Stimulation of glucagon and inhibition of insulin secretion evoked from carotid baroreceptors

1977 ◽  
Vol 33 (2) ◽  
pp. 236-237 ◽  
Author(s):  
J. Järhult ◽  
J. J. Holst
Keyword(s):  
Insulin Secretion ◽  
Carotid Baroreceptors ◽  
Stimulation Of

Stimulation of residual insulin secretion by glibenclamide in insulin dependent diabetics

1980 ◽  
Vol 95 (3) ◽  
pp. 372-375 ◽  
Author(s):  
B. J. Burke ◽  
R. J. Sherriff
Keyword(s):  
Insulin Secretion ◽  
Insulin Therapy ◽  
Metabolic Control ◽  
C Peptide ◽  
Beneficial Effects ◽  
Insulin Dependent ◽  
Serum And Urine ◽  
Stimulation Of

Abstract. Residual insulin secretion, reflected by the presence of C-peptide in serum and urine, has been demonstrated in 5 of 10 insulin-requiring diabetics of less than 10 years' duration tested. The C-peptide response, in the C-peptide secretors, showed a significant increase in both serum and urine after 4 weeks' treatment with 15 mg glibenclamide daily in addition to their usual insulin regime although no beneficial effects in metabolic control were detected. It is suggested that glibenclamide might be a useful adjunct to insulin therapy in insulinrequiring diabetics who still secrete C-peptide.

Stimulation of insulin secretion from isolated rat islets by SaRI 59-801

Diabetes ◽  
1985 ◽  
Vol 34 (6) ◽  
pp. 548-552 ◽  
Author(s):  
R. L. Hanson ◽  
C. M. Isaacson ◽  
L. D. Boyajy
Keyword(s):  
Insulin Secretion ◽  
Rat Islets ◽  
Isolated Rat Islets ◽  
Isolated Rat ◽  
Stimulation Of

scholarly journals GPR40 Is Necessary but Not Sufficient for Fatty Acid Stimulation of Insulin Secretion In Vivo

Diabetes ◽  
2007 ◽  
Vol 56 (4) ◽  
pp. 1087-1094 ◽  
Author(s):  
M. G. Latour ◽  
T. Alquier ◽  
E. Oseid ◽  
C. Tremblay ◽  
T. L. Jetton ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Fatty Acid ◽  
Insulin Secretion In Vivo ◽  
Stimulation Of

Interactions between cholinergic agonists and enteric factors in the regulation of insulin secretion from isolated perifused rat islets

1989 ◽  
Vol 120 (6) ◽  
pp. 702-707 ◽  
Author(s):  
Walter S. Zawalich ◽  
Kathleen C. Zawalich ◽  
Howard Rasmussen
Keyword(s):  
Insulin Secretion ◽  
Gastric Inhibitory Polypeptide ◽  
Moderate Increase ◽  
Rat Islets ◽  
Insulin Requirements ◽  
Isolated Rat Islets ◽  
First Phase Insulin Secretion ◽  
Sensitizing Effect ◽  
Stimulation Of

Abstract. The ability of the cholinergic agonist carbachol to sensitize islets to the action of combined glucose, cholecystokinin and gastric inhibitory polypeptide was determined in isolated rat islets. In response to this combination, peak first phase insulin secretion from control islets averages 85 ± 5 pg · islet−1 · min−1 (mean ± sem) and the insulin secretory rates measured 35–40 min after the onset of stimulation averages 127 ± 34 pg · islet−1 · min−1. A prior 20 min exposure to 1 mmol/l carbachol potentiates the modest insulin stimulatory response to this combination of stimulants: peak first phase release is 354 ± 61 pg · islet−1 · min−1, and release measured 35–40 min after the onset of stimulation is 179 ± 34 pg · islet−1 · min−1. This sensitizing effect of carbachol lasts for at least 40 min and can be duplicated by the natural in vivo agonist acetylcholine. These results demonstrate that cholinergic stimulation of isolated islets primes them to the subsequent stimulatory effect of a moderate increase in the circulating glucose level and to several postulated incretin factors. If operative in vivo, this communications network between cephalic and enteric factors represents a remarkable control system to ensure the release of insulin in amounts commensurate to meet the anticipated and actual insulin requirements for insulin-mediated fuel disposition.

scholarly journals Glucose stimulation of insulin secretion from the isolated pancreas of foetal and newborn rats

Diabetologia ◽  
1969 ◽  
Vol 5 (4) ◽  
pp. 260-262 ◽  
Author(s):  
K. Asplound ◽  
S. Westman ◽  
C. Hellerste�m
Keyword(s):  
Insulin Secretion ◽  
Newborn Rats ◽  
Glucose Stimulation ◽  
Isolated Pancreas ◽  
Stimulation Of

Vagally mediated insulin secretion by stimulation of brain cholinergic neurons with neostigmine in bilateral adrenalectomized rats

1989 ◽  
Vol 493 (1) ◽  
pp. 97-102 ◽  
Author(s):  
Minehiro Gotoh ◽  
Akihisa Iguchi ◽  
Akira Yatomi ◽  
Kazumasa Uemura ◽  
Hisayuki Miura ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Cholinergic Neurons ◽  
Adrenalectomized Rats ◽  
Stimulation Of

scholarly journals Stimulation of Insulin Secretion by Denatonium, One of the Most Bitter-Tasting Substances Known

Diabetes ◽  
2003 ◽  
Vol 52 (2) ◽  
pp. 356-364 ◽  
Author(s):  
S. G. Straub ◽  
J. Mulvaney-Musa ◽  
H. Yajima ◽  
G. A. Weiland ◽  
G. W.G. Sharp
Keyword(s):  
Insulin Secretion ◽  
Stimulation Of

Direct effect of parathyroid hormone on insulin secretion from pancreatic islets

1990 ◽  
Vol 258 (6) ◽  
pp. E975-E984 ◽  
Author(s):  
G. Z. Fadda ◽  
M. Akmal ◽  
L. G. Lipson ◽  
S. G. Massry
Keyword(s):  
Insulin Secretion ◽  
Parathyroid Hormone ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Direct Effect ◽  
Indirect Evidence ◽  
Cytosolic Calcium ◽  
Dependent Manner ◽  
Stimulation Of

Indirect evidence indicates that parathyroid hormone (PTH) interacts with pancreatic islets and modulates their insulin secretion. This property of PTH has been implicated in the genesis of impaired insulin release in chronic renal failure. We examined the direct effect of PTH-(1-84) and PTH-(1-34) on insulin release using in vitro static incubation and dynamic perifusion of pancreatic islets from normal rats. Both moieties of the hormone stimulated in a dose-dependent manner glucose-induced insulin release but higher doses inhibited glucose-induced insulin release. This action of PTH was modulated by the calcium concentration in the media. The stimulatory effect of PTH was abolished by its inactivation and blocked by its antagonist [Tyr-34]bPTH-(7-34)NH2. PTH also augmented phorbol ester (TPA)-induced insulin release, stimulated adenosine 3',5'-cyclic monophosphate (cAMP) generation by pancreatic islets, and significantly increased (+50 +/- 2.7%, P less than 0.01) their cytosolic calcium. Verapamil inhibited the stimulatory effect of PTH on insulin release. The data show that 1) pancreatic islets are a PTH target and may have PTH receptors, 2) stimulation of glucose-induced insulin release by PTH is mediated by a rise in cytosolic calcium, 3) stimulation of cAMP production by PTH and a potential indirect activation of protein kinase C by PTH may also contribute to the stimulatory effect on glucose-induced insulin release, and 4) this action of PTH requires calcium in incubation or perifusion media.

Stimulation of insulin secretion after prostaglandin PGE1 in the anesthetized dog

1973 ◽  
Vol 22 (14) ◽  
pp. 1773-1779 ◽  
Author(s):  
Pierre J. Lefebvre ◽  
Alfred S. Luyckx
Keyword(s):  
Insulin Secretion ◽  
Stimulation Of
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