Organ-specific metabolic pathways distinguish prediabetes, type 2 diabetes, and normal tissues

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Organ-specific metabolic pathways distinguish prediabetes, type 2 diabetes, and normal tissues. / Diamanti, Klev; Cavalli, Marco; Pereira, Maria J.; Pan, Gang; Castillejo-López, Casimiro; Kumar, Chanchal; Mundt, Filip; Komorowski, Jan; Deshmukh, Atul S.; Mann, Matthias; Korsgren, Olle; Eriksson, Jan W.; Wadelius, Claes.

In: Cell Reports Medicine, Vol. 3, No. 10, 100763, 2022.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Diamanti, K, Cavalli, M, Pereira, MJ, Pan, G, Castillejo-López, C, Kumar, C, Mundt, F, Komorowski, J, Deshmukh, AS, Mann, M, Korsgren, O, Eriksson, JW & Wadelius, C 2022, 'Organ-specific metabolic pathways distinguish prediabetes, type 2 diabetes, and normal tissues', Cell Reports Medicine, vol. 3, no. 10, 100763. https://doi.org/10.1016/j.xcrm.2022.100763

APA

Diamanti, K., Cavalli, M., Pereira, M. J., Pan, G., Castillejo-López, C., Kumar, C., Mundt, F., Komorowski, J., Deshmukh, A. S., Mann, M., Korsgren, O., Eriksson, J. W., & Wadelius, C. (2022). Organ-specific metabolic pathways distinguish prediabetes, type 2 diabetes, and normal tissues. Cell Reports Medicine, 3(10), [100763]. https://doi.org/10.1016/j.xcrm.2022.100763

Vancouver

Diamanti K, Cavalli M, Pereira MJ, Pan G, Castillejo-López C, Kumar C et al. Organ-specific metabolic pathways distinguish prediabetes, type 2 diabetes, and normal tissues. Cell Reports Medicine. 2022;3(10). 100763. https://doi.org/10.1016/j.xcrm.2022.100763

Author

Diamanti, Klev ; Cavalli, Marco ; Pereira, Maria J. ; Pan, Gang ; Castillejo-López, Casimiro ; Kumar, Chanchal ; Mundt, Filip ; Komorowski, Jan ; Deshmukh, Atul S. ; Mann, Matthias ; Korsgren, Olle ; Eriksson, Jan W. ; Wadelius, Claes. / Organ-specific metabolic pathways distinguish prediabetes, type 2 diabetes, and normal tissues. In: Cell Reports Medicine. 2022 ; Vol. 3, No. 10.

Bibtex

@article{124e464e03d3471f8f961ae0dedbab50,
title = "Organ-specific metabolic pathways distinguish prediabetes, type 2 diabetes, and normal tissues",
abstract = "Environmental and genetic factors cause defects in pancreatic islets driving type 2 diabetes (T2D) together with the progression of multi-tissue insulin resistance. Mass spectrometry proteomics on samples from five key metabolic tissues of a cross-sectional cohort of 43 multi-organ donors provides deep coverage of their proteomes. Enrichment analysis of Gene Ontology terms provides a tissue-specific map of altered biological processes across healthy, prediabetes (PD), and T2D subjects. We find widespread alterations in several relevant biological pathways, including increase in hemostasis in pancreatic islets of PD, increase in the complement cascade in liver and pancreatic islets of PD, and elevation in cholesterol biosynthesis in liver of T2D. Our findings point to inflammatory, immune, and vascular alterations in pancreatic islets in PD that are hypotheses to be tested for potential contributions to hormonal perturbations such as impaired insulin and increased glucagon production. This multi-tissue proteomic map suggests tissue-specific metabolic dysregulations in T2D.",
keywords = "liver, mass spectrometry, multi-tissue, pancreatic islets, prediabetes, proteomics, skeletal muscle, T2D, type 2 diabetes, visceral adipose tissue",
author = "Klev Diamanti and Marco Cavalli and Pereira, {Maria J.} and Gang Pan and Casimiro Castillejo-L{\'o}pez and Chanchal Kumar and Filip Mundt and Jan Komorowski and Deshmukh, {Atul S.} and Matthias Mann and Olle Korsgren and Eriksson, {Jan W.} and Claes Wadelius",
note = "Publisher Copyright: {\textcopyright} 2022 The Author(s)",
year = "2022",
doi = "10.1016/j.xcrm.2022.100763",
language = "English",
volume = "3",
journal = "Cell Reports Medicine",
issn = "2666-3791",
publisher = "Cell Press",
number = "10",

}

RIS

TY - JOUR

T1 - Organ-specific metabolic pathways distinguish prediabetes, type 2 diabetes, and normal tissues

AU - Diamanti, Klev

AU - Cavalli, Marco

AU - Pereira, Maria J.

AU - Pan, Gang

AU - Castillejo-López, Casimiro

AU - Kumar, Chanchal

AU - Mundt, Filip

AU - Komorowski, Jan

AU - Deshmukh, Atul S.

AU - Mann, Matthias

AU - Korsgren, Olle

AU - Eriksson, Jan W.

AU - Wadelius, Claes

N1 - Publisher Copyright: © 2022 The Author(s)

PY - 2022

Y1 - 2022

N2 - Environmental and genetic factors cause defects in pancreatic islets driving type 2 diabetes (T2D) together with the progression of multi-tissue insulin resistance. Mass spectrometry proteomics on samples from five key metabolic tissues of a cross-sectional cohort of 43 multi-organ donors provides deep coverage of their proteomes. Enrichment analysis of Gene Ontology terms provides a tissue-specific map of altered biological processes across healthy, prediabetes (PD), and T2D subjects. We find widespread alterations in several relevant biological pathways, including increase in hemostasis in pancreatic islets of PD, increase in the complement cascade in liver and pancreatic islets of PD, and elevation in cholesterol biosynthesis in liver of T2D. Our findings point to inflammatory, immune, and vascular alterations in pancreatic islets in PD that are hypotheses to be tested for potential contributions to hormonal perturbations such as impaired insulin and increased glucagon production. This multi-tissue proteomic map suggests tissue-specific metabolic dysregulations in T2D.

AB - Environmental and genetic factors cause defects in pancreatic islets driving type 2 diabetes (T2D) together with the progression of multi-tissue insulin resistance. Mass spectrometry proteomics on samples from five key metabolic tissues of a cross-sectional cohort of 43 multi-organ donors provides deep coverage of their proteomes. Enrichment analysis of Gene Ontology terms provides a tissue-specific map of altered biological processes across healthy, prediabetes (PD), and T2D subjects. We find widespread alterations in several relevant biological pathways, including increase in hemostasis in pancreatic islets of PD, increase in the complement cascade in liver and pancreatic islets of PD, and elevation in cholesterol biosynthesis in liver of T2D. Our findings point to inflammatory, immune, and vascular alterations in pancreatic islets in PD that are hypotheses to be tested for potential contributions to hormonal perturbations such as impaired insulin and increased glucagon production. This multi-tissue proteomic map suggests tissue-specific metabolic dysregulations in T2D.

KW - liver

KW - mass spectrometry

KW - multi-tissue

KW - pancreatic islets

KW - prediabetes

KW - proteomics

KW - skeletal muscle

KW - T2D

KW - type 2 diabetes

KW - visceral adipose tissue

U2 - 10.1016/j.xcrm.2022.100763

DO - 10.1016/j.xcrm.2022.100763

M3 - Journal article

C2 - 36198307

AN - SCOPUS:85140051320

VL - 3

JO - Cell Reports Medicine

JF - Cell Reports Medicine

SN - 2666-3791

IS - 10

M1 - 100763

ER -

ID: 324172333