Abstract
The increase in high-energy dietary intakes is a well-known risk factor for many diseases, and can also negatively impact the tendon. Ancestral lifestyle can mitigate the metabolic harmful effects of offspring exposed to high-fat diet (HF). However, the influence of paternal exercise on molecular pathways associated to offspring tendon remodeling remains to be determined. We investigated the effects of 8 weeks of paternal resistance training (RT) on offspring tendon proteome exposed to standard diet or HF diet. Wistar rats were randomly divided into two groups: sedentary fathers and trained fathers (8 weeks, three times per week, with 8–12 dynamic movements per climb in a stair climbing apparatus). The offspring were obtained by mating with sedentary females. Upon weaning, male offspring were divided into four groups (five animals per group): offspring from sedentary fathers were exposed either to control diet (SFO-C), or to high-fat diet (SFO-HF); offspring from trained fathers were exposed to control diet (TFO-C) or to a high-fat diet (TFO-HF). The Nano-LC-MS/MS analysis revealed 383 regulated proteins among offspring groups. HF diet induced a decrease of abundance in tendon proteins related to extracellular matrix organization, transport, immune response and translation. On the other hand, the changes in the offspring tendon proteome in response to paternal RT were more pronounced when the offspring were exposed to HF diet, resulting in positive regulation of proteins essential for the maintenance of tendon integrity. Most of the modulated proteins are associated to biological pathways related to tendon protection and damage recovery, such as extracellular matrix organization and transport. The present study demonstrated that the father’s lifestyle could be crucial for tendon homeostasis in the first generation. Our results provide important insights into the molecular mechanisms involved in paternal intergenerational effects and potential protective outcomes of paternal RT.
Highlights
The global obesity disease is often causally linked to marked changes in lifestyle and diet, such as increases in high-energy dietary intakes and low levels of physical activity (Hruby and Hu, 2015)
There was no difference between TFO-C and sedentary father exposed to either control diet (SFO-C) group, while paternal resistance training (RT) prevented the body weight gain, and reduced adiposity markers in the TFO-HF when compared to sedentary father exposed to high-fat diet (SFO-HF) group after 24 weeks (p = 0.001)
There were clear differences in the patterns of protein abundance levels among the others offspring groups (SFO-C, SFO-HF and TFO-HF), suggesting that paternal RT modulates the protein profile of the calcaneal tendon, especially noticeable in offspring exposed to HF diet
Summary
The global obesity disease is often causally linked to marked changes in lifestyle and diet, such as increases in high-energy dietary intakes and low levels of physical activity (Hruby and Hu, 2015). Zucker rats displayed disorganized collagen fibril bundles and decreased average fibril diameter accompanied by adverse effects in displacement at maximum load and maximum strain, indicating a significant harmful ECM remodeling in deep digital flexor tendon (Biancalana et al, 2010). In this way, further investigations are necessary to determine strategies to attenuate these detrimental responses on tendons. Paternal obesity is a risk factor for increased adiposity and glucose intolerance in the adult offspring (Ng et al, 2010; McPherson et al, 2015), besides harming the sperm metabolic function and fertility (McPherson et al, 2015). Paternal intergenerational inheritance has important implications in the offspring phenotype
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