p38 MAPK in Glucose Metabolism of Skeletal Muscle: Beneficial or Harmful?

Skeletal muscles respond to environmental and physiological changes by varying their size, fiber type, and metabolic properties. P38 mitogen-activated protein kinase (MAPK) is one of several signaling pathways that drive the metabolic adaptation of skeletal muscle to exercise. p38 MAPK also particip...

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Published inInternational journal of molecular sciences Vol. 21; no. 18; p. 6480
Main Authors Bengal, Eyal, Aviram, Sharon, Hayek, Tony
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 04.09.2020
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Abstract Skeletal muscles respond to environmental and physiological changes by varying their size, fiber type, and metabolic properties. P38 mitogen-activated protein kinase (MAPK) is one of several signaling pathways that drive the metabolic adaptation of skeletal muscle to exercise. p38 MAPK also participates in the development of pathological traits resulting from excessive caloric intake and obesity that cause metabolic syndrome and type 2 diabetes (T2D). Whereas p38 MAPK increases insulin-independent glucose uptake and oxidative metabolism in muscles during exercise, it contrastingly mediates insulin resistance and glucose intolerance during metabolic syndrome development. This article provides an overview of the apparent contradicting roles of p38 MAPK in the adaptation of skeletal muscles to exercise and to pathological conditions leading to glucose intolerance and T2D. Here, we focus on the involvement of p38 MAPK in glucose metabolism of skeletal muscle, and discuss the possibility of targeting this pathway to prevent the development of T2D.
AbstractList Skeletal muscles respond to environmental and physiological changes by varying their size, fiber type, and metabolic properties. P38 mitogen-activated protein kinase (MAPK) is one of several signaling pathways that drive the metabolic adaptation of skeletal muscle to exercise. p38 MAPK also participates in the development of pathological traits resulting from excessive caloric intake and obesity that cause metabolic syndrome and type 2 diabetes (T2D). Whereas p38 MAPK increases insulin-independent glucose uptake and oxidative metabolism in muscles during exercise, it contrastingly mediates insulin resistance and glucose intolerance during metabolic syndrome development. This article provides an overview of the apparent contradicting roles of p38 MAPK in the adaptation of skeletal muscles to exercise and to pathological conditions leading to glucose intolerance and T2D. Here, we focus on the involvement of p38 MAPK in glucose metabolism of skeletal muscle, and discuss the possibility of targeting this pathway to prevent the development of T2D.
Author Bengal, Eyal
Hayek, Tony
Aviram, Sharon
AuthorAffiliation 1 Department of Biochemistry, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, P.O. Box 9649, Haifa 31096, Israel; avirams@technion.ac.il
2 Department of Internal Medicine E, Rambam Medical Center, Haifa 31096, Israel; t_hayek@rambam.health.gov.il
AuthorAffiliation_xml – name: 2 Department of Internal Medicine E, Rambam Medical Center, Haifa 31096, Israel; t_hayek@rambam.health.gov.il
– name: 1 Department of Biochemistry, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, P.O. Box 9649, Haifa 31096, Israel; avirams@technion.ac.il
Author_xml – sequence: 1
  givenname: Eyal
  surname: Bengal
  fullname: Bengal, Eyal
  organization: Department of Biochemistry, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, P.O. Box 9649, Haifa 31096, Israel
– sequence: 2
  givenname: Sharon
  surname: Aviram
  fullname: Aviram, Sharon
  organization: Department of Biochemistry, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, P.O. Box 9649, Haifa 31096, Israel
– sequence: 3
  givenname: Tony
  surname: Hayek
  fullname: Hayek, Tony
  organization: Department of Internal Medicine E, Rambam Medical Center, Haifa 31096, Israel
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32899870$$D View this record in MEDLINE/PubMed
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Issue 18
Keywords exercise
type 2 diabetes
skeletal muscle
signal transduction
p38 MAPK
energy metabolism
Language English
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Snippet Skeletal muscles respond to environmental and physiological changes by varying their size, fiber type, and metabolic properties. P38 mitogen-activated protein...
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SubjectTerms Adaptation
Animals
Biological Transport
Carbohydrate Metabolism
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2 - metabolism
Energy
energy metabolism
Enzymes
Exercise
Gene expression
Glucose
Glucose - metabolism
Glucose Intolerance - metabolism
Glucose tolerance
Homeostasis
Humans
Insulin
Insulin - metabolism
Insulin resistance
Insulin Resistance - physiology
Intolerance
Kinases
Lipids
Liver
MAP kinase
Metabolic disorders
Metabolic syndrome
Metabolism
Mitochondria
Muscle contraction
Muscle, Skeletal - metabolism
Muscles
Musculoskeletal system
Obesity
Obesity - metabolism
Oxidation resistance
Oxidative metabolism
p38 MAPK
p38 Mitogen-Activated Protein Kinases - metabolism
p38 Mitogen-Activated Protein Kinases - physiology
Phosphorylation
Physical fitness
Protein kinase
Proteins
Review
signal transduction
Signal Transduction - physiology
Skeletal muscle
Transcription factors
type 2 diabetes
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Title p38 MAPK in Glucose Metabolism of Skeletal Muscle: Beneficial or Harmful?
URI https://www.ncbi.nlm.nih.gov/pubmed/32899870
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https://search.proquest.com/docview/2441278201
https://pubmed.ncbi.nlm.nih.gov/PMC7555282
https://doaj.org/article/d858107768ee43a5a9fb2ddd7bdc76dd
Volume 21
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