"Exercise Improves Glucose Homeostasis in Old Mice" by Alexandra Canizales, David J. Buckley et al.
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Abstract

Age is an independent risk factor for the development of type 2 diabetes, which is characterized in part by impaired glucose homeostasis, greater body weight and visceral adiposity. In older humans, exercise has been demonstrated to be a viable modality to improve these aforementioned outcomes. Surprisingly, to date, no one has assessed whether exercise improves glucose tolerance in old mice. Further the mechanism(s) of improvement in old animals independent of overt obesity is not well understood. PURPOSE: The purpose of this study was to determine whether 8 weeks of voluntary wheel running would result in improved glucose tolerance and shed light on the potential target tissues, such as the visceral adipose, liver, and/or skeletal muscle that are mechanistically responsible for improvements in glucose homeostasis. METHODS: Old (22-24mo) male C57BL6 mice were randomly selected to undergo 8 weeks of voluntary wheel running (n=13-25) or remain sedentary (n=13-15). The day prior to and following 8 weeks of voluntary wheel running, mice underwent a glucose tolerance test (GTT), which was assessed by i.p. injection of glucose (2g/kg). Blood glucose was measured over 120min using a handheld glucometer. Following euthanasia, the liver, perigonadal visceral adipose tissue (WAT), and quadriceps muscles were dissected and weighed. Differences were assessed by either an independent samples t-test or a simple linear regression. Data expressed as mean±SEM. RESULTS: Mice ran an average of 679.0±134.1 m/day. Mice which ran less than 100m/day were excluded from analysis. Δ(change from pre-post) area under the curve analysis of the GTT revealed that voluntary wheel running resulted in substantial improvements in glucose tolerance (Units Arbitrary (AU); Control: 1047±2037AU, Exercise -6305±1841AU; p=0.0061) and ΔBody weight (Control: 0.9067±0.5192g, Exercise:-3.893±0.5757g; p=0.0003) compared to controls. Interestingly, we observed that exercise only led to a reduction in WAT (Control: 0.7982±0.1346g, Exercise:0.4865±0.08099g; p=0.02) weight, but no differences in the weight of the liver (Control:2.032±0.1357g, Exercise:1.867±0.07141g; p=0.1293) or quadriceps (Control: 0.3311±0.01299g, Exercise: 0.3397±0.01265g; p=0.31). We then sought to determine which of these outcomes (i.e. body weight, tissue weight) was most closely related with glucose tolerance. We correlated body weight, WAT weight, liver weight, and quad weight with post GTT area under the curve. We found that body weight (R2=0.16, p=0.02) and WAT weight (R2=0.26, p=0.0065) were most closely associated with glucose tolerance. Whereas liver (R2=0.001; p=0.84) and surprisingly quad weight (R2=0.05; p=0.25) were not related to AUC. CONCLUSION: Our results are the first to demonstrate that exercise is sufficient to induce improvements in glucose tolerance in old mice. Further, these changes appear to be mostly driven by visceral adiposity and are independent of changes in lean mass and liver weight. Thus, highlighting visceral adipose as a target tissue to further study the mechanism(s) by which exercise improves glucose homeostasis in aging.

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