scholarly journals Effects of monensin on metabolism of isolated rat islets of Langerhans

1984 ◽  
Vol 223 (2) ◽  
pp. 423-432 ◽  
Author(s):  
J E Smith ◽  
S L Howell
Keyword(s):  
Insulin Release ◽  
Islets Of Langerhans ◽  
Islet Cells ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Rat Islets ◽  
Islet Volume ◽  
Isolated Rat Islets ◽  
Rat Islets Of Langerhans ◽  
Isolated Rat

Monensin, a univalent ionophore, is a carboxylic acid produced by Streptomyces cinnamonensis. It will complex various alkali-metal ions, but most readily binds Na+. Because of interest in the possible role of Na+ in the regulation of insulin secretion, we examined its effects on several aspects of the metabolism of isolated rat islets of Langerhans. The ionophore inhibited glucose-stimulated insulin release in a concentration-dependent manner, completely inhibiting secretion evoked by 20 mM-glucose at concentrations as low as 0.1 microM in static incubations. In perifusion experiments, both phases of insulin release were equally affected. Monensin (0.1 microM) had no significant effect on glucose oxidation as measured by the generation of 14CO2 from [14C]glucose. Monensin increased the rate of 22Na+ efflux from preloaded islets and net 22Na+ uptake over 30 min, in the absence of changes in islet volume or extracellular space. The ionophore increased the Rb+/K+ permeability of islet cells, as shown by its inhibition of 86Rb+ retention and stimulation of 86Rb+ efflux. At 0.1 microM, monensin abolished glucose-stimulated 45Ca2+ uptake by islets during 5 min incubations, and stimulated 45Ca2+ efflux from preloaded islets perifused with Ca2+-free medium, even in the complete absence of extracellular Na+. Studies of the uptake of 14C-labelled 5,5-dimethyloxazolidine-2,4-dione showed that 0.1 microM-monensin increased net intracellular pH from 7.05 to 7.13. 7 Monensin has widespread, complex, effects on the secretory responses and ion handling by the B cells, which are difficult to interpret in terms solely of actions as a Na+ ionophore.

scholarly journals Studies on the role of inositol trisphosphate in the regulation of insulin secretion from isolated rat islets of Langerhans

1985 ◽  
Vol 228 (3) ◽  
pp. 713-718 ◽  
Author(s):  
N G Morgan ◽  
G M Rumford ◽  
W Montague
Keyword(s):  
Insulin Secretion ◽  
Islets Of Langerhans ◽  
Islet Cells ◽  
Inositol Trisphosphate ◽  
Rat Islets ◽  
Isolated Rat Islets ◽  
Rat Islets Of Langerhans ◽  
Isolated Rat ◽  
Stimulation Of

Glucose (20 mM) and carbachol (1 mM) produced a rapid increase in [3H]inositol trisphosphate (InsP3) formation in isolated rat islets of Langerhans prelabelled with myo-[3H]inositol. The magnitude of the increase in InsP3 formation was similar when either agent was used alone and was additive when they were used together. In islets prelabelled with 45Ca2+ and treated with carbachol (1 mM), the rise in InsP3 correlated with a rapid, transient, release of 45Ca2+ from the cells, consistent with mobilization of 45Ca2+ from an intracellular pool. Under these conditions, however, insulin secretion was not increased. In contrast, islets prelabelled with 45Ca2+ and exposed to 20mM-glucose exhibited a delayed and decreased 45Ca2+ efflux, but released 7-8-fold more insulin than did those exposed to carbachol. Depletion of extracellular Ca2+ failed to modify the increase in InsP3 elicited by either glucose or carbachol, whereas it selectively inhibited the efflux of 45Ca2+ induced by glucose in preloaded islets. Under these conditions, however, glucose was still able to induce a small stimulation of the first phase of insulin secretion. These results demonstrate that polyphosphoinositide metabolism, Ca2+ mobilization and insulin release can all be dissociated in islet cells, and suggest that glucose and carbachol regulate these parameters by different mechanisms.

Alloxan Stimulation and Inhibition of Insulin Release from Isolated Rat Islets of Langerhans

Diabetes ◽  
1978 ◽  
Vol 27 (12) ◽  
pp. 1205-1214 ◽  
Author(s):  
D. C. Weaver ◽  
M. L. McDaniel ◽  
S. P. Naber ◽  
C. D. Barry ◽  
P. E. Lacy
Keyword(s):  
Insulin Release ◽  
Islets Of Langerhans ◽  
Rat Islets ◽  
Isolated Rat Islets ◽  
Rat Islets Of Langerhans ◽  
Isolated Rat

Propranolol-induced Insulin Release in Isolated Rat Islets of Langerhans

Diabetes ◽  
1973 ◽  
Vol 22 (2) ◽  
pp. 91-93 ◽  
Author(s):  
G. Northrop ◽  
W. G. Ryan ◽  
T. B. Schwartz
Keyword(s):  
Insulin Release ◽  
Islets Of Langerhans ◽  
Rat Islets ◽  
Isolated Rat Islets ◽  
Rat Islets Of Langerhans ◽  
Isolated Rat

EFFECTS OF HYPOPHYSECTOMY AND SHORT-TERM GROWTH HORMONE REPLACEMENT ON INSULIN RELEASE FROM AND GLUCOSE METABOLISM IN ISOLATED RAT ISLETS OF LANGERHANS

1975 ◽  
Vol 67 (1) ◽  
pp. 1-17 ◽  
Author(s):  
A. Ü. PARMAN
Keyword(s):  
Glucose Metabolism ◽  
Adrenal Gland ◽  
Insulin Release ◽  
Islets Of Langerhans ◽  
Short Term ◽  
Rat Islets ◽  
Gh Replacement ◽  
Isolated Rat Islets ◽  
Rat Islets Of Langerhans ◽  
Isolated Rat

SUMMARY The effects of hypophysectomy and short-term GH replacement on insulin release and on some aspects of glucose metabolism in isolated rat islets of Langerhans were investigated. The effects on body, pancreas and adrenal gland weights, and on the levels of blood plasma constituents were also measured. Three to four weeks after hypophysectomy the early and late phases of insulin release from islets incubated with high concentrations of glucose, but not with low concentrations of glucose or with xylitol, leucine, arginine, tolbutamide, citrate or butyrate, were significantly lowered. Short-term GH replacement partially reversed the depression in glucose-stimulated insulin release. This reversal effect was not dependent on the increase in body weight of rats after GH replacement when the fall in adrenal gland but not in pancreas weight was also reversed. Nine out of the 12 plasma constituents measured, including glucose, were maintained in the control range of levels, but albumin, inorganic phosphate and urea nitrogen levels were altered after hypophysectomy or GH replacement. Three to four weeks after hypophysectomy, total glucose oxidation and glucose utilization by the islets were slightly depressed. Hypophysectomy appeared to slow down glucose 6-phosphate utilization in the islets. However, the functional capacity of the glucose phosphorylating, glucose-6-phosphate and 6-phosphogluconate dehydrogenase activities were not changed. Short-term GH replacement caused improvements in these islet functions.

scholarly journals Pentitols and insulin release by isolated rat islets of Langerhans

1968 ◽  
Vol 109 (3) ◽  
pp. 333-339 ◽  
Author(s):  
W Montague ◽  
K W Taylor
Keyword(s):  
Insulin Release ◽  
Islets Of Langerhans ◽  
Pentose Phosphate ◽  
Rat Islets ◽  
Isolated Islets Of Langerhans ◽  
Isolated Rat Islets ◽  
Rat Islets Of Langerhans ◽  
Stimulate Insulin Release ◽  
Isolated Rat

1. Insulin secretion was studied in isolated islets of Langerhans obtained by collagenase digestion of rat pancreas. In addition to responding to glucose and mannose as do whole pancreas and pancreas slices in vitro, isolated rat islets also secrete insulin in response to xylitol, ribitol and ribose, but not to sorbitol, mannitol, arabitol, xylose or arabinose. 2. Xylitol and ribitol readily reduce NAD+ when added to a preparation of ultrasonically treated islets. 3. Adrenaline (1μm) inhibits the effects of glucose and xylitol on insulin release. Mannoheptulose and 2-deoxy-glucose, however, inhibit the response to glucose but not that to xylitol. 4. The intracellular concentration of glucose 6-phosphate is increased when islets are incubated with glucose but not with xylitol, suggesting that xylitol does not promote insulin release by conversion into glucose 6-phosphate. 5. Theophylline (5mm) potentiates the effect of 20mm-glucose on insulin release from isolated rat islets of Langerhans, but has no effect on xylitol-mediated release. These results indicate that xylitol does not stimulate insulin release by alterations in the intracellular concentrations of cyclic AMP. 6. A possible role for the metabolism of hexoses via the pentose phosphate pathway in the stimulation of insulin release is discussed.

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