Nursing sickness, the largest single cause of mortality in adult female mink (Mustela vison), is an example of a metabolic disorder, which develops when the demands for lactation require extensive mobilization of body energy reserves. The condition is characterized by progressive weight loss, emaciation, and dehydration with high concentrations of glucose and insulin in the blood. Morbidity due to nursing sickness can be as high as 15% with mortality around 8%, but the incidence is known to vary from year to year. Stress has been shown to trigger the onset of the disease and old females and females with large litters are most often affected. Increasing demand for gluconeogenesis from amino acids due to heavy milk production may be a predisposing factor. Glucose metabolism is inextricably linked to that of protein and fats. In obesity (or lipodystrophy), the ability of adipose tissue to buffer the daily influx of nutrients is overwhelmed (or absent), interfering with insulin-mediated glucose disposal and leading to insulin resistance. Polyunsaturated fatty acids of the n-3 family play an important role in modulating insulin signalling and glucose uptake by peripheral tissue. The increasing demand on these fatty acids for milk fat synthesis towards late lactation may result in deficiency in the lactating female, thus impairing glucose disposal. It is suggested that the underlying cause of mink nursing sickness is the development of acquired insulin resistance with 3 contributing key elements: obesity (or lipodystrophy), n-3 fatty acid deficiency, and high protein oxidation rate. It is recommended that mink breeder females be kept in moderate body condition during fall and winter to avoid fattening or emaciation. A dietary n-3 fatty acid supplement during the lactation period may be beneficial for improved glycemic control. Lowering of dietary protein reduces (oxidative) stress and improves water balance in the nursing females and may, therefore, prevent the development and help in the management of nursing sickness. It is also surmised that other, thus far unexplained, metabolic disorders seen in male and female mink may be related to acquired insulin resistance.

Objective-To characterize insulin-sensitive glucose-transporter (GLUT-4) protein in equine tissues and determine effects of exercise and glucose administration on content of GLUT-4 protein in equine skeletal muscle. Sample Population-Tissue samples from 9 horses. Procedure-Western blot analyses were performed on crude membrane preparations of equine tissues to characterize GLUT-4. In a crossover, randomized study, horses were strenuously exercised for 3 consecutive days and then administered 13.5% glucose or isotonic saline (0.9% NaCl; control) solution, IV, at similar infusion rates for 12.1 hours. Samples were collected from the middle gluteal muscle before and after exercise and 10.1 hours after completion of an infusion and used for measurements of glycogen concentration and total content of GLUT-4 protein. Results-Immunoblot analyses detected specifically immunoreactive bands for GLUT-4 in insulin-sensitive tissues. Content of GLUT-4 protein in skeletal muscle increased significantly by 27.3 and 12.3% 22.2 hours after exercise for control and glucose groups, respectively. Intravenous infusion of glucose resulted in a significantly higher rate of glycogenesis, compared with results for the control group (mean +/- SD, 3.98 +/- 0.61 and 1.47 +/- 0.20 mmol/kg/h, respectively). Despite enhanced glycogenesis, we did not detect an increase in content of GLUT-4 protein after glucose infusion, compared with values after exercise. Conclusions and Clinical Relevance-GLUT-4 protein was expressed in equine skeletal and cardiac muscles. Exercise increased total content of GLUT-4 protein in skeletal muscle, and replenishment of muscle glycogen stores after glucose infusion attenuated the exercise-induced increase in the content of GLUT-4 protein in equine skeletal muscle.

Objective-To use threshold concentrations of acetone and beta-hydroxybutyrate in milk and serum, respectively; identify risk for ketosis and endometritis; and assess analyses of blood and milk samples as predictors of risk for ketosis in high-yielding dairy cows. Animals-90 multiparous Holstein cows. Procedure-At intervals before and after parturition, blood samples were obtained for determination of glucose, nonesterified fatty acids, leptin, insulin, insulin-like growth factor-1, and beta-hydroxybutyrate concentrations. Samples of milk were obtained at similar intervals after parturition for determination of fat content and concentrations of acetone, protein, and lactose. Reproductive examination of each cow was performed weekly. Results-For each cow, threshold concentrations of acetone and β-hydroxybutyrate were calculated as 75th and 90th percentiles of maximum postpartum concentrations of acetone in milk (0.40 and 0.87 mmol/L) and β-hydroxybutyrate in serum (2.30 and 3.51 mmol/L). Significant decrease in milk production (442 to 654 kg of energy-corrected milk/305-day period per cow) was associated with acetone or beta-hydroxybutyrate in excess of threshold values. Milk acetone concentrations > 0.40 mmol/L were associated with 3.2 times higher risk for endometritis. Low plasma glucose, high serum beta-hydroxybutyrate, and high milk acetone concentrations during week 1 after parturition were indicators of increased risk for ketosis later during lactation. Conclusions and Clinical Relevance-Determination of milk acetone concentration during the week after parturition may identify cows at risk for ketosis and endometritis; with appropriate interventions, development of disease and production losses may be reduced.