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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Healthy Body Weight Research » Research » Publications at this Location » Publication #336060
Title: Both paternal exercise and healthy diet are required to protect offspring from high fat diet-induced obesity and type 2 diabetes risk in mice

Author
item Larson, Kate
item Krout, Danielle
item Garcia Garcia, Rolando
item Roemmich, James

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/1/2016
Publication Date: 4/1/2017
Citation: Larson, K.J., Krout, D.P., Garcia Garcia, R.A., Roemmich, J.N. 2017. Both paternal exercise and healthy diet are required to protect offspring from high fat diet-induced obesity and type 2 diabetes risk in mice [abstract]. Journal of Federation of American Societies for Experimental Biology. 31:456.2.

Interpretive Summary:

Technical Abstract: Objective: Paternal eating and physical activity behaviors peri-conception may influence offspring obesity and type 2 diabetes (T2D) risk. A recent study showed that paternal exercise increased offspring susceptibility to obesity when the offspring consumed a high fat (HF) diet. However, it is not yet known how paternal HF diet and paternal exercise interact to alter offspring adiposity and T2D risk. Method: Three week old male C57BL/6J mice were fed a control normal fat (NF) diet (16% fat) or a HF diet (45% fat) and provided voluntary wheel running exercise or cage activity (sedentary) for 3 months prior to mating with NF diet-fed dams. After weaning, male offspring were fed NF or HF diet for 3 months. Results: Compared to offspring born from cage-active fathers fed a NF diet, offspring of cage-active fathers fed a HF diet had decreased body weights at postnatal days 5, 12, and 21 as well as increased insulin resistance at 5 months of age. Paternal HF diet-induced changes in offspring body weights early in post-natal life and insulin resistance in adulthood were abolished when fathers exercised. In addition, paternal exercise prevented postnatal HF diet-induced body and adipose tissue weight increases in offspring at 5 months of age, but only when fathers were fed NF diets. Conclusion: These findings suggest that paternal exercise reduces risk for adiposity and insulin resistance in offspring exposed to a HF diet, but only when fathers consumed a NF diet and exercised. A paternal NF diet alone, without paternal exercise, did not protect HF diet-induced body and adipose tissue weight gains in offspring. Future studies will determine physiological mechanisms underlying beneficial effects of combined exercise and diet through paternal lineage.