Effect of late gestation low protein supply to mink (Mustela vison) dams on reproductive performance and metabolism of dam and offspring

Abstract

Protein malnutrition in utero that induces permanent changes in metabolism has been investigated intensively in various animals in recent years, but to the best of our knowledge, not yet in the mink, a strict carnivore. In the present study, minks were fed either a low-protein (LP) diet, i.e., with a protein:fat:carbohydrate ratio of 14:51:35% of metabolisable energy (ME), or an adequate-protein diet (AP), i.e. 29:56:15% of ME, from when implantation was completed until parturition (17.9 +/- 3.6 days). Respiration and balance experiments were performed during both gestation and lactation. Plasma concentrations of leptin, IGF-1, and insulin were determined by radioimmunoassay; the relative abundances of glucose-6-phosphatase (G-6-Pase), fructose-1,6-bisphosphatase (Fru-1,6-P2ase), phosphoenol-pyruvate carboxykinase (PEPCK), and pyruvate kinase (PKM2) were determined in liver, and abundances of adiponectin and leptin in adipose tissue were determined by real-time quantitative PCR (q PCR). The protein supply only affected quantitative metabolism traits during the period of differentiated feeding. The dietary composition was reflected in the nitrogen metabolism and substrate oxidation, but no effects remained during lactation. The LP dams tended to have a smaller liver mass in relation to body weight than did AP dams (2.5% vs. 2.9%; p = 0.09), significantly less leptin mRNA (p < 0.05), and 30.6% fewer kits per mated female (p = 0.03). Furthermore, F1-generation kits exposed to protein restriction during foetal life (FLP1; 10.3 g) had a lower birth weight (p = 0.004) than did F1-generation kits exposed to adequate protein (FAP1; 11.3 g). Differences remained significant until 21 days of age (120.4 g vs. 127.6 g; p = 0.005). The FLP1 foetuses displayed a lower abundance of Fru-1,6-P2ase mRNA (p = 0.007) and of PKM2 mRNA (p = 0.002) than did FAP1 foetuses. Whether these changes during foetal life cause permanent changes in the glucose homeostasis of the offspring and result in the transmission of epigenetic phenotypic changes, as seen in the rat, needs further investigation.

Foetal life protein restriction in male mink (Neovison vison) kits lowers post-weaning protein oxidation and the relative abundance of hepatic fructose-1,6-bisphosphatase mRNA

“…The postweaning dietary protein provision was clearly reflected in the N balance data and supported by the OXP during postweaning growth. This was similar to findings among female dams fed an LP or an AP where the amount of dietary protein was also clearly reflected in both the N metabolism and the level of protein oxidation (Matthiesen et al, 2010a).…”

“…Studies in mink have shown that low protein provision to pregnant dams leads to foetal adaptations, resulting in a lower mRNA expression of some key hepatic gluconeogenic and glycolytic enzymes in both F 1 - (Matthiesen et al, 2010a) and F 2 -generation foetuses (Matthiesen et al, 2010b). These findings indicate that protein provision to the mother plays an important role for the offspring.…”

“…Kits exposed to low protein provision during foetal life (FL) had significantly lower birth weight (10.3 g v. 11.3 g; P 5 0.004) than kits given adequate protein provision during foetal life (FA). The FL kits continued to have significantly lower body weight (BW) until 28 days of age, when the BW was found to be similar between the groups (Matthiesen et al, 2010a). Further information about the late gestation diets and the mothers of the male kits is provided elsewhere (Matthiesen et al, 2010a).…”

“…The FL kits continued to have significantly lower body weight (BW) until 28 days of age, when the BW was found to be similar between the groups (Matthiesen et al, 2010a). Further information about the late gestation diets and the mothers of the male kits is provided elsewhere (Matthiesen et al, 2010a). The dams and their offspring were fed conventional feed containing adequate protein from parturition until weaning.…”

“…Further, Russell et al (2002) found that protein oxidation was correlated to some extent to dietary protein intake in cats, but only if the protein requirement was met (Green et al, 2008). Studies in mink have, however, shown that the rates of amino acid decarboxylation (Tauson et al, 2001) and protein oxidation are regulated according to the dietary protein supply, even if the level of dietary protein is low (Fink et al, 2004) or below the requirement (Matthiesen et al, 2010a). These findings indicate some metabolic flexibility in the strict carnivores.…”