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

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

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.

Transgenic overexpression of intraislet ghrelin does not affect insulin secretion or glucose metabolism in vivo

2012 ◽  
Vol 302 (4) ◽  
pp. E403-E408 ◽  
Author(s):  
Mika Bando ◽  
Hiroshi Iwakura ◽  
Hiroyuki Ariyasu ◽  
Hiroshi Hosoda ◽  
Go Yamada ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Medium Chain Triglyceride ◽  
Physiological Role ◽  
Standard Diet ◽  
Entry Site ◽  
Insulin Secretion In Vivo

Whereas ghrelin is produced primarily in the stomach, a small amount of it is produced in pancreatic islets. Although exogenous administration of ghrelin suppresses insulin secretion in vitro or in vivo, the role of intraislet ghrelin in the regulation of insulin secretion in vivo remains unclear. To understand the physiological role of intraislet ghrelin in insulin secretion and glucose metabolism, we developed a transgenic (Tg) mouse model, rat insulin II promoter ghrelin-internal ribosomal entry site-ghrelin O-acyl transferase (RIP-GG) Tg mice, in which mouse ghrelin cDNA and ghrelin O-acyltransferase are overexpressed under the control of the rat insulin II promoter. Although pancreatic desacyl ghrelin levels were elevated in RIP-GG Tg mice, pancreatic ghrelin levels were not altered in animals on a standard diet. However, when Tg mice were fed a medium-chain triglyceride-rich diet (MCTD), pancreatic ghrelin levels were elevated to ∼16 times that seen in control animals. It seems likely that the gastric ghrelin cells possess specific machinery to provide the octanoyl acid necessary for ghrelin acylation but that this machinery is absent from pancreatic β-cells. Despite the overexpression of ghrelin, plasma ghrelin levels in the portal veins of RIP-GG Tg mice were unchanged from control levels. Glucose tolerance, insulin secretion, and islet architecture in RIP-GG Tg mice were not significantly different even when the mice were fed a MCTD. These results indicate that intraislet ghrelin does not play a major role in the regulation of insulin secretion in vivo.

The glucose-lowering potential of exendin-4 orally delivered via a pH-sensitive nanoparticle vehicle and effects on subsequent insulin secretion in vivo

Biomaterials ◽  
2011 ◽  
Vol 32 (10) ◽  
pp. 2673-2682 ◽  
Author(s):  
Ho-Ngoc Nguyen ◽  
Shiaw-Pyng Wey ◽  
Jyuhn-Huarng Juang ◽  
Kiran Sonaje ◽  
Yi-Cheng Ho ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Ph Sensitive ◽  
Glucose Lowering ◽  
Insulin Secretion In Vivo

scholarly journals Aldosterone decreases glucose-stimulated insulin secretion in vivo in mice and in murine islets

Diabetologia ◽  
2011 ◽  
Vol 54 (8) ◽  
pp. 2152-2163 ◽  
Author(s):  
J. M. Luther ◽  
P. Luo ◽  
M. T. Kreger ◽  
M. Brissova ◽  
C. Dai ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Insulin Secretion In Vivo ◽  
Glucose Stimulated Insulin Secretion

scholarly journals The Fatty Acid Receptor GPR40 Plays a Role in Insulin Secretion In Vivo After High-Fat Feeding

Diabetes ◽  
2008 ◽  
Vol 57 (9) ◽  
pp. 2432-2437 ◽  
Author(s):  
M. Kebede ◽  
T. Alquier ◽  
M. G. Latour ◽  
M. Semache ◽  
C. Tremblay ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Fatty Acid ◽  
High Fat ◽  
Acid Receptor ◽  
Insulin Secretion In Vivo ◽  
Fat Feeding ◽  
Fatty Acid Receptor

Pulsatile insulin secretion accounts for 70% of total insulin secretion during fasting

1995 ◽  
Vol 269 (3) ◽  
pp. E478-E488 ◽  
Author(s):  
N. Porksen ◽  
S. Munn ◽  
J. Steers ◽  
S. Vore ◽  
J. Veldhuis ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Portal Vein ◽  
Basal Insulin ◽  
Deconvolution Analysis ◽  
Insulin Secretion In Vivo ◽  
Endogenous Insulin Secretion ◽  
Endogenous Insulin ◽  
Basal Insulin Secretion ◽  
Secretion Rates

The purpose of the present study was to determine the contributions of discrete insulin secretory bursts vs. basal insulin release to total insulin secretion in vivo. Quantification of the partitioning of pulsatile and basal insulin secretion is complicated by physiological delivery of these pulses into the portal vein and the absence of validated methods of measuring the rates of pulsatile and basal insulin secretion in vivo. We therefore 1) developed a canine model with chronically implanted portal vein catheters, 2) validated an established deconvolution technique as well as a novel direct catheterization technique (Clustcath) for measurement of pulsatile and nonpulsatile insulin secretion rates in this model, and 3) applied these methods to study insulin secretion in the overnight-fasted dog in vivo to determine the contribution of pulsatile vs. basal insulin secretion to total rates of endogenous insulin secretion. Rates of total, pulsatile, and nonpulsatile endogenous insulin secretion measured by Cluscath closely parallel those measured by deconvolution analysis (54 +/- 15 vs. 51 +/- 11, 38 +/- 12 vs. 36 +/- 11, and 16 +/- 4 vs. 14 +/- 4 pmol/min, respectively). Clustcath and deconvolution indicated that the majority of insulin was secreted as pulses (70 +/- 6 and 66 +/- 7%, respectively). These data infer that any process that selectively decreases the pulsatile component of insulin secretion (e.g., diabetes mellitus) will likely have a major impact on total insulin secretion.

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