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Published in: Diabetology International 3/2017

01-08-2017 | Review Article

Immune regulation of glucose and lipid metabolism

Author: Tsuguhito Ota

Published in: Diabetology International | Issue 3/2017

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Abstract

The immune response and metabolic regulation are highly integrated, and their interface maintains a homeostatic system. Their dysfunction can cause obesity and its comorbidities, including insulin resistance, type 2 diabetes, and nonalcoholic fatty liver disease (NAFLD). Endoplasmic reticulum (ER) stress is a central abnormality linking obesity, insulin resistance, and NAFLD. ER stress in response to increased hepatic lipids may decrease the ability of the liver to secrete triglyceride by limiting apolipoprotein B secretion, thereby worsening fatty liver. Overnutrition or obesity activates the innate immune system, with the subsequent recruitment of immune cells that contributes to the development of insulin resistance. A significant advance in our understanding of obesity-induced inflammation and insulin resistance has been a recognition of the critical role of adipose tissue macrophages. A role for chemokines, small proteins that direct the trafficking of immune cells to sites of inflammation, has also been demonstrated. Chemokines activate the production of inflammatory cytokines through specific chemokine receptors. This review highlights the chemokine systems linking obesity to inflammation and insulin resistance. Treatment options that target immune cells with the aim of halting the development of insulin resistance and type 2 diabetes remain limited. DPP-4 inhibitors or micronutrients may contribute to the immune regulation of glucose and lipid metabolism by regulating macrophage polarization, thereby reducing insulin resistance and preventing the progression of NAFLD. A detailed understanding of the immune regulation of glucose and lipid homeostasis can lead to the development of a novel therapy for insulin resistance, type 2 diabetes, and NAFLD.
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Metadata
Title
Immune regulation of glucose and lipid metabolism
Author
Tsuguhito Ota
Publication date
01-08-2017
Publisher
Springer Japan
Published in
Diabetology International / Issue 3/2017
Print ISSN: 2190-1678
Electronic ISSN: 2190-1686
DOI
https://doi.org/10.1007/s13340-017-0331-1

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