Paternal obesity programs metabolic syndrome in offspring. Low-impact exercise in obese males improves the metabolic health of female offspring, however whether this occurred in male offspring remained unknown. C57BL/6NHsd (Harlan) mice were fed a control diet (CD; 6% fat, n = 7) or a high-fat diet (HFD; 21% fat, n = 16) for 18 weeks. After 9 weeks, HFD-fed mice either remained sedentary (HH, n = 8) or undertook low-moderate exercise (HE, n = 8) for another 9 weeks. Male offspring were assessed for glucose/insulin tolerance, body composition, plasma lipids, pancreatic islet cell morphology and microRNA expression. Founder HH induced glucose intolerance, insulin insensitivity, and hyperlipidaemia in male offspring (p < 0.05). Metabolic health was fully restored in male offspring by founder exercise to control levels. Founder HH reduced pancreatic β-cell area and islet cell size in male offspring, and altered the expression of 13 pancreatic microRNAs (p < 0.05). Founder HE led to partial restoration of pancreatic islet cell morphology and the expression of two pancreatic microRNAs (let7d-5p, 194-5p) in male offspring. Founder HE reduced male offspring adiposity, increased muscle mass, reduced plasma free fatty acids (FFAs), and further altered pancreatic microRNAs (35 vs. HH; 32 vs. CD) (p < 0.05). Low-impact exercise in obese fathers prior to conception, without dietary change, may be a viable intervention strategy to reduce the illeffects of obesity-induced paternal programming in male offspring.
Keywords: sperm; fertility; nutrition.