Pancreatic β-cells respond to fuel pressure with an early metabolic switch
Pancreatic β-cells become irreversibly damaged by long-term exposure to excessive glucose concentrations and lose their ability to carry out glucose stimulated insulin secretion (GSIS) upon damage. The β-cells are not able to control glucose uptake and they are therefore left vulnerable for endogeno...
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Published in | Scientific reports Vol. 10; no. 1; p. 15413 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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22.09.2020
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Abstract | Pancreatic β-cells become irreversibly damaged by long-term exposure to excessive glucose concentrations and lose their ability to carry out glucose stimulated insulin secretion (GSIS) upon damage. The β-cells are not able to control glucose uptake and they are therefore left vulnerable for endogenous toxicity from metabolites produced in excess amounts upon increased glucose availability. In order to handle excess fuel, the β-cells possess specific metabolic pathways, but little is known about these pathways. We present a study of β-cell metabolism under increased fuel pressure using a stable isotope resolved NMR approach to investigate early metabolic events leading up to β-cell dysfunction. The approach is based on a recently described combination of
13
C metabolomics combined with signal enhanced NMR via dissolution dynamic nuclear polarization (dDNP). Glucose-responsive INS-1 β-cells were incubated with increasing concentrations of [U-
13
C] glucose under conditions where GSIS was not affected (2–8 h). We find that pyruvate and DHAP were the metabolites that responded most strongly to increasing fuel pressure. The two major divergence pathways for fuel excess, the glycerolipid/fatty acid metabolism and the polyol pathway, were found not only to operate at unchanged rate but also with similar quantity. |
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AbstractList | Pancreatic β-cells become irreversibly damaged by long-term exposure to excessive glucose concentrations and lose their ability to carry out glucose stimulated insulin secretion (GSIS) upon damage. The β-cells are not able to control glucose uptake and they are therefore left vulnerable for endogenous toxicity from metabolites produced in excess amounts upon increased glucose availability. In order to handle excess fuel, the β-cells possess specific metabolic pathways, but little is known about these pathways. We present a study of β-cell metabolism under increased fuel pressure using a stable isotope resolved NMR approach to investigate early metabolic events leading up to β-cell dysfunction. The approach is based on a recently described combination of
C metabolomics combined with signal enhanced NMR via dissolution dynamic nuclear polarization (dDNP). Glucose-responsive INS-1 β-cells were incubated with increasing concentrations of [U-
C] glucose under conditions where GSIS was not affected (2-8 h). We find that pyruvate and DHAP were the metabolites that responded most strongly to increasing fuel pressure. The two major divergence pathways for fuel excess, the glycerolipid/fatty acid metabolism and the polyol pathway, were found not only to operate at unchanged rate but also with similar quantity. Pancreatic β-cells become irreversibly damaged by long-term exposure to excessive glucose concentrations and lose their ability to carry out glucose stimulated insulin secretion (GSIS) upon damage. The β-cells are not able to control glucose uptake and they are therefore left vulnerable for endogenous toxicity from metabolites produced in excess amounts upon increased glucose availability. In order to handle excess fuel, the β-cells possess specific metabolic pathways, but little is known about these pathways. We present a study of β-cell metabolism under increased fuel pressure using a stable isotope resolved NMR approach to investigate early metabolic events leading up to β-cell dysfunction. The approach is based on a recently described combination of 13 C metabolomics combined with signal enhanced NMR via dissolution dynamic nuclear polarization (dDNP). Glucose-responsive INS-1 β-cells were incubated with increasing concentrations of [U- 13 C] glucose under conditions where GSIS was not affected (2–8 h). We find that pyruvate and DHAP were the metabolites that responded most strongly to increasing fuel pressure. The two major divergence pathways for fuel excess, the glycerolipid/fatty acid metabolism and the polyol pathway, were found not only to operate at unchanged rate but also with similar quantity. Abstract Pancreatic β-cells become irreversibly damaged by long-term exposure to excessive glucose concentrations and lose their ability to carry out glucose stimulated insulin secretion (GSIS) upon damage. The β-cells are not able to control glucose uptake and they are therefore left vulnerable for endogenous toxicity from metabolites produced in excess amounts upon increased glucose availability. In order to handle excess fuel, the β-cells possess specific metabolic pathways, but little is known about these pathways. We present a study of β-cell metabolism under increased fuel pressure using a stable isotope resolved NMR approach to investigate early metabolic events leading up to β-cell dysfunction. The approach is based on a recently described combination of 13 C metabolomics combined with signal enhanced NMR via dissolution dynamic nuclear polarization (dDNP). Glucose-responsive INS-1 β-cells were incubated with increasing concentrations of [U- 13 C] glucose under conditions where GSIS was not affected (2–8 h). We find that pyruvate and DHAP were the metabolites that responded most strongly to increasing fuel pressure. The two major divergence pathways for fuel excess, the glycerolipid/fatty acid metabolism and the polyol pathway, were found not only to operate at unchanged rate but also with similar quantity. |
ArticleNumber | 15413 |
Author | Mandrup-Poulsen, Thomas Jensen, Pernille R. Ghiasi, Seyed M. Malinowski, Ronja M. Ardenkjær-Larsen, Jan H. Meier, Sebastian Lerche, Mathilde H. |
Author_xml | – sequence: 1 givenname: Ronja M. surname: Malinowski fullname: Malinowski, Ronja M. organization: Department of Health Technology, Technical University of Denmark – sequence: 2 givenname: Seyed M. surname: Ghiasi fullname: Ghiasi, Seyed M. organization: Department of Biomedical Sciences, University of Copenhagen, Department of Metabolism, Digestion and Reproduction, Imperial College London – sequence: 3 givenname: Thomas surname: Mandrup-Poulsen fullname: Mandrup-Poulsen, Thomas organization: Department of Biomedical Sciences, University of Copenhagen – sequence: 4 givenname: Sebastian surname: Meier fullname: Meier, Sebastian organization: Department of Chemistry, Technical University of Denmark – sequence: 5 givenname: Mathilde H. surname: Lerche fullname: Lerche, Mathilde H. organization: Department of Health Technology, Technical University of Denmark – sequence: 6 givenname: Jan H. surname: Ardenkjær-Larsen fullname: Ardenkjær-Larsen, Jan H. organization: Department of Health Technology, Technical University of Denmark – sequence: 7 givenname: Pernille R. surname: Jensen fullname: Jensen, Pernille R. email: peroje@dtu.dk organization: Department of Health Technology, Technical University of Denmark |
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CitedBy_id | crossref_primary_10_1016_j_jbc_2022_101729 crossref_primary_10_1016_j_celrep_2024_114047 crossref_primary_10_3389_fnetp_2021_802881 crossref_primary_10_3390_nu15224791 |
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Snippet | Pancreatic β-cells become irreversibly damaged by long-term exposure to excessive glucose concentrations and lose their ability to carry out glucose stimulated... Abstract Pancreatic β-cells become irreversibly damaged by long-term exposure to excessive glucose concentrations and lose their ability to carry out glucose... |
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Title | Pancreatic β-cells respond to fuel pressure with an early metabolic switch |
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