Ryanodine receptors of pancreatic β‐cells mediate a distinct context‐dependent signal for insulin secretion

Bruton, Joseph D.; Lemmens, Raf; Shi, Chun-Liang; Persson–Sjögren, Solveig; Westerblad, Håkan; Ahmed, Muhammad Adeel; Pyne, Nigel J.; Frame, Mhairi; Furman, Brian L.; Islam, Shahidul

doi:10.1096/fj.02-0481fje

Cited by 60 publications

(53 citation statements)

References 39 publications

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“…In several studies of primary - In most studies of CICR in insulin-secreting cells, the phenomenon has been attributed to RyRs [12,14,[17][18][19]. Both type 2 RyR mRNA and RyR protein are expressed in primary as well as clonal -cells [13][14][15].…”

Section: Discussionmentioning

confidence: 99%

“…Both type 2 RyR mRNA and RyR protein are expressed in primary as well as clonal -cells [13][14][15]. Convincing evidence for functional RyRs come only from the clonal -cells RINm-5F [54], HIT-T15 [14], MIN6 [15] and INS-1 [17,18,55] in which caffeine exhibits the characteristic acute effect on Ca 2+ mobilization. The present data confirm functional ryanodine receptors in INS-1 cells [17] by showing a Ca 2+ -mobilizing effect of caffeine and that ryanodine pre-treatment abolishes such mobilization.…”

Section: Discussionmentioning

confidence: 99%

“…Even though RyRs are expressed in -cells [13][14][15], the physiological role of cADPr and RyRs remains controversial [16]. Nevertheless, there are several suggestions that RyRs mediate CICR in -cells [12,14,[17][18][19].…”

Section: Introductionmentioning

confidence: 99%

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Ca2+-induced Ca2+ release by activation of inositol 1,4,5-trisphosphate receptors in primary pancreatic β-cells

2004

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The effect of sarcoendoplasmic reticulum Ca 2+ -ATPase (SERCA) inhibition on the The results indicate that leakage of Ca 2+ from the endoplasmic reticulum after SERCA inhibition is feedback-accelerated by Ca 2+ -induced Ca 2+ release (CICR). In primary pancreatic -cells this CICR is due to activation of inositol 1,4,5-trisphosphate receptors.CICR by ryanodine receptor activation may be restricted to clonal -cells.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Ca2+-induced Ca2+ release by activation of inositol 1,4,5-trisphosphate receptors in primary pancreatic β-cells

2004

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“…The RyR is a Ca 2+ channel composed of four ~550 kDa ryanodine protomers and four 12 kDa FK506 binding proteins that are the regulatory units FKBP12 or FKB12.6 (Thearle and Brillantes, 2005). There are three distinct genes encoding three ryanodine receptors, types 1, 2, and 3, RyR1, RyR2 and RyR3 respectively and there is some debate over the most prevalent and the most important types in the β cell (reviewed in Bruton et al, 2003). It appears from RNAse protection assays and RT-PCR that RyR2 is the most prevalent form (Islam et al, 1998).…”

Section: Elevation Of [Ca 2+ ] Imentioning

confidence: 99%

Mechanisms of action of glucagon-like peptide 1 in the pancreas

Doyle

Egan

2007

Pharmacology & Therapeutics

561

465

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Glucagon-like peptide-1 is a hormone that is encoded in the proglucagon gene. It is mainly produced in enteroendocrine L cells of the gut and is secreted into the blood stream when food containing fat, protein hydrolysate and/or glucose enters the duodenum. Its particular effects on insulin and glucagon secretion have generated a flurry of research activity over the past twenty years culminating in a naturally occurring GLP-1 receptor agonist, exendin-4, now being used to treat type 2 diabetes. GLP-1 engages a specific G-protein coupled receptor that is present in tissues other than the pancreas (brain, kidney, lung, heart, major blood vessels). The most widely studied cell activated by GLP-1 is the insulin-secreting beta cell where its defining action is augmentation of glucose-induced insulin secretion. Upon GLP-1 receptor activation, adenylyl cyclase is activated and cAMP generated, leading, in turn, to cAMP-dependent activation of second messenger pathways, such as the PKA and Epac pathways. As well as short-term effects of enhancing glucose-induced insulin secretion, continuous GLP-1 receptor activation also increases insulin synthesis, and beta cell proliferation and neogenesis. Although these latter effects cannot be currently monitored in humans, there are substantial improvements in glucose tolerance and increases in both first phase and plateau phase insulin secretory responses in type 2 diabetic patients treated with exendin-4. This review we will focus on the effects resulting from GLP-1 receptor activation in islets of Langerhans

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“…Caffeine acutely lowered insulin sensitivity [18,19,20,21,22] and increased glucose concentrations [23,24,25,26,27] in short-term metabolic studies in humans. However, these effects may not persist during chronic coffee consumption [19], and beneficial effects of caffeine on insulin sensitivity [28] and glucose-induced insulin secretion [29] have also been suggested. In several cohort studies, magnesium intake was associated with a lower risk of type 2 diabetes [30,31,32], and in intervention studies, pharmacological doses of magnesium improved glucose metabolism [33].…”

Section: Introductionmentioning

confidence: 99%

Coffee consumption and incidence of impaired fasting glucose, impaired glucose tolerance, and type 2 diabetes: the Hoorn Study

Dam¹,

et al. 2004

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Aims/hypothesis. Coffee contains several substances that may affect glucose metabolism. The aim of this study was to evaluate the relationship between habitual coffee consumption and the incidence of IFG, IGT and type 2 diabetes. Methods. We used cross-sectional and prospective data from the population-based Hoorn Study, which included Dutch men and women aged 50-74 years. An OGTT was performed at baseline and after a mean follow-up period of 6.4 years. Associations were adjusted for potential confounders including BMI, cigarette smoking, physical activity, alcohol consumption and dietary factors. Results. At baseline, a 5 cup per day higher coffee consumption was significantly associated with lower fasting insulin concentrations (−5.6%, 95% CI −9.3 to −1.6%) and 2-h glucose concentrations (−8.8%, 95% CI −11.8 to −5.6%), but was not associated with lower fasting glucose concentrations (−0.8%, 95% CI −2.1 to 0.6%). In the prospective analyses, the odds ratio (OR) for IGT was 0.59 (95% CI 0.36-0.97) for 3-4 cups per day, 0.46 (95% CI 0.26-0.81) for 5-6 cups per day, and 0.37 (95% CI 0.16-0.84) for 7 or more cups per day, as compared with the corresponding values for the consumption of 2 or fewer cups of coffee per day (p=0.001 for trend). Higher coffee consumption also tended to be associated with a lower incidence of type 2 diabetes (OR 0.69, CI 0.31-1.51 for ≥7 vs ≤2 cups per day, p=0.09 for trend), but was not associated with the incidence of IFG (OR 1.35, CI 0.80-2.27 for ≥7 vs ≤2 cups per day, p=0.49 for trend). Conclusions/interpretation. Our findings indicate that habitual coffee consumption can reduce the risk of IGT, and affects post-load rather than fasting glucose metabolism.

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Ryanodine receptors of pancreatic β‐cells mediate a distinct context‐dependent signal for insulin secretion

Cited by 60 publications

References 39 publications

Ca2+-induced Ca2+ release by activation of inositol 1,4,5-trisphosphate receptors in primary pancreatic β-cells

Ca2+-induced Ca2+ release by activation of inositol 1,4,5-trisphosphate receptors in primary pancreatic β-cells

Mechanisms of action of glucagon-like peptide 1 in the pancreas

Coffee consumption and incidence of impaired fasting glucose, impaired glucose tolerance, and type 2 diabetes: the Hoorn Study

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