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)

TY - JOUR

T1 - 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)

AU - Vesterdorf, Kristine Høvelt

AU - Blanche, D.

AU - Harrison, Adrian Paul

AU - Matthiesen, Connie Frank

AU - Tauson, Anne-Helene

PY - 2014/4

Y1 - 2014/4

N2 - 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.

AB - 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.

U2 - 10.1111/jpn.12108

DO - 10.1111/jpn.12108

M3 - Journal article

C2 - 23909380

SN - 0931-2439

VL - 98

SP - 357

EP - 372

JO - Journal of Animal Physiology and Animal Nutrition

JF - Journal of Animal Physiology and Animal Nutrition

IS - 2

ER -