Low protein provision during the first year of life,but not during foetal life,affects metabolic traits,organ mass development and growth in male mink (Neovison vison)

Low protein provision in utero and post‐partum may induce metabolic disorders in adulthood. Studies in mink have mainly focused on short‐term consequences of low protein provision in utero whereas the long‐term responses to low protein (LP) provision in metabolically programmed mink are unknown. We investigated whether low protein provision in utero affects the long‐term response to adequate (AP) or LP provision after weaning in male mink. Eighty‐six male mink were exposed to low (19% of ME from CP; crude protein) or adequate (31% of ME from CP) protein provision in utero, and to LP (~20% of ME from CP) or AP (30–42% of ME from CP) provision post‐weaning. Being metabolically programmed by low protein provision in utero did not affect the response to post‐weaning diets. Dietary protein content in the LP feed after weaning was below requirements; evidenced by lower nitrogen retention (p < 0.001) preventing LP mink from attaining their growth potential (p < 0.02). LP mink had a lower liver, pancreas and kidney weight (p < 0.05) as well as lower plasma IGF‐1 concentrations at 8 and 25 (p < 0.05) weeks, and a higher incidence of hepatic lipidosis at 25 weeks (p < 0.05). Furthermore, LP mink had a higher body fat (p < 0.05) and lower body CP content (p < 0.05) at 50 weeks of age. It is concluded that some effects of low protein provision in utero can be alleviated by an adequate nutrient supply post‐partum. However, long‐term exposure to low protein provision in mink reduces their growth potential and induces transient hepatic lipidosis and modified body composition.