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.

Keywords:

• foetal programming
• gene expression
• glucose
• nitrogen metabolism
• energy metabolism
• protein deficiencies

Acknowledgements

This study was part of the “Interdisciplinary Animal Research” research programme, grant no. 5414114.95.304. We gratefully acknowledge the financial support of the Danish Food Industry Agency of the Ministry of Food, Agriculture and Fisheries to perform this research. Skilful technical assistance with collection routines and chemical analyses was provided by Merethe Stubgaard, Lotte Ørbæk, and Ebba de Neergaard Harrison, with animal handling by Boye Pedersen, respiration unit operation by Abdalla Ali, radioimmunoassay measurements by Margaret Blackberry, and q PCR by Anne Friis Petersen, assistance for which the authors wish to express their sincere gratitude.