Effect of restricted suckling on milk yield, milk composition and udder health in cows and behaviour and weight gain in calves, in dual-purpose cattle in the tropics.

The study was conducted to evaluate the effects of restricted suckling (RS) in dual-purpose cows and calves compared to artificial rearing (AR). Twelve Holstein-Zebu cows with calves were assigned to each treatment. Cows were milked once daily in the morning with calves present to stimulate milk let-down. RS calves suckled 30 min after milking and 30 min in the afternoon, whereas AR calves were milk-fed from nipple bottles. The daily saleable milk yield was higher in RS than in AR cows (p < 0.01; 7.44 vs 6.50 kg/day), whereas RS cows had lower milk-fat content (p < 0.001). AR cows had higher California Mastitis Test scores (p < 0.001) and lower lactose content (p < 0.001) compared to RS cows, which indicates an improved udder health in RS cows. AR calves displayed more 'cross-suck' during suckling/milk feeding (p < 0.001) and during observations of general behaviour (p < 0.05), and more 'lick and sniff interior' during milking (p < 0.05) and suckling/milk feeding (p < 0.01), compared to RS calves. During observations of general behaviour the RS calves were more often observed to 'walk' (p < 0.01) and 'lick self' (p < 0.05) and less frequently to 'eat concentrate' (p < 0.05) than AR calves. Results support the hypothesis that RS increases milk yield, influences milk composition and improves udder health in cows, and decreases abnormal sucking in calves.

AMP-activated protein kinase (AMPK) is activated in muscle of subjects with type 2 diabetes during exercise.

Insulin-stimulated GLUT4 translocation is impaired in people with type 2 diabetes. In contrast, exercise results in a normal increase in GLUT4 translocation and glucose uptake in these patients. Several groups have recently hypothesized that exercise increases glucose uptake via an insulin-independent mechanism mediated by the activation of AMP-activated protein kinase (AMPK). If this hypothesis is correct, people with type 2 diabetes should have normal AMPK activation in response to exercise. Seven subjects with type 2 diabetes and eight matched control subjects exercised on a cycle ergometer for 45 min at 70% of maximum workload. Biopsies of vastus lateralis muscle were taken before exercise, after 20 and 45 min of exercise, and at 30 min postexercise. Blood glucose concentrations decreased from 7.6 to 4.77 mmol/l with 45 min of exercise in the diabetic group and did not change in the control group. Exercise significantly increased AMPK alpha2 activity 2.7-fold over basal at 20 min in both groups and remained elevated throughout the protocol, but there was no effect of exercise on AMPK alpha1 activity. Subjects with type 2 diabetes had similar protein expression of AMPK alpha1, alpha2, and beta1 in muscle compared with control subjects. AMPK alpha2 was shown to represent approximately two-thirds of the total alpha mRNA in the muscle from both groups. In conclusion, people with type 2 diabetes have normal exercise-induced AMPK alpha2 activity and normal expression of the alpha1, alpha2 and beta1 isoforms. Pharmacological activation of AMPK may be an attractive target for the treatment of type 2 diabetes.

Relation between triglycerides in human skeletal muscle and serum and the fractional elimination rate of exogenous plasma triglycerides.

Muscle triglycerides, serum lipid and lipoprotein concentrations and an intravenous fat tolerance test were determined on thirteen survivors of myocardial infarction and on fourteen subjects referred to a Lipid Clinic but without myocardial infarction. The mean concentration of triglycerides in muscle and the fractional removal rate k2 of intravenous injected Intralipid were similar in patients with and without MI. In seventeen of these subjects type IV hyperlipoproteinaemia was found. In type IV patients the muscle triglyceride concentration was twice that found in patients without hypertriglyceridaemia. A negative correlation between muscle triglyceride concentration and the k2 value was found for all subjects with a correlation coefficient of -0.62 (P less than 0.001). No independent correlations were found between muscle triglyceride and serum triglyceride concentration or the triglyceride concentrations of the major lipoproteins.

Effect of noradrenaline on triglyceride and glycogen concentrations in liver and muscle from man.

Fifteen male subjects aged 21-29 were given noradrenaline infusions for 4 hr. The noradrenaline infusions started at a rate of 0.1 mug/kg/min and were increased stepwise at hourly intervals. Blood was sampled before and at hourly intervals during and after the noradrenaline infusions. Needle biopsies were taken from the femoral muscle in 10 subjects and frim the liver in 8 subjects before and after the noradrenaline infusion. The concentrations of FFA in lasma and of beta-hydroxybutyric acid in blood were markedly elevated during noradrenaline infusion. The concentrations of plasma TG and blood glucose were slightly elevated. In liver the TG concentration increased from 23.1 to 32.7 mmole/kh (p smaller than 0.001). It was estimated that the de novo synthesis of TG in the liver could have required about 30% of the plasma FFA entering the slanchnic region. In muscle the TG concentration was 3.6 mmole/kh lower after the noradrenaline infusion (p smaller than 0.001). No change was found in the concentrations of cholesterol and phospholipids in muscle or of cholesterol in liver. The glycogen concentration in muscle did not change during noradrenaline infusion. The decrease in liver glycogen concentration was of the same order of magnitude as previously observed in fasting man. The results suggest that noradrenaline was without major net effects on the metabolism of glycogen in liver and muscle.