Mechanisms of Sulfonylurea's Stimulation of Insulin Secretion In Vivo: Selective Amplification of Insulin Secretory Burst Mass

Diabetes ◽  
1996 ◽  
Vol 45 (12) ◽  
pp. 1792-1797 ◽  
Author(s):  
N. K. Porksen ◽  
S. R. Munn ◽  
J. L. Steers ◽  
O. Schmitz ◽  
J. D. Veldhuis ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Selective Amplification ◽  
Insulin Secretion In Vivo ◽  
Stimulation Of

Mechanisms of sulfonylurea's stimulation of insulin secretion in vivo: selective amplification of insulin secretory burst mass

Diabetes ◽  
1996 ◽  
Vol 45 (12) ◽  
pp. 1792-1797 ◽  
Author(s):  
N. K. Porksen ◽  
S. R. Munn ◽  
J. L. Steers ◽  
O. Schmitz ◽  
J. D. Veldhuis ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Selective Amplification ◽  
Insulin Secretion In Vivo ◽  
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 Disruption of GPR39 Impairs Insulin Secretion In Vivo

2009 ◽  
Vol 94 (4) ◽  
pp. 1472-1472
Author(s):  
Frédéric Tremblay ◽  
Ann-Marie T. Richard ◽  
Sarah Will ◽  
Jameel Syed ◽  
Nancy Stedman ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Insulin Secretion In Vivo

Hyperinsulinemia of preobese and obese fa/fa rats is partly vagus nerve mediated

1983 ◽  
Vol 244 (4) ◽  
pp. E317-E322 ◽  
Author(s):  
F. Rohner-Jeanrenaud ◽  
A. C. Hochstrasser ◽  
B. Jeanrenaud
Keyword(s):  
Electrical Stimulation ◽  
Insulin Secretion ◽  
B Cells ◽  
Vagus Nerve ◽  
Zucker Rats ◽  
Glucose Load ◽  
Parasympathetic System ◽  
Enhanced Sensitivity ◽  
Stimulation Of

In vivo glucose-induced insulin secretion was greater in preweaned preobese 17-day-old Zucker rats than in the corresponding controls. This hypersecretion of insulin was reversed to normal by acute pretreatment with atropine. A short-lived (30 s) electrical stimulation of the vagus nerve preceding a glucose load potentiated the in vivo glucose-induced insulin release in adult animals (6-9 wk) and more so in obese Zucker (fa/fa) than in lean rats. This suggested the existence of enhanced sensitivity and/or responsiveness of the B cells of obese animals to the parasympathetic system. That the parasympathetic tone was increased in adult obese Zucker (fa/fa) rats was corroborated by the observation that acute vagotomy of these animals resulted in a significant decrease in glucose-induced insulin secretion, whereas no such effect was seen in lean rats. Also, perfused pancreases from adult obese (fa/fa) rats oversecreted insulin during a stimulation by arginine when compared with controls, an oversecretion that was restored toward normal by superimposed infusion of atropine. It is concluded that a) the increased insulin secretion of preobese Zucker fa/fa rats is an early abnormality that is mediated by the vagus nerve, and b) increased secretion of insulin in adult obese fa/fa rats continues to be partly vagus-nerve mediated, although a decreased sympathetic tone and other unknown defects could conceivably play a role as well.

In Vivo Stimulation of Insulin Secretion by Guanidine Derivatives in the Rat

1974 ◽  
Vol 6 (02) ◽  
pp. 115-120 ◽  
Author(s):  
A. Aynsley-Green ◽  
K.G.M.M. Alberti
Keyword(s):  
Insulin Secretion ◽  
Guanidine Derivatives ◽  
Stimulation Of

scholarly journals Action of β-cell tropin on insulin secretion in vivo and on lipid synthesis

FEBS Letters ◽  
1982 ◽  
Vol 139 (2) ◽  
pp. 230-232 ◽  
Author(s):  
Anne Beloff-Chain ◽  
Pamela Carr ◽  
Allan Watkinson
Keyword(s):  
Insulin Secretion ◽  
Lipid Synthesis ◽  
Β Cell ◽  
Insulin Secretion In Vivo

scholarly journals In Vivo Deletion of β-Cell Drp1 Impairs Insulin Secretion Without Affecting Islet Oxygen Consumption

Endocrinology ◽  
2018 ◽  
Vol 159 (9) ◽  
pp. 3245-3256 ◽  
Author(s):  
Thomas G Hennings ◽  
Deeksha G Chopra ◽  
Elizabeth R DeLeon ◽  
Halena R VanDeusen ◽  
Hiromi Sesaki ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Insulin Secretion ◽  
Tricarboxylic Acid Cycle ◽  
Mitochondrial Fission ◽  
Calcium Handling ◽  
Mitochondrial Morphology ◽  
Second Phase ◽  
Β Cell ◽  
Insulin Secretion In Vivo

Abstract Mitochondria are dynamic organelles that undergo frequent fission and fusion events. Mitochondrial fission is required for ATP production, the tricarboxylic acid cycle, and processes beyond metabolism in a cell-type specific manner. Ex vivo and cell line studies have demonstrated that Drp1, a central regulator of mitochondrial fission, is required for glucose-stimulated insulin secretion (GSIS) in pancreatic β cells. Herein, we set out to interrogate the role of Drp1 in β-cell insulin secretion in vivo. We generated β-cell–specific Drp1 knockout (KO) mice (Drp1β-KO) by crossing a conditional allele of Drp1 to Ins1cre mice, in which Cre recombinase replaces the coding region of the Ins1 gene. Drp1β-KO mice were glucose intolerant due to impaired GSIS but did not progress to fasting hyperglycemia as adults. Despite markedly abnormal mitochondrial morphology, Drp1β-KO islets exhibited normal oxygen consumption rates and an unchanged glucose threshold for intracellular calcium mobilization. Instead, the most profound consequences of β-cell Drp1 deletion were impaired second-phase insulin secretion and impaired glucose-stimulated amplification of insulin secretion. Our data establish Drp1 as an important regulator of insulin secretion in vivo and demonstrate a role for Drp1 in metabolic amplification and calcium handling without affecting oxygen consumption.

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