Adipokines, Myokines, and Hepatokines: Crosstalk and Metabolic Repercussions

Abstract

Adipose, skeletal, and hepatic muscle tissues are the main endocrine organs that produce adipokines, myokines, and hepatokines. These biomarkers can be harmful or beneficial to an organism and still perform crosstalk, acting through the endocrine, paracrine, and autocrine pathways. This study aims to review the crosstalk between adipokines, myokines, and hepatokines. Far beyond understanding the actions of each biomarker alone, it is important to underline that these cytokines act together in the body, resulting in a complex network of actions in different tissues, which may have beneficial or non-beneficial effects on the genesis of various physiological disorders and their respective outcomes, such as type 2 diabetes mellitus (DM2), obesity, metabolic syndrome, and cardiovascular diseases (CVD). Overweight individuals secrete more pro-inflammatory adipokines than those of a healthy weight, leading to an impaired immune response and greater susceptibility to inflammatory and infectious diseases. Myostatin is elevated in pro-inflammatory environments, sharing space with pro-inflammatory organokines, such as tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), resistin, and chemerin. Fibroblast growth factor FGF21 acts as a beta-oxidation regulator and decreases lipogenesis in the liver. The crosstalk mentioned above can interfere with homeostatic disorders and can play a role as a potential therapeutic target that can assist in the methods of diagnosing metabolic syndrome and CVD.

Effect of Exercise Training on Fat Loss—Energetic Perspectives and the Role of Improved Adipose Tissue Function and Body Fat Distribution

“…Physical activity has proven to be an effective intervention for treating and preventing NAFLD (van der Windt et al, 2018;Wang et al, 2020). Exactly how exercise improves NAFLD is not completely understood (van der Windt et al, 2018); however, complex crosstalk between adipokines, hepatokines, and myokines has been suggested to play a central role in this improvement (de Oliveira Dos Santos et al, 2021).…”

Effects of Intermittent Hypoxia on Cytokine Expression Involved in Insulin Resistance

“…The excessive accumulation of triglycerides in the liver induces oxidative stress and inflammation, leading to the development of nonalcoholic steatohepatitis (NASH). In addition, abnormalities in hepatic lipid metabolism caused by insulin resistance lead to increased secretion of atherosclerosis-inducing lipoprotein abnormalities, inflammatory cytokines, and blood clot promoting factor, which promote atherosclerosis and create high-risk conditions for cardiovascular diseases [ 8 , 39 ].…”

“…The involvement of these pathologies can lead to chronic diseases of multiple organs. A number of conditions may occur including atherosclerosis, cardiovascular disease, cerebrovascular disease, immunodeficiency, and metabolic abnormalities (pancreatic β cell dysfunction, insulin resistance, and increased free-fatty acid [FFA]) may occur [ 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 ].…”

Erythroferrone Expression in Anemic Rheumatoid Arthritis Patients: Is It Disordered Iron Trafficking or Disease Activity?

“… 6 , 34 However, it was recently claimed to be released in resistance modalities of movement. 35 Attempts to move an inflexible joint might be viewed as a direct cause of resistance to movement. However, we cannot verify whether exercise restriction is a direct cause of increased muscle ERFE secretion since the available data are inadequate to accurately correlate the degree of pain or exercise resistance to the increase in ERFE level.…”