Proteomics Analysis of Skeletal Muscle from Leptin-Deficient ob/ob Mice Reveals Adaptive Remodeling of Metabolic Characteristics and Fiber Type Composition

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Proteomics Analysis of Skeletal Muscle from Leptin-Deficient ob/ob Mice Reveals Adaptive Remodeling of Metabolic Characteristics and Fiber Type Composition. / Schönke, Milena; Björnholm, Marie; Chibalin, Alexander V.; Zierath, Juleen R.; Deshmukh, Atul S.

In: Proteomics, Vol. 18, No. 5-6, 2018, p. 1-11.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Schönke, M, Björnholm, M, Chibalin, AV, Zierath, JR & Deshmukh, AS 2018, 'Proteomics Analysis of Skeletal Muscle from Leptin-Deficient ob/ob Mice Reveals Adaptive Remodeling of Metabolic Characteristics and Fiber Type Composition', Proteomics, vol. 18, no. 5-6, pp. 1-11. https://doi.org/10.1002/pmic.201700375

APA

Schönke, M., Björnholm, M., Chibalin, A. V., Zierath, J. R., & Deshmukh, A. S. (2018). Proteomics Analysis of Skeletal Muscle from Leptin-Deficient ob/ob Mice Reveals Adaptive Remodeling of Metabolic Characteristics and Fiber Type Composition. Proteomics, 18(5-6), 1-11. https://doi.org/10.1002/pmic.201700375

Vancouver

Schönke M, Björnholm M, Chibalin AV, Zierath JR, Deshmukh AS. Proteomics Analysis of Skeletal Muscle from Leptin-Deficient ob/ob Mice Reveals Adaptive Remodeling of Metabolic Characteristics and Fiber Type Composition. Proteomics. 2018;18(5-6):1-11. https://doi.org/10.1002/pmic.201700375

Author

Schönke, Milena ; Björnholm, Marie ; Chibalin, Alexander V. ; Zierath, Juleen R. ; Deshmukh, Atul S. / Proteomics Analysis of Skeletal Muscle from Leptin-Deficient ob/ob Mice Reveals Adaptive Remodeling of Metabolic Characteristics and Fiber Type Composition. In: Proteomics. 2018 ; Vol. 18, No. 5-6. pp. 1-11.

Bibtex

@article{1a43ddba0ec94306b555ac2167caa0f2,
title = "Proteomics Analysis of Skeletal Muscle from Leptin-Deficient ob/ob Mice Reveals Adaptive Remodeling of Metabolic Characteristics and Fiber Type Composition",
abstract = "Skeletal muscle insulin resistance, an early metabolic defect in the pathogenesis of type 2 diabetes (T2D), may be a cause or consequence of altered protein expression profiles. Proteomics technology offers enormous promise to investigate molecular mechanisms underlying pathologies, however, the analysis of skeletal muscle is challenging. Using state-of-the-art multienzyme digestion and filter-aided sample preparation (MED-FASP) and a mass spectrometry (MS)-based workflow, we performed a global proteomics analysis of skeletal muscle from leptin-deficient, obese, insulin resistant (ob/ob) and lean mice in mere two fractions in a short time (8 h per sample). We identified more than 6000 proteins with 118 proteins differentially regulated in obesity. This included protein kinases, phosphatases, and secreted and fiber type associated proteins. Enzymes involved in lipid metabolism in skeletal muscle from ob/ob mice were increased, providing evidence against reduced fatty acid oxidation in lipid-induced insulin resistance. Mitochondrial and peroxisomal proteins, as well as components of pyruvate and lactate metabolism, were increased. Finally, the skeletal muscle proteome from ob/ob mice displayed a shift toward the {"}slow fiber type.{"} This detailed characterization of an obese rodent model of T2D demonstrates an efficient workflow for skeletal muscle proteomics, which may easily be adapted to other complex tissues.",
author = "Milena Sch{\"o}nke and Marie Bj{\"o}rnholm and Chibalin, {Alexander V.} and Zierath, {Juleen R.} and Deshmukh, {Atul S.}",
note = "Special Issue: Reviews 2018 ‐ Part I",
year = "2018",
doi = "10.1002/pmic.201700375",
language = "English",
volume = "18",
pages = "1--11",
journal = "Proteomics",
issn = "1615-9853",
publisher = "Wiley - V C H Verlag GmbH & Co. KGaA",
number = "5-6",

}

RIS

TY - JOUR

T1 - Proteomics Analysis of Skeletal Muscle from Leptin-Deficient ob/ob Mice Reveals Adaptive Remodeling of Metabolic Characteristics and Fiber Type Composition

AU - Schönke, Milena

AU - Björnholm, Marie

AU - Chibalin, Alexander V.

AU - Zierath, Juleen R.

AU - Deshmukh, Atul S.

N1 - Special Issue: Reviews 2018 ‐ Part I

PY - 2018

Y1 - 2018

N2 - Skeletal muscle insulin resistance, an early metabolic defect in the pathogenesis of type 2 diabetes (T2D), may be a cause or consequence of altered protein expression profiles. Proteomics technology offers enormous promise to investigate molecular mechanisms underlying pathologies, however, the analysis of skeletal muscle is challenging. Using state-of-the-art multienzyme digestion and filter-aided sample preparation (MED-FASP) and a mass spectrometry (MS)-based workflow, we performed a global proteomics analysis of skeletal muscle from leptin-deficient, obese, insulin resistant (ob/ob) and lean mice in mere two fractions in a short time (8 h per sample). We identified more than 6000 proteins with 118 proteins differentially regulated in obesity. This included protein kinases, phosphatases, and secreted and fiber type associated proteins. Enzymes involved in lipid metabolism in skeletal muscle from ob/ob mice were increased, providing evidence against reduced fatty acid oxidation in lipid-induced insulin resistance. Mitochondrial and peroxisomal proteins, as well as components of pyruvate and lactate metabolism, were increased. Finally, the skeletal muscle proteome from ob/ob mice displayed a shift toward the "slow fiber type." This detailed characterization of an obese rodent model of T2D demonstrates an efficient workflow for skeletal muscle proteomics, which may easily be adapted to other complex tissues.

AB - Skeletal muscle insulin resistance, an early metabolic defect in the pathogenesis of type 2 diabetes (T2D), may be a cause or consequence of altered protein expression profiles. Proteomics technology offers enormous promise to investigate molecular mechanisms underlying pathologies, however, the analysis of skeletal muscle is challenging. Using state-of-the-art multienzyme digestion and filter-aided sample preparation (MED-FASP) and a mass spectrometry (MS)-based workflow, we performed a global proteomics analysis of skeletal muscle from leptin-deficient, obese, insulin resistant (ob/ob) and lean mice in mere two fractions in a short time (8 h per sample). We identified more than 6000 proteins with 118 proteins differentially regulated in obesity. This included protein kinases, phosphatases, and secreted and fiber type associated proteins. Enzymes involved in lipid metabolism in skeletal muscle from ob/ob mice were increased, providing evidence against reduced fatty acid oxidation in lipid-induced insulin resistance. Mitochondrial and peroxisomal proteins, as well as components of pyruvate and lactate metabolism, were increased. Finally, the skeletal muscle proteome from ob/ob mice displayed a shift toward the "slow fiber type." This detailed characterization of an obese rodent model of T2D demonstrates an efficient workflow for skeletal muscle proteomics, which may easily be adapted to other complex tissues.

U2 - 10.1002/pmic.201700375

DO - 10.1002/pmic.201700375

M3 - Journal article

VL - 18

SP - 1

EP - 11

JO - Proteomics

JF - Proteomics

SN - 1615-9853

IS - 5-6

ER -

ID: 191300727