Effect of purified phospholipases on glucose transport, insulin binding, and insulin action in isolated rat adipocytes

The influence of alterations in phospholipid structure by phospholipase treatment on insulin action and glucose transport in rat adipocytes was studied. It appeared that phospholipase A2 from bee venom caused a breakdown of approximately 50% of phosphotidylcholine without lysis of the cells. Because of this treatment, insulin binding was increased, resulting in an increased sensitivity of glucose transport towards lower insulin concentrations. Moreover, an increased affinity of the transport system for 2-deoxyglucose was observed. Phospholipase C from Clostridium welchii caused complete lysis of adipocytes. Phospholipase A2 from Crotalus adamenteus was without effect.     

Effect of glucose load and of insulin on the metabolism of glucose and of palmitate in sheep

1. Simultaneous measurements of the entry rates of palmitate and glucose have been made in Merino sheep (wethers), starved for 24hr., by using constant infusions of [9,10-(3)H(2)]palmitate and [U-(14)C]glucose. 2. The infusion of glucose into the peripheral circulation of the sheep lowered the endogenous entry of both glucose and palmitate. Since palmitate is roughly metabolically representative of the free fatty acid fraction, there was no marked change in the calories available to the sheep. 3. The infusion of insulin into either the peripheral or portal circulation increased the uptake of glucose and decreased the uptake of palmitate by the tissues of the sheep. 4. The infusion of insulin into the peripheral circulation produced a depression in glucose entry after about 80min., whereas the infusion of insulin into the portal circulation produced an almost immediate depression in glucose entry. 5. The hypoglycaemia produced gave rise to an increase in free fatty acid production followed by an increase in glucose production. 6. No direct effect of insulin on the metabolism of free fatty acids has been demonstrated by the techniques used. The effect of insulin on the metabolism of free fatty acids is apparently mediated through its effect on glucose metabolism.     

Effect of parathyroid hormone on the increase in serum glucose and insulin levels after a glucose load to thyroparathyroidectomized rats.

Thyroparathyroidectomy (TPTX) caused a significant increase in serum glucose and a corresponding fall in serum calcium in both fed and fasted rats. The increase in serum glucose, induced by TPTX, was markedly potentiated by a single intraperitoneal administration of calcium (2 mg/100 g BW) which caused a significant elevation of serum calcium in thyroparathyroidectomized rats. Parathyroid hormone (PTH; 20 U/100 g BW) administered subcutaneously to thyroparathyroidectomized rats, caused a significant decrease in serum glucose (0.1 g/100 g BW) to sham-operated rats significantly increased both serum glucose and insulin. The rise of serum glucose produced by a glucose load was markedly potentiated by TPTX, but the increase in serum insulin was not promoted significantly. The administration of PTH decreased both serum glucose and insulin levels increased by a glucose load to thyroparathyroidectomized rats, in a dose-dependent manner. The administration of calcitonin (80 MRC mU/100 g BW) significantly prevented the effect of PTH to decrease serum glucose after a glucose load to thyroparathyroidectomized rats, and calcitonin increased serum insulin. These results suggest that the effect of PTH on serum glucose does not involve insulin secretion.