CPT1a-Dependent Long-Chain Fatty Acid Oxidation Contributes to Maintaining Glucagon Secretion from Pancreatic Islets

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CPT1a-Dependent Long-Chain Fatty Acid Oxidation Contributes to Maintaining Glucagon Secretion from Pancreatic Islets. / Briant, Linford J B; Dodd, Michael S; Chibalina, Margarita V; Rorsman, Nils J G; Johnson, Paul R V; Carmeliet, Peter; Rorsman, Patrik; Knudsen, Jakob G.

I: Cell Reports, Bind 23, Nr. 11, 2018, s. 3300-3311.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Briant, LJB, Dodd, MS, Chibalina, MV, Rorsman, NJG, Johnson, PRV, Carmeliet, P, Rorsman, P & Knudsen, JG 2018, 'CPT1a-Dependent Long-Chain Fatty Acid Oxidation Contributes to Maintaining Glucagon Secretion from Pancreatic Islets', Cell Reports, bind 23, nr. 11, s. 3300-3311. https://doi.org/10.1016/j.celrep.2018.05.035

APA

Briant, L. J. B., Dodd, M. S., Chibalina, M. V., Rorsman, N. J. G., Johnson, P. R. V., Carmeliet, P., Rorsman, P., & Knudsen, J. G. (2018). CPT1a-Dependent Long-Chain Fatty Acid Oxidation Contributes to Maintaining Glucagon Secretion from Pancreatic Islets. Cell Reports, 23(11), 3300-3311. https://doi.org/10.1016/j.celrep.2018.05.035

Vancouver

Briant LJB, Dodd MS, Chibalina MV, Rorsman NJG, Johnson PRV, Carmeliet P o.a. CPT1a-Dependent Long-Chain Fatty Acid Oxidation Contributes to Maintaining Glucagon Secretion from Pancreatic Islets. Cell Reports. 2018;23(11):3300-3311. https://doi.org/10.1016/j.celrep.2018.05.035

Author

Briant, Linford J B ; Dodd, Michael S ; Chibalina, Margarita V ; Rorsman, Nils J G ; Johnson, Paul R V ; Carmeliet, Peter ; Rorsman, Patrik ; Knudsen, Jakob G. / CPT1a-Dependent Long-Chain Fatty Acid Oxidation Contributes to Maintaining Glucagon Secretion from Pancreatic Islets. I: Cell Reports. 2018 ; Bind 23, Nr. 11. s. 3300-3311.

Bibtex

@article{e58a8e3f647741f8a8efeb1b61b36deb,

title = "CPT1a-Dependent Long-Chain Fatty Acid Oxidation Contributes to Maintaining Glucagon Secretion from Pancreatic Islets",

abstract = "Glucagon, the principal hyperglycemic hormone, is secreted from pancreatic islet α cells as part of the counter-regulatory response to hypoglycemia. Hence, secretory output from α cells is under high demand in conditions of low glucose supply. Many tissues oxidize fat as an alternate energy substrate. Here, we show that glucagon secretion in low glucose conditions is maintained by fatty acid metabolism in both mouse and human islets, and that inhibiting this metabolic pathway profoundly decreases glucagon output by depolarizing α cell membrane potential and decreasing action potential amplitude. We demonstrate, by using experimental and computational approaches, that this is not mediated by the KATP channel, but instead due to reduced operation of the Na+-K+ pump. These data suggest that counter-regulatory secretion of glucagon is driven by fatty acid metabolism, and that the Na+-K+ pump is an important ATP-dependent regulator of α cell function.",

author = "Briant, {Linford J B} and Dodd, {Michael S} and Chibalina, {Margarita V} and Rorsman, {Nils J G} and Johnson, {Paul R V} and Peter Carmeliet and Patrik Rorsman and Knudsen, {Jakob G}",

year = "2018",

doi = "10.1016/j.celrep.2018.05.035",

language = "English",

volume = "23",

pages = "3300--3311",

journal = "Cell Reports",

issn = "2211-1247",

publisher = "Cell Press",

number = "11",

}

RIS

TY - JOUR

T1 - CPT1a-Dependent Long-Chain Fatty Acid Oxidation Contributes to Maintaining Glucagon Secretion from Pancreatic Islets

AU - Briant, Linford J B

AU - Dodd, Michael S

AU - Chibalina, Margarita V

AU - Rorsman, Nils J G

AU - Johnson, Paul R V

AU - Carmeliet, Peter

AU - Rorsman, Patrik

AU - Knudsen, Jakob G

PY - 2018

Y1 - 2018

N2 - Glucagon, the principal hyperglycemic hormone, is secreted from pancreatic islet α cells as part of the counter-regulatory response to hypoglycemia. Hence, secretory output from α cells is under high demand in conditions of low glucose supply. Many tissues oxidize fat as an alternate energy substrate. Here, we show that glucagon secretion in low glucose conditions is maintained by fatty acid metabolism in both mouse and human islets, and that inhibiting this metabolic pathway profoundly decreases glucagon output by depolarizing α cell membrane potential and decreasing action potential amplitude. We demonstrate, by using experimental and computational approaches, that this is not mediated by the KATP channel, but instead due to reduced operation of the Na+-K+ pump. These data suggest that counter-regulatory secretion of glucagon is driven by fatty acid metabolism, and that the Na+-K+ pump is an important ATP-dependent regulator of α cell function.

AB - Glucagon, the principal hyperglycemic hormone, is secreted from pancreatic islet α cells as part of the counter-regulatory response to hypoglycemia. Hence, secretory output from α cells is under high demand in conditions of low glucose supply. Many tissues oxidize fat as an alternate energy substrate. Here, we show that glucagon secretion in low glucose conditions is maintained by fatty acid metabolism in both mouse and human islets, and that inhibiting this metabolic pathway profoundly decreases glucagon output by depolarizing α cell membrane potential and decreasing action potential amplitude. We demonstrate, by using experimental and computational approaches, that this is not mediated by the KATP channel, but instead due to reduced operation of the Na+-K+ pump. These data suggest that counter-regulatory secretion of glucagon is driven by fatty acid metabolism, and that the Na+-K+ pump is an important ATP-dependent regulator of α cell function.

U2 - 10.1016/j.celrep.2018.05.035

DO - 10.1016/j.celrep.2018.05.035

M3 - Journal article

C2 - 29898400

VL - 23

SP - 3300

EP - 3311

JO - Cell Reports

JF - Cell Reports

SN - 2211-1247

IS - 11

ER -

ID: 220850730

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