Anti-diabetic effects of GLP1 analogs are mediated by thermogenic interleukin-6 signaling in adipocytes
Cell Reports Medicine, ISSN: 2666-3791, Vol: 3, Issue: 11, Page: 100813
2022
- 18Citations
- 32Captures
- 2Mentions
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Metrics Details
- Citations18
- Citation Indexes18
- 18
- CrossRef11
- Captures32
- Readers32
- 32
- Mentions2
- News Mentions2
- News2
Most Recent News
University of Texas Health Science Center Houston Details Findings in Interleukin-6 (Anti-diabetic Effects of Glp1 Analogs Are Mediated By Thermogenic Interleukin-6 Signaling In Adipocytes)
2023 JAN 20 (NewsRx) -- By a News Reporter-Staff News Editor at NewsRx Diabetes Daily -- Data detailed on Intercellular Signaling Peptides and Proteins -
Article Description
Mechanisms underlying anti-diabetic effects of GLP1 analogs remain incompletely understood. We observed that in prediabetic humans exenatide treatment acutely induces interleukin-6 (IL-6) secretion by monocytes and IL-6 in systemic circulation. We hypothesized that GLP1 analogs signal through IL-6 in adipose tissue (AT) and used the mouse model to test if IL-6 receptor (IL-6R) signaling underlies the effects of the GLP1-IL-6 axis. We show that liraglutide transiently increases IL-6 in mouse circulation and IL-6R signaling in AT. Metronomic liraglutide treatment resulted in AT browning and thermogenesis linked with STAT3 activation. IL-6-blocking antibody treatment inhibited STAT3 activation in AT and suppressed liraglutide-induced increase in thermogenesis and glucose utilization. We show that adipose IL-6R knockout mice still display liraglutide-induced weight loss but lack thermogenic adipocyte browning and metabolism activation. We conclude that the anti-diabetic effects of GLP1 analogs are mediated by transient upregulation of IL-6, which activates canonical IL-6R signaling and thermogenesis.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S266637912200372X; http://dx.doi.org/10.1016/j.xcrm.2022.100813; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85142205832&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/36384099; https://linkinghub.elsevier.com/retrieve/pii/S266637912200372X; https://dx.doi.org/10.1016/j.xcrm.2022.100813
Elsevier BV
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