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Immunometabolism of AMPK in insulin resistance and atherosclerosis.
Mol Cell Endocrinol. 2013 Feb 25; 366(2):224-34.MC

Abstract

Obesity leads to insulin resistance and atherosclerosis, which precede Type 2 diabetes and cardiovascular disease. Immunometabolism addresses how metabolic and inflammatory pathways converge to maintain health and a contemporary problem is determining how obesity-induced inflammation precipitates chronic diseases such as insulin resistance and atherosclerosis. AMP-activated protein kinase (AMPK) is an important serine/threonine kinase well known for regulating metabolic processes and maintaining energy homeostasis. However, both metabolic and immunological AMPK-mediated effects play a role in disease. Pro-inflammatory mediators suppress AMPK activity and hinder lipid oxidation. In addition, AMPK activation curbs inflammation by directly inhibiting pro-inflammatory signaling pathways and limiting the build-up of specific lipid intermediates that elicit immune responses. In the context of obesity and chronic disease, these reciprocal responses involve both immune and metabolic cells. Therefore, the immunometabolism of AMPK-mediated processes and therapeutics should be considered in atherosclerosis and insulin resistance.

Authors+Show Affiliations

Division of Endocrinology and Metabolism, Department of Medicine, McMaster University, Hamilton, Ontario, Canada.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

22361321

Citation

Fullerton, Morgan D., et al. "Immunometabolism of AMPK in Insulin Resistance and Atherosclerosis." Molecular and Cellular Endocrinology, vol. 366, no. 2, 2013, pp. 224-34.
Fullerton MD, Steinberg GR, Schertzer JD. Immunometabolism of AMPK in insulin resistance and atherosclerosis. Mol Cell Endocrinol. 2013;366(2):224-34.
Fullerton, M. D., Steinberg, G. R., & Schertzer, J. D. (2013). Immunometabolism of AMPK in insulin resistance and atherosclerosis. Molecular and Cellular Endocrinology, 366(2), 224-34. https://doi.org/10.1016/j.mce.2012.02.004
Fullerton MD, Steinberg GR, Schertzer JD. Immunometabolism of AMPK in Insulin Resistance and Atherosclerosis. Mol Cell Endocrinol. 2013 Feb 25;366(2):224-34. PubMed PMID: 22361321.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Immunometabolism of AMPK in insulin resistance and atherosclerosis. AU - Fullerton,Morgan D, AU - Steinberg,Gregory R, AU - Schertzer,Jonathan D, Y1 - 2012/02/14/ PY - 2011/12/12/received PY - 2012/02/06/accepted PY - 2012/2/25/entrez PY - 2012/3/1/pubmed PY - 2013/7/3/medline SP - 224 EP - 34 JF - Molecular and cellular endocrinology JO - Mol Cell Endocrinol VL - 366 IS - 2 N2 - Obesity leads to insulin resistance and atherosclerosis, which precede Type 2 diabetes and cardiovascular disease. Immunometabolism addresses how metabolic and inflammatory pathways converge to maintain health and a contemporary problem is determining how obesity-induced inflammation precipitates chronic diseases such as insulin resistance and atherosclerosis. AMP-activated protein kinase (AMPK) is an important serine/threonine kinase well known for regulating metabolic processes and maintaining energy homeostasis. However, both metabolic and immunological AMPK-mediated effects play a role in disease. Pro-inflammatory mediators suppress AMPK activity and hinder lipid oxidation. In addition, AMPK activation curbs inflammation by directly inhibiting pro-inflammatory signaling pathways and limiting the build-up of specific lipid intermediates that elicit immune responses. In the context of obesity and chronic disease, these reciprocal responses involve both immune and metabolic cells. Therefore, the immunometabolism of AMPK-mediated processes and therapeutics should be considered in atherosclerosis and insulin resistance. SN - 1872-8057 UR - https://www.unboundmedicine.com/medline/citation/22361321/Immunometabolism_of_AMPK_in_insulin_resistance_and_atherosclerosis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0303-7207(12)00081-0 DB - PRIME DP - Unbound Medicine ER -