Quantitative Glucose Metabolism in Lactating Mink ( Mustela vison ) - Effects of Dietary Levels of Protein, Fat and Carbohydrates

Abstract

Quantitative glucose metabolism in lactating mink (Mustela Øison) -Effects of dietary levels of protein, fat and carbohydrates .Glucose metabolism was measured during two consecutive years, 4 weeks postpartum, in a total of 36 yearling female mink, tted with jugular vein catheters and raising litters of six to seven kits. The dams were fed ad libitum from parturition on diets with different ratios of metabolizable energy (ME) derived from protein:fat:carbohydrate s (experiment 1: 61:37:2, 46:37:17, 31:37:32; experiment 2: 61:38:1, 47:52:1, 33:66:1). After 3 h fasting the dams were fed 210 kJ ME of the experimental diets. Two hours postprandially a single dose of 50 mCi U-1 4 C-and 2-3 H-labelled glucose was administered to each dam and blood samples were drawn 5, 10, 20, 30, 45 and 60 min after the tracer administration. Glucose turnover rates were 4 -5% min ¼ 1 in all dams, and the approximate daily glucose ux was 12 -17 g day ¼ 1 ; however, these were not signi cantly affected by dietary treatment. In conclusion, the mink is able both to synthesize large amounts of glucose de no×o and to utilize high levels of dietary digestible carbohydrates, and thereby to tolerate large variations in dietary carbohydrate supply.

A first estimate of the amino acid requirement for milk production of the high‐producing female mink (Mustela vison)

“…Our estimates on milk yield and amino acid excretion in milk may therefore be considered reliable. The present data demonstrate, in good agreement with previous findings (Fink and Børsting, 2002; Fink et al., 2002,2004), that carbohydrate sources with a high content of pre‐gelatinised starch are well utilised as glucose source of the lactating mink dam with beneficial effects on milk yield. The poorer performance of HP dams in the present study was probably caused by a combination of a lower intake of ME than MP and LP dams, although the energy densities of all diets were within the range where mink can be expected to regulate their intake (Tauson, 1988), and the higher energetic costs of using amino acids as glucose precursors, as demonstrated by Fink et al.…”

“…Current recommendations for protein supply during the lactation period are based on production experiments with pre‐weaning kit growth as a measure of dietary adequacy (Skrede, 1978; Glem‐Hansen, 1979), and state that a minimum of 40% of metabolisable energy (ME) should be provided by protein (Hansen et al., 1991). Mink has a high activity of hepatic gluconeogenic enzymes (Sørensen et al., 1995) and capacity of gluconeogenesis (Børsting and Damgaard, 1995; Fink and Børsting, 2002), whereas the α ‐amylase (Elnif et al., 1988) and intestinal microbial activity (Williams et al., 1998) are low, and carbohydrates have to be supplied either by monosaccharides or gelatinised starch to ensure high digestibility. However, the glycolytic capacity in mink is large (Sørensen et al., 1995), and lactating dams are able to utilise high amounts of digestible carbohydrates without negative effects on blood glucose concentration and animal welfare (Fink and Børsting, 2002; Fink et al., 2002).…”

“…Mink has a high activity of hepatic gluconeogenic enzymes (Sørensen et al., 1995) and capacity of gluconeogenesis (Børsting and Damgaard, 1995; Fink and Børsting, 2002), whereas the α ‐amylase (Elnif et al., 1988) and intestinal microbial activity (Williams et al., 1998) are low, and carbohydrates have to be supplied either by monosaccharides or gelatinised starch to ensure high digestibility. However, the glycolytic capacity in mink is large (Sørensen et al., 1995), and lactating dams are able to utilise high amounts of digestible carbohydrates without negative effects on blood glucose concentration and animal welfare (Fink and Børsting, 2002; Fink et al., 2002). Furthermore, recent research has shown that lactating mink are able to regulate protein oxidation rate and that milk yield, during the first 4 week postpartum , was improved and dam weight loss reduced, when protein supply was reduced below current recommendations (Fink et al., 2004).…”

Glycemic control in minks with tendency to obesity in the perinatal period with the use of HbA1C

“…The study by Fink and Børsting (2002) confirmed that both excess and lack of body fat in feeding minks can cause the accumulation of fat in cells that metabolize glucose, causing insulin resistance and break in the peripheral glucose circulation. In animals with clear insulin resistance, the ability to stimulate the translocation of the GLUT-4 glucose transporter in the blood is impaired, which causes binding of glucose by the peripheral cells, for instance muscle and fat cells (Clausen et al, 1996).…”

“…Wamberg et al (1992), in their study, found average blood glucose levels for healthy lactating females as 5.3±0.3 mmol L −1 (95.4±5.3 mg dL −1 ). Fink and Børsting (2002) suggested that uncontrollable gluconeogenesis causes hyperglycemia in female minks during lactation. Therefore, the older mink dams may be more prone to poor glycemic regulation due to their higher demands for hepatic glucose production in support of the higher milk production, as well as increased hepatic glucose output caused by their heavier body condition.…”