Publication Date:
1979-02-16
Description:
The mouse mutant genes obese (ob) and diabetes (db) cause similar obesity-diabetes states in homozygotes. These obesity syndromes are characterized by a more efficient conversion of food to lipid and, once stored, a slower rate of catabolism on fasting. Heterozygous mice, either ob/+ or db/+, survived a prolonged fast significantly longer than normal homozygotes (+/+); this suggests that the heterozygotes exhibited increased metabolic efficiency, a feature normally associated with both homozygous mutants. The existence of this thriftiness trait, if manifested by heterozygous carriers in wild populations, would lend credence to the thrifty gene concept of diabetes. Beneficial effects of normally deleterious genes may have played a role in the development of diabetes-susceptible human populations, as well as having provided the survival advantage that has allowed both the development and successful establishment of species in desert and other less affluent regions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coleman, D L -- New York, N.Y. -- Science. 1979 Feb 16;203(4381):663-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/760211" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Body Temperature Regulation
;
Diabetes Mellitus, Experimental/*genetics/metabolism
;
Fasting
;
Glucose/metabolism
;
Heterozygote
;
Insulin/blood
;
Mice
;
Mice, Obese/*genetics
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
