Fetal life malnutrition was not reflected in the relative abundances of adiponectin and leptin mRNAs in adipose tissue in male mink kits at 9.5 weeks of age.

BACKGROUND: Malnutrition in fetal life and during suckling have in some animal studies resulted in adaptive changes related to the fat and glucose metabolism, which in the long term might predispose the offspring for metabolic disorders such as obesity later in life. The objective was to study the effect of fetal life malnutrition in male mink on the gene expression of leptin and adiponectin in different adipose tissue sites. RESULTS: Thirty-two male mink, strict carnivore species, exposed to low (FL) or adequate (FA) protein provision the last 16.3 ± 1.8 days of fetal life and randomly assigned to a low (LP) or adequate (AP) protein diet from 7 to 9.5 weeks of age were used. Adipose tissues (subcutaneous, perirenal and mesenteric) were analyzed using qPCR. Fetal life or post-weaning protein provision did not affect the relative abundances of leptin and adiponectin mRNAs in adipose tissue at 9.5 weeks of age. Relative abundances of leptin and adiponectin mRNAs were different between adipose tissue sites and were significantly higher in subcutaneous than in perirenal and mesenteric tissues. CONCLUSION: Fetal life protein malnutrition in male mink, did not result in adaptive changes in the gene expression of leptin and adiponectin mRNAs in adipose tissue at 9.5 weeks of age as found in rodents. However, both leptin and adiponectin mRNAs were significantly differently expressed between tissue sites.

Feeding mink (Neovison vison) a protein-restricted diet during pregnancy induces higher birth weight and altered hepatic gene expression in the F(2) offspring.

Malnutrition during foetal life can induce modifications in the phenotype of an individual. The present study aimed to observe effects of low foetal life protein provision on modifications of the phenotype and changes in the progeny of 1-year-old female mink (F(1) generation) offspring of mothers fed a low-protein diet. Traits studied included reproductive performance, energy and protein metabolism, and key hepatic enzymes associated with glucose homeostasis and metabolic hormones. The F(0) generation offspring were fed either a low-protein (14 % of metabolisable energy (ME) from protein - FLP1) or an adequate-protein (29 % of ME from protein - FAP1) diet for the last 17.9 (sd 3.6) d of gestation. The F(1) dams were studied at birth and at 1 year of age, during their first reproductive cycle, after maintenance on an adequate diet from birth and thereafter. Metabolic traits during gestation and lactation were largely unaffected by foetal life protein provision, but birth weight in the F(2) generation was higher (P = 0.003) among FLP2 kits than among FAP2 kits. Furthermore, the relative abundance of pyruvate kinase mRNA was significantly (P = 0.007) lower, and fructose-1,6-bisphosphatase mRNA tended (P = 0.08) to be lower in FLP2 foetuses than in FAP2 foetuses, showing some similar difference in the F(2) generation and F(1) generation foetuses, suggesting an effect on some hepatic enzymes affecting glucose homeostasis being transmitted from the F(1) to the F(2) generation. These findings indicate that even though energy and nitrogen metabolism displayed no effect of protein provision during early life, programming effects still appeared at the molecular level in the following generation.