Skip to main content
ARS Home » Plains Area » Clay Center, Nebraska » U.S. Meat Animal Research Center » Livestock Bio-Systems » Research » Publications at this Location » Publication #170950
Title: THE M16 MOUSE: AN OUTBRED ANIMAL MODEL OF EARLY ONSET POLYGENIC OBESITY AND DIABESITY

Author
item Allan, Mark
item EISEN, EUGENE - NORTH CAROLINA STATE UNIV
item POMP, DANIEL - UNIV OF NEBRASKA, LINCOLN

Submitted to: Obesity Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/1/2004
Publication Date: 9/1/2004
Citation: Allan, M.F., Eisen, E.J., Pomp, D. 2004. The M16 mouse: An outbred animal model of early onset polygenic obesity and diabesity. Obesity Research. 12(9):1397-1407.

Interpretive Summary: Obesity in the US has been identified as an epidemic for over two decades, and yet the number of individuals classified as obese continues to grow. We evaluated the M16 mouse to understand the consequences of long-term selective breeding for rapid weight gain, with an emphasis on obesity and obesity-induced diabetes (diabesity). M16 is the result of long-term selection for 3 to 6 week weight gain from an Institute Cancer Research (ICR) base population. Experiment 1 characterized males from both lines for body weights (3, 6, 8 wk), feed (4 to 8 wk) and H2O (6 to 8 wk) consumption, and heat loss, body composition and levels of several plasma proteins at 8 weeks of age. Experiment 2 characterized differences between lines for both sexes, at three ages (6, 8, 16 wks) and fed two diets (high and normal fat). Body weight, composition, blood glucose, and plasma insulin and leptin levels were evaluated after an 8 hour fast. At all ages measured, M16 mice were heavier, fatter, consume more feed, with increased insulin and leptin relative to ICR. M16 males and females were hyperglycemic relative to ICR, with 56 and 22% higher fasted blood glucose levels, at 8 weeks of age. M16 mice represent an outbred animal model to facilitate gene discovery and pathway regulation controlling early onset polygenic obesity and Type II diabetic phenotypes. Phenotypes prevalent in the M16 model, with obesity and diabesity exhibited at a young age, closely mirrors current trends in human populations.

Technical Abstract: Objective: To characterize the phenotypic consequences of long-term selective breeding for rapid weight gain, with an emphasis on obesity and obesity-induced diabetes (diabesity). Research Methods and Procedures: M16 is the result of long-term selection for 3- to 6-week weight gain from an Institute Cancer Research (ICR) base population. Experiment 1 characterized males from both lines for body weights (3, 6, and 8 weeks), feed (4 to 8 weeks) and H2O (6 to 8 weeks) consumption, and heat loss, body composition, and levels of several plasma proteins at 8 weeks of age. Experiment 2 characterized differences between lines for both sexes at three ages (6, 8, and 16 weeks) and fed two diets (high and normal fat). Body weight, composition, blood glucose, and plasma insulin and leptin levels were evaluated after an 8-hour fast. Results: At all ages measured, M16 mice were heavier, fatter, hyperphagic, hyperinsulinemic, and hyperleptinemic relative to ICR. M16 males and females were hyperglycemic relative to ICR, with 56% and 22% higher fasted blood glucose levels at 8 weeks of age. Discussion: M16 mice represent an outbred animal model to facilitate gene discovery and pathway regulation controlling controlling early onset polygenic obesity and type 2 diabetic phenotypes. Phenotypes prevalent in the M16 model, with obesity and diabesity exhibited at a young age, closely mirror current trends in human populations.