Abstract

Obesity and type II diabetes are characterized by insulin resistance in peripheral tissues. A high caloric intake combined with a sedentary lifestyle is the leading cause of these conditions. Whole-body insulin resistance and its improvement are the result of the combined actions of each insulin-sensitive organ. Among the fundamental molecular mechanisms by which each organ is able to communicate and engage in cross-talk are cytokines or peptides which stem from secretory organs. Recently, it was reported that several cytokines or peptides are secreted from muscle (myokines), adipose tissue (adipokines) and liver (hepatokines) in response to certain nutrition and/or physical activity conditions. Cytokines exert autocrine, paracrine or endocrine effects for the maintenance of energy homeostasis. The present review is focused on the relationship and cross-talk amongst muscle, adipose tissue and the liver as secretory organs in metabolic diseases.

Highlights

  • Metabolic disease is characterized by insulin resistance in peripheral tissues

  • Understanding the regulation of endocrine hormones secreted from each metabolic organ is important for improving metabolic diseases such as obesity and type II diabetes, as metabolic diseases are not a local problem

  • We demonstrate that a sedentary lifestyle combined with excessive calorie intake alters the pattern of cytokine secretion from many organs

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Summary

Introduction

Metabolic disease is characterized by insulin resistance in peripheral tissues. Impaired insulin action increases hepatic glucose production, decreases muscle glucose uptake, and promotes lipid accumulation in insulin-sensitive organs such as muscle, liver and fat [1,2,3]. Recent evidence has identified skeletal muscle and the liver, as well as adipocytes, as secretory organs [4,5,6,7] These metabolic organs communicate with each other regarding the regulation of energy homeostasis and insulin sensitivity. Circulating irisin levels in humans were positively correlated with adiposity parameters such as body weight, fat mass, body mass index (BMI), waist-to-hip ratio and homeostasis model assessment of insulin resistance (HOMA-IR) [25,27,28,29,30,31,32,33]. These reports suggest that adiposity would be one of the main contributors to increase circulating irisin levels in humans

Fibroblast Growth Factor 21
Interleukin 6
Interleukin 4
Interleukin 7
Interleukin 8
Interleukin 15
Myostatin
2.10. Brain-Derived Neurotrophic Factor
2.11. Leukemia Inhibitory Factor
2.12. Secreted Protein Acidic and Rich in Cysteine
2.13. Insulin-Like Growth Factor-1 and Fibroblast Growth Factor 2
2.14. Follistatin-Related Protein 1
2.15. Erythropoietin
2.16.1. Hepatocyte Growth Factor
2.16.2. Semaphorin 3A
Adipokines
Adiponectin
Secreted Frizzled-Related Protein 5
Leptin
Resistin
Tumor Necrosis Factor α
Retinol Binding Protein 4
Irisin
Hepatokines
Leukocyte Cell-Derived Chemotaxin 2
Selenoprotein P
Chemerin
Concluding Remarks

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