Rethinking the Golden Rule.
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D S Blanchard
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What women can do to protect against osteoporosis.
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Inhibition of somatomedin-like activity by serum from streptozotocin-diabetic rats: prevention by insulin treatment and correlation with skeletal growth.
Diabetes mellitus was induced in rats by streptozotocin. This gave rise to a loss of somatomedin activity in serum. The loss of somatomedin activity was due to the presence of inhibitors associated with serum proteins having mol wts of less than 1, 1-10, 30-50, and 300 K. Whereas less than 1, 1-10, and 30-50 kilodalton fractions were not inhibitory in control and insulin-treated animals, greater than 300 kilodalton fraction was inhibitory in control and insulin-treated animals; the inhibitory activity of this fraction in diabetic animals was significantly greater than that in controls and insulin-treated animals. The appearance of these inhibitors in diabetic animals was accompanied by reduced skeletal growth. Treatment of diabetic animals with insulin abolished the somatomedin-inhibitory activity of serum and corrected the skeletal growth deficit. Serum inhibitors of somatomedin may, therefore, be involved in the causation of some of the complications of diabetes, including impaired skeletal growth.
Animals↗
The effect of continuous subcutaneous insulin infusion therapy on morphological and biochemical abnormalities of peripheral nerves in experimental diabetes.
Diabetes mellitus was induced in rats by the administration of streptozotocin and observations have been made over a period of 2 months in 3 groups of animals: controls, untreated diabetics and diabetics treated with continuous subcutaneous insulin infusion (CSII) therapy, using a 14-day Alzet osmotic minipump. Optimal control of day-to-day and 24-h blood glucose levels was achieved in diabetic animals treated with CSII. Body weight and skeletal growth, assessed by measurements of tibial length, were decreased in untreated diabetic rats and were normalized by insulin treatment. The concentrations of glucose, sorbitol and fructose in the nerves of diabetic animals were significantly increased and that of myoinositol significantly decreased; CSII therapy normalized these levels to those of age-matched controls. External myelinated fibre diameter in the tibial nerve was significantly less in untreated diabetic rats as compared with age-matched controls. In the insulin-treated group, fibre diameter significantly increased as compared with untreated diabetics and there was no significant difference between insulin-treated and control animals. Teased fibre preparations from the tibial nerve revealed very few abnormal fibres in all the three groups and no significant difference was detected between any of the groups. Continuous subcutaneous insulin infusion therapy, therefore, corrected biochemical abnormalities and also normalized myelinated fibre diameter in the peripheral nerves of experimental diabetic animals. The paradoxical excess of axonal degeneration that has been reported with conventional insulin treatment was not observed.
Animals↗
The effect of insulin treatment on myelinated nerve fibre maturation and integrity and on body growth in streptozotocin-diabetic rats.
Diabetes mellitus was produced in rats by the administration of streptozotocin and observations made over a period of 2 months. Four groups of animals were studied: onset and end controls, untreated diabetic rats and rats treated daily with a long-acting insulin preparation. Body weight increased in the end controls and insulin-treated diabetic animals to a similar degree over the observation period but was reduced in the untreated diabetic rats. Skeletal growth, assessed by measurements of tibial length, was also reduced in the untreated diabetic rats and partially corrected by insulin treatment. Myelinated fibre diameter in the tibial and sural nerves increased over the observation period in the controls, but the increase was less in the untreated animals and the growth deficit was not corrected by insulin treatment. Myelinated fibre numbers did not alter in the tibial or sural nerves between the onset and end controls. Numbers were significantly less in the tibial nerves of both the untreated and insulin-treated diabetic rats as compared with the two control groups; in the sural nerves, fibre numbers did not differ significantly between the four groups. Finally, the number of degenerating axons, assessed in teased fibre preparations, was very small in the control and untreated diabetic animals but was significantly increased in the insulin-treated group. Measurements of plasma glucose concentrations did not suggest that the axonal degeneration could be related to hypoglycaemia. The explanation for this paradoxical effect of insulin therapy is uncertain. It may be dependent upon fluctuations in blood glucose levels or other metabolic actions of insulin apart from its hypoglycaemic effect.
Animals↗