scholarly journals Effects of streptozotocin in vitro on proinsulin biosynthesis, insulin release and ATP content of isolated rat islets of Langerhans

Diabetologia ◽  
1976 ◽  
Vol 12 (5) ◽  
pp. 471-481 ◽  
Author(s):  
A. Maldonato ◽  
P. A. Trueheart ◽  
A. E. Renold ◽  
G. W. G. Sharp
Keyword(s):  
Insulin Release ◽  
Islets Of Langerhans ◽  
Atp Content ◽  
Rat Islets ◽  
Proinsulin Biosynthesis ◽  
Isolated Rat Islets ◽  
Rat Islets Of Langerhans ◽  
Isolated Rat

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.

Low concentrations of interleukin-1 stimulate and high concentrations inhibit insulin release from isolated rat islets of Langerhans

1986 ◽  
Vol 113 (4) ◽  
pp. 551-558 ◽  
Author(s):  
Giatgen A. Spinas ◽  
Thomas Mandrup-Poulsen ◽  
Jens Mølvig ◽  
Leif Bæk ◽  
Klaus Bendtzen ◽  
...  
Keyword(s):  
Insulin Release ◽  
Interleukin 1 ◽  
Insulin Biosynthesis ◽  
Rat Islets ◽  
Low Concentrations ◽  
Isolated Rat Islets ◽  
High Concentrations ◽  
Rat Islets Of Langerhans ◽  
Isolated Rat

Abstract. Isolated rat islets were incubated either with crude, affinity-purified or recombinant human interleukin-1 for 1 to 6 days. A significant (20–60%) increase of insulin release was observed at low concentrations of all three interleukin-1-containing preparations. In contrast, higher concentrations dose-dependently inhibited the insulin release. The increased insulin secretion occurred at concentrations below those necessary to augment the mitogen response to phytohaemagglutinin of murine thymocytes in vitro. These doses (0.05-0.5 U/ml) correspond to 0.2-2 ng of recombinant interleukin-1 per ml, equal to approximately 0.01-0.1 pmol/ml. In doses of 0.6-1.8 U/ml affinitypurified interleukin-1 significantly increased the islet insulin content per ng of DNA, indicating a stimulation of insulin-biosynthesis. The data support the concept that low concentrations of interleukin-1 may play a role in priming the physiological secretion of insulin.

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.

Evidence That Cholecystokinin Interacts with Specific Receptors and Regulates Insulin Release in Isolated Rat Islets of Langerhans

Diabetes ◽  
1986 ◽  
Vol 35 (1) ◽  
pp. 38-43 ◽  
Author(s):  
E. J. Verspohl ◽  
H. P. T. Ammon ◽  
J. A. Williams ◽  
I. D. Goldfine
Keyword(s):  
Insulin Release ◽  
Islets Of Langerhans ◽  
Rat Islets ◽  
Isolated Rat Islets ◽  
Specific Receptors ◽  
Rat Islets Of Langerhans ◽  
Isolated Rat

Effects of flavonoids on insulin secretion and 45Ca2+ handling in rat islets of Langerhans

1985 ◽  
Vol 107 (1) ◽  
pp. 1-8 ◽  
Author(s):  
C.S.T. Hii ◽  
S.L. Howell
Keyword(s):  
Insulin Secretion ◽  
Insulin Release ◽  
Islets Of Langerhans ◽  
Hormone Release ◽  
Short Term ◽  
Rat Islets ◽  
Naturally Occurring ◽  
Isolated Rat Islets ◽  
Rat Islets Of Langerhans ◽  
Isolated Rat

ABSTRACT The effects of some flavonoids, a group of naturally occurring pigments one of which has been claimed to possess antidiabetic activities, on insulin release and 45Ca2+ handling have been studied in isolated rat islets of Langerhans. Insulin release was enhanced by approximately 44–70% when islets were exposed to either (−)epicatechin (0·8 mmol/l) or quercetin (0·01–0·1 mmol/l); others such as naringenin (0·1 mmol/l) and chrysin (0·08 mmol/l) inhibited hormone release by approximately 40–60%. These effects were observed only in the presence of 20 mmol glucose/l. Quercetin (0·01 mmol/l) and (−)epicatechin (0·8 mmol/l) both inhibited 45Ca2+ efflux in the presence and absence of extracellular Ca2+. In the presence of 20 mmol glucose/l both the short-term (5 min) and steady-state (30 min) uptake of 45Ca2+ were significantly increased by either quercetin or (−)epicatechin. These results suggest that the stimulatory compounds such as quercetin and (−)epicatechin may, at least in part, exert their effects on insulin release via changes in Ca2+ metabolism. J. Endocr. (1985) 107, 1–8

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