Calcium signaling in pancreatic β-cells in health and in Type 2 diabetes

Gilon, Patrick; Chae, Heeyoung; Rutter, Guy A.; Ravier, Magalie A.

doi:10.1016/j.ceca.2014.09.001

Cited by 179 publications

(185 citation statements)

References 352 publications

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“…Numerous studies have demonstrated that calcium (Ca 2+ ) plays a pivotal role in insulin secretion from the islets of Langerhans and that altered cellular Ca 2+ homeostasis may be involved in defective insulin release (7)(8)(9)(10)(11). Nevertheless, according to the classical view of the glucose-sensing machinery, insulin secretion largely depends on voltage-activated Ca 2+ influx, whereas the role of intracellular Ca 2+ release in pancreatic β cells in response to glucose has not been fully elucidated (12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

Calcium release channel RyR2 regulates insulin release and glucose homeostasis

Santulli¹,

Pagano²,

Sardu³

et al. 2015

J. Clin. Invest.

196

175

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Section: Introductionmentioning

confidence: 99%

Calcium release channel RyR2 regulates insulin release and glucose homeostasis

Santulli¹,

Pagano²,

Sardu³

et al. 2015

J. Clin. Invest.

196

175

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“…An occasional event following the addition of high glucose to islets (305,506) and dissociated cells (179,221,434) is a transient decrease in [Ca 2ϩ ] c prior to the initiation of oscillations, which has been ascribed to enhanced uptake into the endoplasmic reticulum (ER) (23,121). This indicates that the ⌬G p maintained in low glucose restricts the activity of one or more pathways sequestering cytosolic Ca 2ϩ , such as the plasma membrane and ER Ca 2ϩ -ATPases.…”

Section: Ion Pumpsmentioning

confidence: 99%

The Pancreatic β-Cell: A Bioenergetic Perspective

Nicholls

2016

Physiological Reviews

123

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The pancreatic ␤-cell secretes insulin in response to elevated plasma glucose. This review applies an external bioenergetic critique to the central processes of glucose-stimulated insulin secretion, including glycolytic and mitochondrial metabolism, the cytosolic adenine nucleotide pool, and its interaction with plasma membrane ion channels. The control mechanisms responsible for the unique responsiveness of the cell to glucose availability are discussed from bioenergetic and metabolic control standpoints. The concept of coupling factor facilitation of secretion is critiqued, and an attempt is made to unravel the bioenergetic basis of the oscillatory mechanisms controlling secretion. The need to consider the physiological constraints operating in the intact cell is emphasized throughout. The aim is to provide a coherent pathway through an extensive, complex, and sometimes bewildering literature, particularly for those unfamiliar with the field.

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“…Ca 2+ -induced Ca 2+ release (CICR) through RyRs may also occur upon large VDCC-mediated Ca 2+ influx. However, this process is still controversial (reviewed in Gilon et al 2014).…”

Section: Soce In Insulin Secretion: From Capacitative Ca 2+ Entry To mentioning

confidence: 99%

“…The sudden rise in intracellular Ca 2+ levels causes exocytosis of insulincontaining vesicles. In addition to K ATP channels and VDCC, a complex interplay between additional ion channels and intracellular Ca 2+ stores produces unique patterns of oscillatory depolarization and [Ca 2+ ] i changes controlling insulin release (Gilon et al 2014).…”

Section: Introductionmentioning

confidence: 99%

Store-operated Ca2+ entry: a key component of the insulin secretion machinery

Sabourin

Allagnat

2016

Journal of Molecular Endocrinology

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Normal plasma glucose level is ensured by the action of insulin, the major hypoglycemic hormone. Therefore, it is not surprising that insulin release from pancreatic β-cells of the islets of Langerhans is controlled by an array of balanced mechanisms in which glucose plays the leading role. Glucose triggers insulin secretion through the well-described pathway of ATP-driven closure of ATP-sensitive potassium channels (KATP), depolarization of the plasma membrane, and opening of the voltage-dependent Ca2+ channels (VDCC). The subsequent rapid rise in cytoplasmic free Ca2+ concentration triggers insulin exocytosis. However, despite more than 40 years of investigation, certain aspects of the intracellular Ca2+ responses to glucose and secretagogues remain unexplained, suggesting the involvement of additional Ca2+ channels. Here, we discuss the emerging role of store-operated Ca2+ channels carried by Orai1 and transient receptor potential canonical 1 (TRPC1) proteins and regulated by the stromal interaction molecule 1 (STIM1) in the control of glucose-induced insulin secretion. The role of other voltage-independent cation channels formed by other members of the TRP channels family is also addressed.

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Calcium signaling in pancreatic β-cells in health and in Type 2 diabetes

Cited by 179 publications

References 352 publications

Calcium release channel RyR2 regulates insulin release and glucose homeostasis

Calcium release channel RyR2 regulates insulin release and glucose homeostasis

The Pancreatic β-Cell: A Bioenergetic Perspective

Store-operated Ca2+ entry: a key component of the insulin secretion machinery

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