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S Hagg

Publications and source records attributed to S Hagg.

7 recordsLinked to original sources

Does self-monitoring of blood glucose levels improve dietary compliance for obese patients with type II diabetes?

Self-monitoring of blood glucose levels is currently being recommended for obese patients with type II diabetes to improve weight loss and glycemic control. To determine whether self-monitoring of blood glucose levels improves dietary compliance in these patients, 50 obese patients with type II diabetes were randomly assigned either to a standard behavioral weight control program or to a weight control program that included self-monitoring of blood glucose levels and focused on the weight-blood glucose relationship. Both groups lost significant amounts of weight and maintained their losses for at least one year; reductions in medication could be made for 70 percent of patients. These data suggest that the behavioral weight control used in this study may be of benefit to patients with type II diabetes. However, there was no evidence that the addition of self-monitoring of blood glucose levels to the treatment program improved the outcome in terms of weight loss, reduction in medication, dietary compliance, or mood state.

Adult↗

Effect of starvation on the production and peripheral metabolism of 3,3',5'-triiodothyronine in euthyroid obese subjects.

The effect of starvation on the peripheral metabolism of rT3 was evaluated in four obese euthyroid patients. During starvation, the serum rT3 concentration increased by 69% while the MCR of rT3 decreased in all four patients from control values of 96 +/- 23 (mean +/- SD) to 68 +/- 17 liters/70 kg . day, resulting in a slight increase in the mean production rate of rT3. These findings are in contrast to the marked decrease in T3 production rate associated with fasting, indicating that inner and outer ring deiodination of T4 can be varied independently.

Female↗

Effect of starvation on muscle glucose metabolism: studies with the isolated perfused rat hindquarter.

Studies in man and experimental animals suggest that the metabolism of glucose by skeletal muscle is depressed during starvation. To investigate the basis for this, the effect of starvation on the uptake and disposition of glucose in skeletal muscle was studied in the isolated perfused rat hindquarter. In contrast to earlier work carried out in heart, neither glucose uptake, whether stimulated by insulin or exercise, nor glycolysis were depressed by 48 hr of starvation or by perfusion of the hindquarter with acetoacetate, palmitate, or octanoate. Glucose oxidation, assessed from the oxidation of 1-[14C]lactate, was depressed by approximately 75% in starved rats and by 30% in fed rats perfused with acetoacetate. Exercise increased lactate oxidation 10-fold in both fed and starved rats; however, the relative difference between the groups persisted. In general, changes in lactate oxidation were paralleled by changes in the activity of pyruvate dehycrogenase (active form). The data suggest that glucose metabolism in skeletal muscle is inhibited during starvation at the step of pyruvate oxidation and that this inhibition persists during exercise. The also suggest that the diminution of glucose uptake that occurs in skeletal muscle of intact organisms during starvation may not be related to the presence of high concentrations of free fatty acids and ketone bodies.

Acetyl Coenzyme A↗

Glucose metabolism in perfused skeletal muscle. Interaction of insulin and exercise on glucose uptake.

1. The interaction of insulin and isometric exercise on glucose uptake by skeletal muscle was studied in the isolated perfused rat hindquarter. 2. Insulin, 10 m-i.u./ml, added to the perfusate, increased glucose uptake more than 10-fold, from 0.3-0.5 to 5.2-5.4 mumol/min per 30g of muscle in hindquarters of fed and 48h-starved rats respectively. In contrast, it did not stimulate glucose uptake in hindquarters from rats in diabetic ketoacidosis. 3. In the absence of added insulin, isometric exercise, induced by sciatic-nerve stimulation, increased glucose uptake to 4 and 3.4 mumol/min per 30g of muscle in fed and starved rats respectively. It had a similar effect in rats with moderately severe diabetes, but it did not increase glucose uptake in rats with diabetic ketoacidosis or in hindquarters of fed rats that had been "washed out" with an insulin-free perfusate. Insulin, at concentrations which did not stimulate glucose uptake in resting muscle, restored the stimulatory effect of exercise in these situations. 4. The stimulation of glucose uptake by exercise was independent of blood flow and the degree of tissue hypoxia; also it could not be reproduced by perfusing resting muscle with a medium previously used in an exercise experiment. 5. At rest glucose was not detectable in muscle cell water of fed and starved rats even when perfused with insulin. In the presence of insulin, a small accumulation of glucose, 0.25 mM, was noted in the muscle of ketoacidotic diabetic rats, suggesting inhibition of glucose phosphorylation, as well as of transport. 6. During exercise, the calculated intracellular concentration of glucose in the contracting muscle increased to 1.1-1.6mM in the fed, starved and moderately diabetic groups. Insulin significantly increased the already high rates of glucose uptake by the hindquarters of these animals but it did not alter the elevated intracellular concentration of glucose. 7. In severely diabetic rats, exercise did not cause glucose to accumulate in the cell in the absence of insulin. In the presence of insulin, it increased glucose uptake to 6.1 mumol/min per 30g of muscle and intracellular glucose to 0.72 mM. 8. The data indicate that the stimulatory effect of exercise on glucose uptake requires the presence of insulin. They suggest that in the absence of insulin, glucose uptake is not enhanced by exercise owing to inhibition of glucose transport into the cell.

Animals↗