Extracellular calcium influx activates adenylate cyclase 1 and potentiates insulin secretion in MIN6 cells

Kitaguchi, Tetsuya; Oya, Manami; Wada, Yoshiko; Tsuboi, Takashi; Miyawaki, Atsushi

doi:10.1042/bj20121022

Cited by 80 publications

(78 citation statements)

References 39 publications

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“…We have observed an increase in [Ca 2+ ] i rather than a loss of glucose effects after knock-down of ADCY1 and have no ready explanation for this effect, which may stem from adaptation. Note also that in contrast with our study, the clone of MIN6 cells used in the ADCY1 study [35] did not express ADCY8, in contrast to INS-1E or primary beta cells [6,7] (or MIN6 cells used by us, see ESM Fig. 1).…”

Section: Discussioncontrasting

confidence: 46%

“…The recently reported effects of knock-down of ADCY1 in MIN6 cells also underlines a tight link between cAMP, regulation of [Ca 2+ ] i and insulin secretion [35]. We have observed an increase in [Ca 2+ ] i rather than a loss of glucose effects after knock-down of ADCY1 and have no ready explanation for this effect, which may stem from adaptation.…”

Section: Discussioncontrasting

confidence: 45%

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Multilevel control of glucose homeostasis by adenylyl cyclase 8

et al. 2014

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Aims/hypothesis Nutrient homeostasis requires integration of signals generated by glucose metabolism and hormones. Expression of the calcium-stimulated adenylyl cyclase ADCY8 is regulated by glucose and the enzyme is capable of integrating signals from multiple pathways. It may thus have an important role in glucose-induced signalling and glucose homeostasis. Methods We used pharmacological and genetic approaches in beta cells to determine secretion and calcium metabolism. Furthermore, Adcy8 knockout mice were characterised. Results In clonal beta cells, inhibitors of adenylyl cyclases or their downstream targets reduced the glucose-induced increase in cytosolic calcium and insulin secretion. This was reproduced by knock-down of ADCY8, but not of ADCY1. These agents also inhibited glucose-induced increase in cytosolic calcium and electrical activity in primary beta cells and similar effects were observed after ADCY8 knock-down.Moreover, insulin secretion was diminished in islets from Adcy8 knockout mice. These mice were glucose intolerant after oral or intraperitoneal administration of glucose whereas their levels of glucagon-like peptide-1 remained unaltered. Finally, we knocked down ADCY8 in the ventromedial hypothalamus to evaluate the need for ADCY8 in the central regulation of glucose homeostasis. Whereas mice fed a standard diet had normal glucose levels, high-fat diet exacerbated glucose intolerance and knock-down mice were incapable of raising their plasma insulin levels. Finally we confirmed that ADCY8 is expressed in human islets. Conclusions/interpretations Collectively, our findings demonstrate that ADCY8 is required for the physiological activation of glucose-induced signalling pathways in beta cells, for glucose tolerance and for hypothalamic adaptation to a high-fat diet via regulation of islet insulin secretion.Electronic supplementary material The online version of this article (doi:10.1007/s00125-014-3445-z) contains peer-reviewed but unedited supplementary material, which is available to authorised users.

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Section: Discussioncontrasting

confidence: 46%

Section: Discussioncontrasting

confidence: 45%

Multilevel control of glucose homeostasis by adenylyl cyclase 8

et al. 2014

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“…Despite Cav1.2 being the principal L-type Ca 21 channel in mouse, Cav1.3 is the most important L-type channel in rat and human beta cells. Cav1.3 plays a role in cAMP homeostasis through adenylate cyclase 1 and may participate in insulin secretion in an indirect manner (Kitaguchi et al, 2013). Recent work suggests that Cav1.2 LII-III loop interactions may play a significant role in the glucosestimulated excitability.…”

Section: Pharmacology Of Cav Channels In Pancreatic Beta Cellsmentioning

confidence: 99%

Modulation of Ionic Channels and Insulin Secretion by Drugs and Hormones in Pancreatic Beta Cells

Velasco

Díaz‐García

Larqué

et al. 2016

Molecular Pharmacology

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Pancreatic beta cells, unique cells that secrete insulin in response to an increase in glucose levels, play a significant role in glucose homeostasis. Glucose-stimulated insulin secretion (GSIS) in pancreatic beta cells has been extensively explored. In this mechanism, glucose enters the cells and subsequently the metabolic cycle. During this process, the ATP/ADP ratio increases, leading to ATP-sensitive potassium (K ATP ) channel closure, which initiates depolarization that is also dependent on the activity of TRP nonselective ion channels. Depolarization leads to the opening of voltage-gated Na 1 channels (Nav) and subsequently voltage-dependent Ca 21 channels (Cav).The increase in intracellular Ca 21 triggers the exocytosis of insulin-containing vesicles. Thus, electrical activity of pancreatic beta cells plays a central role in GSIS. Moreover, many growth factors, incretins, neurotransmitters, and hormones can modulate GSIS, and the channels that participate in GSIS are highly regulated. In this review, we focus on the principal ionic channels (K ATP , Nav, and Cav channels) involved in GSIS and how classic and new proteins, hormones, and drugs regulate it. Moreover, we also discuss advances on how metabolic disorders such as metabolic syndrome and diabetes mellitus change channel activity leading to changes in insulin secretion.

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“…9 Vit-D is necessary for the absorption of calcium and also has a role in the regulation of insulin secretion from pancreatic beta cells. 10 It is thought that vit-D may be involved in stimulating glucose transport and preventing systemic inflammation, which is associated with insulin resistance. 11,12 Low vit-D levels have been associated with abdominal obesity, hypertension and dyslipidemia.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D: prescription audit in tertiary health care centre

Dashputra¹,

Badwaik²,

Borker³

et al. 2017

Int J Basic Clin Pharmacol

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Background: Vitamin-D is critically important for development, growth and maintenance of health of human being. Many evidences show association between vit-D deficiency and several serious health conditions. Data collection on use of drugs is being obtained with the aim of optimizing drug therapy. So far till date only few studies about prescription pattern of vit-D have been found. Hence it is very important to do audit of prescriptions of vit-D. The aim of the study is to provide concise and updated information about the use of vit-D in tertiary care hospital and to record demographic details of patients. Methods: After ethical approval, this cross sectional study was conducted at tertiary health centre. Patient and drug data (name of drug, dose, dosage form and route of administration) was collected from the patient's prescriptions in OPD. Results: Highest prescriptions of vit-D were found in orthopedic department (22% of total prescriptions of that department). Prescribing percentage of vit-D in medicine department was 4.6%, dermatology 1.5% and in psychiatry 0.8% of total prescriptions. Prescriptions of vit-D in combination with calcium were found in orthopedics (52%), medicine (7%) and obstetrics and gynecology (10%) departments. Conclusions: Highest prescriptions of vit-D alone and with calcium found in orthopedic department. Periodic therapeutic audit is necessary to rationalise the use of vit D.

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Extracellular calcium influx activates adenylate cyclase 1 and potentiates insulin secretion in MIN6 cells

Cited by 80 publications

References 39 publications

Multilevel control of glucose homeostasis by adenylyl cyclase 8

Multilevel control of glucose homeostasis by adenylyl cyclase 8

Modulation of Ionic Channels and Insulin Secretion by Drugs and Hormones in Pancreatic Beta Cells

Vitamin D: prescription audit in tertiary health care centre

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