Faculty Research 1980 - 1989


Thermogenesis in diabetes-obesity syndromes in mutant mice.


D L. Coleman

Document Type


Publication Date



Animal, Blood-Glucose: an, Body-Temperature, Body-Temperature-Regulation, Caloric-Intake, Diabetes-Mellitus-Experimental: pp, pa, Eating, Fatty-Acids-Nonesterified, Genotype, Mice, Mice-Mutant-Strains, Mice-Obese, Obesity-in-Diabetes: pp, pa, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S, Temperature

JAX Location


JAX Source

Diabetologia. 1982 Mar; 22(3):205-11.


AM14461, AM20725


The two mouse mutants, obese (ob) and diabetes (db), cause similar diabetes-obesity syndromes that are characterized by a marked increase in apparent metabolic efficiency with regard to utilization of energy. A failure to thermoregulate in a normal fashion would save energy which could then be diverted to other functions and be reflected as increased metabolic efficiency. This study assesses the contribution of a defect in thermogenesis to the increased metabolic efficiency. Thermogenesis in obese (ob) and diabetes (db) mutant mice was quantified at various environmental temperatures. Both mutants maintained body temperatures near normal when maintained at ambient temperatures (23 degrees C), and if exposed to cold at 10 degrees C for a brief period, became cold-adapted and would survive indefinitely at 4 degrees C. Rectal temperatures of mutants maintained at 4 degrees C were only 1 degree -2 degrees C less than those seen in normal mice. This maintenance of nearly normal body temperature at temperatures less than thermoneutral was reflected by increased food consumption in all mice maintained in the cold. The data presented suggest that the defect in thermogenesis in both mutants is not a major cause of the increased metabolic efficiency. Hyperinsulinaemia, a consistent feature of both mutants, might by increasing anabolic processes (synthesis) and decreasing degradation spare energy normally used for tissue turnover and account for some of this increased metabolic efficiency.

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