Role of mitochondria in metabolism-secretion coupling of insulin release in the pancreatic β-cell

BioFactors ◽  
1998 ◽  
Vol 8 (3-4) ◽  
pp. 255-262 ◽  
Author(s):  
Pierre Maechler ◽  
Claes B. Wollheim
Keyword(s):  
Insulin Release ◽  
Pancreatic Β Cell ◽  
Β Cell

Role of Ca2+ in alloxan-induced pancreatic β-cell damage

1994 ◽  
Vol 1227 (1-2) ◽  
pp. 87-91 ◽  
Author(s):  
Hyung-Rho Kim ◽  
Hye-Won Rho ◽  
Byung-Hyun Park ◽  
Jin-Woo Park ◽  
Jong-Suk Kim ◽  
...  
Keyword(s):  
Cell Damage ◽  
Pancreatic Β Cell ◽  
Β Cell

The agouti gene product stimulates pancreatic β-cell Ca2+ signaling and insulin release

1999 ◽  
Vol 1 (1) ◽  
pp. 11-19 ◽  
Author(s):  
B. Z. XUE ◽  
W. O. WILKISON ◽  
R. L. MYNATT ◽  
N. MOUSTAID ◽  
M. GOLDMAN ◽  
...  
Keyword(s):  
Gene Product ◽  
Insulin Release ◽  
Fold Increase ◽  
Cell Types ◽  
Human Pancreas ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Agouti Protein ◽  
Intracellular Ca ◽  
Agouti Gene

Xue, B. Z., W. O. Wilkison, R. L. Mynatt, N. Moustaid, M. Goldman, and M. B. Zemel. The agouti gene product stimulates pancreatic β-cell Ca2+ signaling and insulin release. Physiol. Genomics 1: 11-19, 1999.—Ubiquitous expression of the mouse agouti gene results in obesity and hyperinsulinemia. Human agouti is expressed in adipose tissue, and we found recombinant agouti protein to stimulate lipogenesis in adipocytes in a Ca2+-dependent fashion. However, adipocyte-specific agouti transgenic mice only became obese in the presence of hyperinsulinemia. Because intracellular Ca2+ concentration ([Ca2+]i) is a primary signal for insulin release, and we have shown agouti protein to increase [Ca2+]i in several cell types, we examined the effects of agouti on [Ca2+]i and insulin release. We demonstrated the expression of agouti in human pancreas and generated recombinant agouti to study its effects on Ca2+ signaling and insulin release. Agouti (100 nM) stimulated Ca2+ influx, [Ca2+]i increase, and a marked stimulation of insulin release in two β-cell lines (RIN-5F and HIT-T15; P < 0.05). Agouti exerted comparable effects in isolated human pancreatic islets and β-cells, with a 5-fold increase in Ca2+ influx ( P < 0.001) and a 2.2-fold increase in insulin release ( P < 0.01). These data suggest a potential role for agouti in the development of hyperinsulinemia in humans.

scholarly journals Role of AKT/mTORC1 pathway in pancreatic β-cell proliferation

2012 ◽  
pp. 235-243 ◽  
Author(s):  
Norman Balcazar Morales ◽  
Cecilia Aguilar de Plata
Keyword(s):  
Cell Cycle ◽  
Growth Factors ◽  
Cell Cycle Progression ◽  
Cell Mass ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cycle Progression ◽  
Mtorc1 Signaling

Growth factors, insulin signaling and nutrients are important regulators of β-cell mass and function. The events linking these signals to regulation of β-cell mass are not completely understood. Recent findings indicate that mTOR pathway integrates signals from growth factors and nutrients with transcription, translation, cell size, cytoskeleton remodeling and mitochondrial metabolism. mTOR is a part of two distinct complexes; mTORC1 and mTORC2. The mammalian TORC1 is sensitive to rapamycin and contains Raptor, deptor, PRAS40 and the G protein β-subunit-like protein (GβL). mTORC1 activates key regulators of protein translation; ribosomal S6 kinase (S6K) and eukaryote initiation factor 4E-binding protein 1. This review summarizes current findings about the role of AKT/mTORC1 signaling in regulation of pancreatic β cell mass and proliferation. mTORC1 is a major regulator of β-cell cycle progression by modulation of cyclins D2, D3 and cdk4/cyclin D activity. These studies uncovered key novel pathways controlling cell cycle progression in β-cells in vivo. This information can be used to develop alternative approaches to expand β-cell mass in vivo and in vitro without the risk of oncogenic transformation. The acquisition of such knowledge is critical for the design of improved therapeutic strategies for the treatment and cure of diabetes as well as to understand the effects of mTOR inhibitors in β-cell function.

Life and death decisions of the pancreatic β-cell: the role of fatty acids

2006 ◽  
Vol 112 (1) ◽  
pp. 27-42 ◽  
Author(s):  
Philip Newsholme ◽  
Deirdre Keane ◽  
Hannah J. Welters ◽  
Noel G. Morgan
Keyword(s):  
Fatty Acids ◽  
Insulin Release ◽  
Chronic Exposure ◽  
Cell Function ◽  
Pancreatic Β Cell ◽  
Β Cells ◽  
Β Cell ◽  
Endogenous Fatty Acid ◽  
Gene And Protein Expression ◽  
Β Cell Function

Both stimulatory and detrimental effects of NEFAs (non-esterified fatty acids) on pancreatic β-cells have been recognized. Acute exposure of the pancreatic β-cell to high glucose concentrations and/or saturated NEFAs results in a substantial increase in insulin release, whereas chronic exposure results in desensitization and suppression of secretion, followed by induction of apoptosis. Some unsaturated NEFAs also promote insulin release acutely, but they are less toxic to β-cells during chronic exposure and can even exert positive protective effects. Therefore changes in the levels of NEFAs are likely to be important for the regulation of β-cell function and viability under physiological conditions. In addition, the switching between endogenous fatty acid synthesis or oxidation in the β-cell, together with alterations in neutral lipid accumulation, may have critical implications for β-cell function and integrity. Long-chain acyl-CoA (formed from either endogenously synthesized or exogenous fatty acids) controls several aspects of β-cell function, including activation of specific isoenzymes of PKC (protein kinase C), modulation of ion channels, protein acylation, ceramide formation and/or NO-mediated apoptosis, and transcription factor activity. In this review, we describe the effects of exogenous and endogenous fatty acids on β-cell metabolism and gene and protein expression, and have explored the outcomes with respect to insulin secretion and β-cell integrity.

The role of aging and senescence on pancreatic β-cell function and proliferation

2017 ◽  
Vol 108 ◽  
pp. S71
Author(s):  
Richard Kehm ◽  
Oliver Kluth ◽  
Annette Schürmann ◽  
Tilman Grune ◽  
Annika Höhn
Keyword(s):  
Cell Function ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Β Cell Function

scholarly journals Role of TRPV channels in regulating various pancreatic β-cell functions: Lessons from in vitro studies

2017 ◽  
Vol 11 (1) ◽  
pp. 9-15
Author(s):  
Marek Skrzypski ◽  
Maria Billert ◽  
Stefan Mergler ◽  
Noushafarin Khajavi ◽  
Krzysztof W. Nowak ◽  
...  
Keyword(s):  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Functions ◽  
Trpv Channels

scholarly journals Erratum: Role of the SIK2–p35–PJA2 complex in pancreatic β-cell functional compensation

2014 ◽  
Vol 16 (4) ◽  
pp. 382-382
Author(s):  
Jun-Ichi Sakamaki ◽  
Accalia Fu ◽  
Courtney Reeks ◽  
Stephen Baird ◽  
Chantal Depatie ◽  
...  
Keyword(s):  
Pancreatic Β Cell ◽  
Β Cell ◽  
Functional Compensation
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