An Integrated View of Immunometabolism

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The worldwide obesity epidemic has emerged as a major cause of insulin resistance and Type 2 diabetes. Chronic tissue inflammation is a well-recognized feature of obesity, and the field of immunometabolism has witnessed many advances in recent years. Here, we review the major features of our current understanding with respect to chronic obesity-related inflammation in metabolic tissues and focus on how these inflammatory changes affect insulin sensitivity, insulin secretion, food intake, and glucose homeostasis. There is a growing appreciation of the varied and sometimes integrated crosstalk between cells within a tissue (intraorgan) and tissues within an organism (interorgan) that supports inflammation in the context of metabolic dysregulation. Understanding these pathways and modes of communication has implications for translational studies. We also briefly summarize the state of this field with respect to potential current and developing therapeutics.
Publisher
CELL PRESS
Issue Date
2018-01
Language
English
Article Type
Review
Keywords

INDUCED INSULIN-RESISTANCE; NECROSIS-FACTOR-ALPHA; DIET-INDUCED OBESITY; BETA-CELL DEDIFFERENTIATION; ADIPOSE-TISSUE MACROPHAGES; ACTIVATED PROTEIN-KINASE; FATTY LIVER-DISEASE; ISLET-ASSOCIATED MACROPHAGES; GLUCAGON-LIKE PEPTIDE-1; HUMAN SKELETAL-MUSCLE

Citation

CELL, v.172, no.1-2, pp.22 - 40

ISSN
0092-8674
DOI
10.1016/j.cell.2017.12.025
URI
http://hdl.handle.net/10203/240099
Appears in Collection
MSE-Journal Papers(저널논문)
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