candidates Nr1i3, Apoa2, Atp1a2, Prox1, and Hsd11b1. We conclude that obesity and hyperglycemia of NZO is to a large part caused by variant genes located in Nob3 on chromosome 1. Since these exert robust effects on a B6 background, the QTL Nob3 is a prime target for identification of a novel diabesity gene.


SLEEP ◽  
2007 ◽  
Vol 30 (10) ◽  
pp. 1255-1263 ◽  
Author(s):  
Jonathan P. Wisor ◽  
Martin Striz ◽  
Jason DeVoss ◽  
Greer M. Murphy ◽  
Dale M. Edgar ◽  
...  

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