title: 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.
authors.affiliation: Department of Basic Animal and Veterinary Sciences, Faculty of Life Sciences, University of Copenhagen, Denmark.
authors.forename: Connie Frank
authors.initials: CF
authors.lastname: Matthiesen
authors.forename: Dominique
authors.initials: D
authors.lastname: Blache
authors.forename: Preben Dybdahl
authors.initials: PD
authors.lastname: Thomsen
authors.forename: Niels Enggaard
authors.initials: NE
authors.lastname: Hansen
authors.forename: Anne-Helene
authors.initials: AH
authors.lastname: Tauson
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000821:Animal Feed / Q000032:analysis*; D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D001835:Body Weight; D004032:Diet / Q000662:veterinary*; D004044:Dietary Proteins / Q000494:pharmacology*; D004435:Eating; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D007774:Lactation; D008098:Litter Size; D008099:Liver / Q000378:metabolism; D008907:Mink / Q000502:physiology*; D009584:Nitrogen / Q000378:metabolism; D011247:Pregnancy; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012098:Reproduction / Q000187:drug effects*
chemical_list: D004044:Dietary Proteins; D012333:RNA, Messenger; D009584:Nitrogen