GSE202295: Distinctive exercise-induced inflammatory response and exerkine induction in skeletal muscle of people with type 2 diabetes

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Vastus Lateralis
GSM6107907 GSM6107918 GSM6107921 GSM6107927 GSM6107933 GSM6107939 GSM6107945 GSM6107951 GSM6107957 GSM6107963 GSM6107969 GSM6107975 GSM6107981 GSM6107987 GSM6107993 GSM6107998 GSM6108001 GSM6108007 GSM6108010 GSM6108015
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GSM6107910 GSM6107915 GSM6107924 GSM6107930 GSM6107936 GSM6107942 GSM6107948 GSM6107954 GSM6107960 GSM6107966 GSM6107972 GSM6107978 GSM6107984 GSM6107990 GSM6108004 GSM6108012
GSM6107909 GSM6107914 GSM6107923 GSM6107929 GSM6107935 GSM6107941 GSM6107947 GSM6107953 GSM6107959 GSM6107965 GSM6107971 GSM6107977 GSM6107983 GSM6107989 GSM6107995 GSM6108003 GSM6108011
GSM6107906 GSM6107912 GSM6107917 GSM6107920 GSM6107926 GSM6107932 GSM6107938 GSM6107944 GSM6107950 GSM6107956 GSM6107962 GSM6107968 GSM6107974 GSM6107980 GSM6107986 GSM6107992 GSM6107997 GSM6108000 GSM6108006 GSM6108009 GSM6108014
GSM6107908 GSM6107913 GSM6107919 GSM6107922 GSM6107928 GSM6107934 GSM6107940 GSM6107946 GSM6107952 GSM6107958 GSM6107964 GSM6107970 GSM6107976 GSM6107982 GSM6107988 GSM6107994 GSM6107999 GSM6108002 GSM6108008 GSM6108016
Description

Submission Date: May 05, 2022

Summary: Mechanistic insights into the molecular events by which exercise enhances the skeletal muscle phenotype are lacking, particularly in the context of type 2 diabetes. Here we unravel a fundamental role for exercise-responsive cytokines (exerkines) on skeletal muscle development and growth in individuals with normal glucose tolerance or type 2 diabetes. Acute exercise triggered an inflammatory response in skeletal muscle, concomitant with an infiltration of immune cells. These exercise effects were potentiated in type 2 diabetes. In response to contraction or hypoxia, cytokines were mainly produced by endothelial cells and macrophages. The chemokine CXCL12 was induced by hypoxia in endothelial cells, as well as by conditioned medium from contracted myotubes in macrophages. We found that CXCL12 was associated with skeletal muscle remodeling after exercise and differentiation of cultured muscle. Collectively, acute aerobic exercise mounts a non-canonical inflammatory response, with an atypical production of exerkines, which is potentiated in type 2 diabetes.

GEO Accession ID: GSE202295

PMID: 36070371

Description

Submission Date: May 05, 2022

Summary: Mechanistic insights into the molecular events by which exercise enhances the skeletal muscle phenotype are lacking, particularly in the context of type 2 diabetes. Here we unravel a fundamental role for exercise-responsive cytokines (exerkines) on skeletal muscle development and growth in individuals with normal glucose tolerance or type 2 diabetes. Acute exercise triggered an inflammatory response in skeletal muscle, concomitant with an infiltration of immune cells. These exercise effects were potentiated in type 2 diabetes. In response to contraction or hypoxia, cytokines were mainly produced by endothelial cells and macrophages. The chemokine CXCL12 was induced by hypoxia in endothelial cells, as well as by conditioned medium from contracted myotubes in macrophages. We found that CXCL12 was associated with skeletal muscle remodeling after exercise and differentiation of cultured muscle. Collectively, acute aerobic exercise mounts a non-canonical inflammatory response, with an atypical production of exerkines, which is potentiated in type 2 diabetes.

GEO Accession ID: GSE202295

PMID: 36070371

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