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Glucose metabolism is altered after loss of L cells and α-cells but not influenced by loss of K cells

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Standard

Glucose metabolism is altered after loss of L cells and α-cells but not influenced by loss of K cells. / Pedersen, J; Ugleholdt, Randi Kjærsgaard; Jørgensen, Signe Marie; Windeløv, Johanne Agerlin; Grunddal, Kaare Villum; Schwartz, T W; Füchtbauer, Ernst-Martin; Poulsen, S S; Holst, P J; Holst, J J.

I: American Journal of Physiology: Endocrinology and Metabolism, Bind 304, Nr. 1, 01.01.2013, s. E60-E73.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Harvard

Pedersen, J, Ugleholdt, RK, Jørgensen, SM, Windeløv, JA, Grunddal, KV, Schwartz, TW, Füchtbauer, E-M, Poulsen, SS, Holst, PJ & Holst, JJ 2013, 'Glucose metabolism is altered after loss of L cells and α-cells but not influenced by loss of K cells', American Journal of Physiology: Endocrinology and Metabolism, bind 304, nr. 1, s. E60-E73. https://doi.org/10.1152/ajpendo.00547.2011

APA

Pedersen, J., Ugleholdt, R. K., Jørgensen, S. M., Windeløv, J. A., Grunddal, K. V., Schwartz, T. W., ... Holst, J. J. (2013). Glucose metabolism is altered after loss of L cells and α-cells but not influenced by loss of K cells. American Journal of Physiology: Endocrinology and Metabolism, 304(1), E60-E73. https://doi.org/10.1152/ajpendo.00547.2011

CBE

Pedersen J, Ugleholdt RK, Jørgensen SM, Windeløv JA, Grunddal KV, Schwartz TW, Füchtbauer E-M, Poulsen SS, Holst PJ, Holst JJ. 2013. Glucose metabolism is altered after loss of L cells and α-cells but not influenced by loss of K cells. American Journal of Physiology: Endocrinology and Metabolism. 304(1):E60-E73. https://doi.org/10.1152/ajpendo.00547.2011

MLA

Pedersen, J o.a.. "Glucose metabolism is altered after loss of L cells and α-cells but not influenced by loss of K cells". American Journal of Physiology: Endocrinology and Metabolism. 2013, 304(1). E60-E73. https://doi.org/10.1152/ajpendo.00547.2011

Vancouver

Pedersen J, Ugleholdt RK, Jørgensen SM, Windeløv JA, Grunddal KV, Schwartz TW o.a. Glucose metabolism is altered after loss of L cells and α-cells but not influenced by loss of K cells. American Journal of Physiology: Endocrinology and Metabolism. 2013 jan 1;304(1):E60-E73. https://doi.org/10.1152/ajpendo.00547.2011

Author

Pedersen, J ; Ugleholdt, Randi Kjærsgaard ; Jørgensen, Signe Marie ; Windeløv, Johanne Agerlin ; Grunddal, Kaare Villum ; Schwartz, T W ; Füchtbauer, Ernst-Martin ; Poulsen, S S ; Holst, P J ; Holst, J J. / Glucose metabolism is altered after loss of L cells and α-cells but not influenced by loss of K cells. I: American Journal of Physiology: Endocrinology and Metabolism. 2013 ; Bind 304, Nr. 1. s. E60-E73.

Bibtex

@article{52b36c51c9154c629d7be63988b288eb,
title = "Glucose metabolism is altered after loss of L cells and α-cells but not influenced by loss of K cells",
abstract = "The enteroendocrine K and L cells are responsible for secretion of glucose-dependent insulinotropic polypeptide (GIP) and glucagon like-peptide 1 (GLP-1), whereas pancreatic α-cells are responsible for secretion of glucagon. In rodents and humans, dysregulation of the secretion of GIP, GLP-1, and glucagon is associated with impaired regulation of metabolism. This study evaluates the consequences of acute removal of Gip- or Gcg-expressing cells on glucose metabolism. Generation of the two diphtheria toxin receptor cellular knockout mice, TgN(GIP.DTR) and TgN(GCG.DTR), allowed us to study effects of acute ablation of K and L cells and α-cells. Diphtheria toxin administration reduced the expression of Gip and content of GIP in the proximal jejunum in TgN(GIP.DTR) and expression of Gcg and content of proglucagon-derived peptides in both proximal jejunum and terminal ileum as well as content of glucagon in pancreas in TgN(GCG.DTR) compared with wild-type mice. GIP response to oral glucose was attenuated following K cell loss, but oral and intraperitoneal glucose tolerances were unaffected. Intraperitoneal glucose tolerance was impaired following combined L cell and α-cell loss and normal following α-cell loss. Oral glucose tolerance was improved following L cell and α-cell loss and supernormal following α-cell loss. We present two mouse models that allow studies of the effects of K cell or L cell and α-cell loss as well as isolated α-cell loss. Our findings show that intraperitoneal glucose tolerance is dependent on an intact L cell mass and underscore the diabetogenic effects of α-cell signaling. Furthermore, the results suggest that K cells are less involved in acute regulation of mouse glucose metabolism than L cells and α-cells.",
keywords = "Animals, Apoptosis, Diphtheria Toxin, Enteroendocrine Cells, Female, Gastric Inhibitory Polypeptide, Gene Knockdown Techniques, Genes, Transgenic, Suicide, Glucagon-Secreting Cells, Glucose, Male, Mice, Mice, Inbred C57BL, Mice, Inbred DBA, Mice, Transgenic, Organ Specificity",
author = "J Pedersen and Ugleholdt, {Randi Kj{\ae}rsgaard} and J{\o}rgensen, {Signe Marie} and Windel{\o}v, {Johanne Agerlin} and Grunddal, {Kaare Villum} and Schwartz, {T W} and Ernst-Martin F{\"u}chtbauer and Poulsen, {S S} and Holst, {P J} and Holst, {J J}",
year = "2013",
month = "1",
day = "1",
doi = "10.1152/ajpendo.00547.2011",
language = "English",
volume = "304",
pages = "E60--E73",
journal = "American Journal of Physiology: Endocrinology and Metabolism",
issn = "0193-1849",
publisher = "American Physiological Society",
number = "1",

}

RIS

TY - JOUR

T1 - Glucose metabolism is altered after loss of L cells and α-cells but not influenced by loss of K cells

AU - Pedersen, J

AU - Ugleholdt, Randi Kjærsgaard

AU - Jørgensen, Signe Marie

AU - Windeløv, Johanne Agerlin

AU - Grunddal, Kaare Villum

AU - Schwartz, T W

AU - Füchtbauer, Ernst-Martin

AU - Poulsen, S S

AU - Holst, P J

AU - Holst, J J

PY - 2013/1/1

Y1 - 2013/1/1

N2 - The enteroendocrine K and L cells are responsible for secretion of glucose-dependent insulinotropic polypeptide (GIP) and glucagon like-peptide 1 (GLP-1), whereas pancreatic α-cells are responsible for secretion of glucagon. In rodents and humans, dysregulation of the secretion of GIP, GLP-1, and glucagon is associated with impaired regulation of metabolism. This study evaluates the consequences of acute removal of Gip- or Gcg-expressing cells on glucose metabolism. Generation of the two diphtheria toxin receptor cellular knockout mice, TgN(GIP.DTR) and TgN(GCG.DTR), allowed us to study effects of acute ablation of K and L cells and α-cells. Diphtheria toxin administration reduced the expression of Gip and content of GIP in the proximal jejunum in TgN(GIP.DTR) and expression of Gcg and content of proglucagon-derived peptides in both proximal jejunum and terminal ileum as well as content of glucagon in pancreas in TgN(GCG.DTR) compared with wild-type mice. GIP response to oral glucose was attenuated following K cell loss, but oral and intraperitoneal glucose tolerances were unaffected. Intraperitoneal glucose tolerance was impaired following combined L cell and α-cell loss and normal following α-cell loss. Oral glucose tolerance was improved following L cell and α-cell loss and supernormal following α-cell loss. We present two mouse models that allow studies of the effects of K cell or L cell and α-cell loss as well as isolated α-cell loss. Our findings show that intraperitoneal glucose tolerance is dependent on an intact L cell mass and underscore the diabetogenic effects of α-cell signaling. Furthermore, the results suggest that K cells are less involved in acute regulation of mouse glucose metabolism than L cells and α-cells.

AB - The enteroendocrine K and L cells are responsible for secretion of glucose-dependent insulinotropic polypeptide (GIP) and glucagon like-peptide 1 (GLP-1), whereas pancreatic α-cells are responsible for secretion of glucagon. In rodents and humans, dysregulation of the secretion of GIP, GLP-1, and glucagon is associated with impaired regulation of metabolism. This study evaluates the consequences of acute removal of Gip- or Gcg-expressing cells on glucose metabolism. Generation of the two diphtheria toxin receptor cellular knockout mice, TgN(GIP.DTR) and TgN(GCG.DTR), allowed us to study effects of acute ablation of K and L cells and α-cells. Diphtheria toxin administration reduced the expression of Gip and content of GIP in the proximal jejunum in TgN(GIP.DTR) and expression of Gcg and content of proglucagon-derived peptides in both proximal jejunum and terminal ileum as well as content of glucagon in pancreas in TgN(GCG.DTR) compared with wild-type mice. GIP response to oral glucose was attenuated following K cell loss, but oral and intraperitoneal glucose tolerances were unaffected. Intraperitoneal glucose tolerance was impaired following combined L cell and α-cell loss and normal following α-cell loss. Oral glucose tolerance was improved following L cell and α-cell loss and supernormal following α-cell loss. We present two mouse models that allow studies of the effects of K cell or L cell and α-cell loss as well as isolated α-cell loss. Our findings show that intraperitoneal glucose tolerance is dependent on an intact L cell mass and underscore the diabetogenic effects of α-cell signaling. Furthermore, the results suggest that K cells are less involved in acute regulation of mouse glucose metabolism than L cells and α-cells.

KW - Animals

KW - Apoptosis

KW - Diphtheria Toxin

KW - Enteroendocrine Cells

KW - Female

KW - Gastric Inhibitory Polypeptide

KW - Gene Knockdown Techniques

KW - Genes, Transgenic, Suicide

KW - Glucagon-Secreting Cells

KW - Glucose

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Inbred DBA

KW - Mice, Transgenic

KW - Organ Specificity

U2 - 10.1152/ajpendo.00547.2011

DO - 10.1152/ajpendo.00547.2011

M3 - Journal article

C2 - 23115082

VL - 304

SP - E60-E73

JO - American Journal of Physiology: Endocrinology and Metabolism

JF - American Journal of Physiology: Endocrinology and Metabolism

SN - 0193-1849

IS - 1

ER -