Calves intensively fed milk replacers frequently develop postprandial insulin resistance, characterized by excessively elevated plasma insulin concentrations, hyperglycemia, and glucosuria. To test the hypothesis that insulin secretion and insulin-dependent dependent glucose metabolism are modified by age and carbohydrate intake, 20 male calves (Simmental x Red Holstein) were fed a milk replacer containing 290 and 423 g lactose/kg DM from 60-70 to 190-200 kg BW. Responses of insulin and glucose to milk replacer intake and orally administered glucose and pre- and postprandial glucose responses to i.v. infused glucose and i.v. injected insulin were tested at 75-105 and 160-200 kg BW. Urine was collected during 24h to determine glucose, galactose, dopamine, noradrenaline, and creatinine excretion. Insulin resistance, hyperinsulinemia, hyperglycemia, glucosuria, and galactosuria developed with increasing age and occurred primarily postprandially. High lactose intake enhanced postprandial hyperglycemia but did not significantly increase glucosuria, galactosuria, and hyperinsulinemia. Based on urinary excretion of dopamine and noradrenaline there was a marked age-dependent increase in the activity of the sympathetic nervous system, which was not modified by lactose intake. high feeding intensity and lactose intake, excessive hyperinsulinemia per se and enhanced activity of the sympathetic nervous system possibly contributed to the development of insulin resistance. Glucose-dependent insulinotropic polypeptide, growth hormone and cortisol concentrations, and iron intake were low and comparable in both groups and therefore were etiologically not involved in the development of insulin resistance. Increasing circulating concentrations of insulin-like growth factor I during growth may have in part allowed high growth rates in the presence of insulin resistance.

Summary Changes of blood metabolites and hormones were studied in female breeding calves before, during and after weaning from 4 to 18 weeks of age. Calves were initially fed increasing amounts of whole milk (up to 7 kg/day in week 8 of life). Milk intake was then gradually decreased up to the age of 16 weeks, when calves were completely weaned and only fed hay and concentrates. Average daily gain was 0.85 kg. Postprandial concentrations of glucose, insulin, insulin‐like growth factor‐I and 3.5.3′‐triiodothyronine concentrations gradually decreased (P < 0.05) with age, while those of β‐hydroxybutyrate, protein, albumin, haemoglobin and iron increased (P < 0.05). Concentrations of cholesterol transiently increased, whereas those of urea reversibly decreased. Non‐esterified fatty acids, triglycerides and growth hormone did not consistently change during the duration of the study. In conclusion, changes of glucose, β‐hydroxybutyrate, haemoglobin, iron, insulin, insulin‐like growth factor‐I and 3.5.3′‐triiodothyronine were markedly different from those usually seen in veal calves of the same age.

Postprandial insulin resistance with excessive hyperinsulinemia, hyperglycemia and glucosuria develops with increasing age in veal calves intensively fed milk replacers. We tested the age dependency of insulin resistance, modulated by high lactose intake, glucose oxidation and insulin receptor number and affinity after an overnight period without food. Male calves were fed a milk replacer containing 290 or 423 g lactose and 310 and 541 g total sugar/kg from 69-195 kg body weight. At mean body weights of 95 and 170 kg, insulin-dependent glucose metabolism was studied in euglycemic-hyperinsulinemic glucose clamps (EGC), and glucose-dependent insulin responses were tested in hyperglycemic clamps (HGC). EGC were combined with infusions of [13C6]glucose to measure glucose kinetics and glucose oxidation by determination of 13CO2 exhalation. During EGC and HGC, insulin concentrations were similar in both groups, indicating comparable insulin secretion and metabolic clearance rates. On the basis of glucose infusion rates required to maintain eu- or hyperglycemia in EGC and HGC, respectively, insulin-dependent glucose utilization was not age dependent. However, in calves receiving a high lactose intake, insulin-dependent glucose utilization was enhanced in the early phases, but was reduced in the late stages of the growth trial. Insulin-dependent glucose utilization behaved inversely with atom % excess of [13C6]glucose, but changed in a manner similar to that of the rate of glucose appearance. Inhibition of endogenous glucose output, exhalation of 13CO2 and amounts of oxidized glucose exhibited no group differences. More glucose was therefore stored in lactose-supplemented calves. A reduced insulin receptor number in skeletal muscle in calves fed high amounts of lactose likely contributed to low insulin-dependent glucose utilization.

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Summary Veal calves often develop insulin resistance, hyperglycaemia and glucosuria. We have studied effects of age and nutrition on blood metabolites and hormones, with major emphasis on glucose and insulin, in four groups of veal calves from 66–69 kg until slaughter at 175–196 kg. Calves were fed milk replacers which differed with respect to lactose, total sugar, protein and fat content. Mean intakes in groups 1, 2, 3 and 4 of lactose (1.24, 1.08, 0.95 and 0.66 kg/d), total sugar (1.27, 1.10, 1.01 and 96 kg/d), crude protein (0.40, 0.48, 0.65 and 0.49 kg/d) and crude fat (0.32, 0.31, 0.37 and 0.46 kg/d) were different. Average daily gains were 1.46–1.49 kg and feed/gain ratios were 1.49–1.61 kg/kg. Glucose and insulin concentrations were not associated with protein and fat intakes, but followed lactose and total sugar intakes, albeit differently at the start and end of the growth trial. Thus, insulin concentrations were higher (P < 0.05) at the end than at start of the growth trial in all 4 groups, whereas glucose concentrations increased (P < 0.05) with increasing age in only group 2. In conclusion, lactose and total sugar intakes affected the degree of hyperglycaemia and modified hyperinsulinemia at a given age, but the age‐dependent rise of insulin concentrations could not be explained by hyperglycaemia alone.