To evaluate the role of serum calcium in human insulin secretion, insulin responses after a 100-g oral glucose load were studied in nine patients with primary hyperparathyroidism, five with idiopathic hypoparathyroidism, three with pseudohypoparathyroidism and one with normocalcemic secondary hyperparathyroidism. Glucose tolerance values in these disorders were almost normal. Insulin responses in primary hyperparathyroidism were increased, and those in idiopathic hypoparathyroidism and pseudohypoparathyroidism were reduced significantly as compared to normal subjects. Isulin response in secondary hyperparathyroidism was normal. The calculated insulin area during an oral glucose load was significantly correlated with serum calcium (5.1 to 12.2 mg per deciliter), and a linear relation was obtained (y = 1.59x - 3.3, r = 0.81, p less than 0.001), although a relation with the glucose area was not found. These observations indicate that serum calcium has an important effect on insulin secretion in parathyroid disorders.

Calcium↗

PubMed1975

Defective early phase insulin release in perifused isolated pancreatic islets of spiny mice (Acomys cahirinus).

In order to characterize pancreatic beta cell function in Geneva bred spiny mice (acomys cahirinus), the dynamics of immunoreactive insulin release were examined during perifusion of pancreatic islets isolated from normoglycemic acomys. The initial insulin response of acomys was slow: no clear-cut early (1 to 10 min) peak of insulin release was observed when glucose in the perifusion medium was abruptly raised from 2.8 mM to concentrations as high as 56 mM. This was true for islets of either young, or older more obese acomys. However, after 20 to 30 min of perifusion at the high glucose concentrations, the rate of insulin release from acomysislets became similar to that from islets of rats or mice. By contrast, glucose-induced insulin release responses observed with islets of Wistar-derived rats, Swiss albino mice, and inbred C57BL/6J lean or obese (ob/ob) mice, were clearly biphasic. Tolbutamide 1.5 mM, arginine 16 mM, and theophylline 10 mM were ineffective in stimulating insulin release from acomys islets in the presence of a substimulatory glucose concentration (2.8 mM), whereas these agents were effective in rat islets at the same substimulatory concentration of glucose. On the other hand, when these agents, as well as cyclic AMP 10 mM or cytochalasin B 10 mug/ml were applied in the presence of a stimulating concentration of glucose (16.8 mM), the glucose-stimulated insulin release from acomys islets was increased to the same or to a greater extent than from rat islets. It is suggested that the failure of all the agents tested to stimulate an early rapid phase of insulin release from acomys islets may be secondary to the observed initial insensitivity to glucose, which insensitivity may in turn reflect a selective impairment in the recognition of glucose as an insulinogenic signal in this species.

Age Factors↗

PubMed1975

Interactions of the inhibitory component of troponin, F-actin, and tropomyosin.

The interaction of the inhibitory component (TN I) of troponin and F-actin in the presence and absence of tropomyosin was studied by a number of physico-chemical techniques: i.e., gel filtration, ultracentrifugation, flow birefringence, viscosity and dynamic viscoelasticity measurements, and electron microscopy. The results indicated that TN I and F-actin interact with each other more strongly in the presence of tropomyosin than in its absence. The physiological implication of this finding is discussed.

Actins↗

PubMed1975

An effect of hyposmolarity on insulin release in vitro.

An abrupt reduction of medium osmolarity by as little as 20 mosM evoked a discrete short-lived insulin secretory response from perifused chopped pancreas or isolated islets. The insulin response occurred earlier than that induced by either glucose or tolbutamide. None of the usual modifiers of insulin secretion significantly altered this secretory response. Glycolytic inhibitors, adrenergic agonists and blocking agents, cholinergic blocking agents, mitotic spindle inhibitors, and agents influencing sodium pump activity failed to alter hyposmolar-induced insulin secretion. Manipulation of the perifusion medium calcium concentration was the only procedure tested that influenced the secretory response. Perturbations of medium calcium concentration that increased the tissue-to-medium calcium gradient augmented the hyposmolar-induced insulin response and those that decreased tissue-to-medium calcium gradient greatly inhibited the response. The precise cause of the insulin response to a decrease in bathing fluid osmolarity remains undefined; however, the stimulus is not specific for insulin because increases in glucagon and amylase were also elicited by the hyposmolar stimulus.

Amiloride↗

PubMed1975