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The Importance of Inflammation as a Link Between Adipokines and Myokines in Obesity

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (20 November 2025) | Viewed by 1311

Special Issue Editor

Special Issue Information

Dear Colleagues,

Obesity triggers inflammation, disrupting adipokine and myokine signaling, which affects metabolic balance, impairs adipose tissue differentiation, and reduces mitochondrial function in both skeletal muscle and adipose tissue. In BMI-discordant twin studies, obese twins showed mitochondrial downregulation and elevated inflammatory markers, particularly in adipose tissue, and had a higher risk of fatty liver and insulin resistance. Sarcopenic obesity, characterized by muscle loss and fat gain, increases cardiometabolic risk, especially in older adults, as pro-inflammatory adipokines like TNFα and IL-6 inhibit muscle regeneration. Myosteatosis worsens muscle function, impairing muscle contractility and metabolism through lipotoxicity and insulin resistance. Understanding adipose–muscle crosstalk and its systemic impact is essential.

This Special Issue is supervised by Prof. Dr. Maria Greabu and assisted by our Topical Advisory Panel Member Dr. Bogdana Virgolici (University of Medicine and Pharmacy).

Prof. Dr. Maria Greabu
Guest Editor

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Keywords

  • inflammation
  • adipokines
  • myokines
  • obesity
  • adipose tissue
  • muscle

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Published Papers (1 paper)

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Review

28 pages, 1145 KB  
Review
Inflammation—Insulin Resistance Crosstalk and the Central Role of Myokines
by Maria-Zinaida Dobre, Bogdana Virgolici, Daciana Costina Andrada Dunca-Stefan, Ioana-Cristina Doicin and Iulia-Ioana Stanescu-Spinu
Int. J. Mol. Sci. 2026, 27(1), 60; https://doi.org/10.3390/ijms27010060 - 20 Dec 2025
Viewed by 851
Abstract
Insulin resistance develops when skeletal muscle (SM), adipose tissue (AT), and the liver fail to respond adequately to insulin, a dysfunction closely intertwined with chronic low-grade inflammation. This combination leads to compensatory hyperinsulinemia, dysglycemia, and metabolic stress, driving major disorders such as type [...] Read more.
Insulin resistance develops when skeletal muscle (SM), adipose tissue (AT), and the liver fail to respond adequately to insulin, a dysfunction closely intertwined with chronic low-grade inflammation. This combination leads to compensatory hyperinsulinemia, dysglycemia, and metabolic stress, driving major disorders such as type 2 diabetes, metabolic syndrome, metabolic dysfunction-associated steatotic liver disease (MASLD), and cardiovascular disease. Both adipokines and myokines are central modulators of this metabolic–inflammatory axis. In obesity, diabetes, MASLD, and thyroid dysfunction, alterations in myokines such as myostatin, irisin, fibroblast growth factor 21 (FGF-21), apelin, brain-derived neurotrophic factor (BDNF), interleukin-6 (IL-6), and interleukin-15 (IL-15) influence glucose uptake, lipid oxidation, mitochondrial function, and systemic inflammation. Exercise-induced myokines exert insulin-sensitizing and anti-inflammatory effects, whereas myostatin and tumor necrosis factor-alpha (TNF-α) promote metabolic impairment. These pathways reveal extensive crosstalk between SM and key metabolic organs—including the liver, pancreas, AT, intestine, heart, and thyroid gland. In metabolic disease, inflammation-driven changes in deiodinase activity and triiodothyronine (T3) availability further link muscle dysfunction with thyroid imbalance. The aim of this narrative review was to elucidate the complex interplay between myokines, adipokines, inflammation, and insulin resistance, and to clarify their clinical relevance in metabolic and thyroid disorders. Given this integrative role of SM, sarcopenia should be recognized as a clinical marker of metabolic or thyroid dysregulation, and preserving muscle mass through structured physical activity should be a core therapeutic target. Full article
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