Cytokines and inflammation in adipogenesis: an updated review

Abstract

The biological relevance of cytokines is known for more than 20 years. Evidence suggests that adipogenesis is one of the biological events involved in the regulation of cytokines, and pro-inflammatory cytokines (e.g., TNFα and IL-1β) inhibit adipogenesis through various pathways. This inhibitory effect can constrain the hyperplastic expandability of adipose tissues. Meanwhile, chronic low-grade inflammation is commonly observed in obese populations. In some individuals, the impaired ability of adipose tissues to recruit new adipocytes to adipose depots during overnutrition results in adipocyte hypertrophy, ectopic lipid accumulation, and insulin resistance. Intervention studies showed that pro-inflammatory cytokine antagonists improve metabolism in patients with metabolic syndrome. This review focuses on the cytokines currently known to regulate adipogenesis under physiological and pathophysiological circumstances. Recent studies on how inhibited adipogenesis leads to metabolic disorders were summarized. Although the interplay of cytokines and lipid metabolism is yet incompletely understood, cytokines represent a class of potential therapeutic targets in the treatment of metabolic disorders.

Brucella abortus Infection Modulates 3T3-L1 Adipocyte Inflammatory Response and Inhibits Adipogenesis

“…Additionally, leptin could significantly reduce lipid accumulation during the adipocyte differentiation process, indicating an inhibitory effect on adipogenesis. The loss of expression of adipokines and the acquisition of an inflammatory phenotype may also involve the secretion of IL-1β, TNF-α, and IL-6 ( 52 ). Here, we have demonstrated an increased secretion of adipokines such as IL-6, but not IL-1β and TNF-α, among infected pre-adipocytes and adipocytes after B. abortus infection, being higher among the former.…”

“…Even though the role of macrophage polarization in the pathogenesis of Brucella species is poorly described until now ( 76 , 77 ). Here, we have demonstrated that proinflammatory cytokines -such as TNF-α- secreted by macrophages in response to B. abortus infection exert an inhibitory effect on adipogenic differentiation ( 52 ). However, we cannot rule out that other cytokines are also present in the conditioned media and contribute to these observations.…”

Salvianolic acid-B improves fat graft survival by promoting proliferation and adipogenesis

“…In addition, we observed some interesting results in our experiment, and the degree of in ammatory cell in ltration in the salvianolic acid B-treated group was lower than that of the control group. Researchers have found that in ammation could inhibit adipogenesis [29]. Moreover, overactivation of in ammation reduces the survival rate of fat transplantation [11,30,31].…”

Severe hyperlipemia-induced pseudoerythrocytosis - Implication for misdiagnosis and blood transfusion: A case report and literature review

“…SHLE could be the complication of various diseases mainly involving diseases in the cardiovascular system, endocrine system, liver, pancreas and kidneys, in which hyperlipemia may the consequence of metabolic abnormalities and play an essential role in the pathogenesis of targeted tissue damages[ 8 - 21 ]. In the genetically predisposed individuals, systemic inflammatory conditions and dietary regimen may be the major environmental factors to influence the lipid metabolism and insulin resistance[ 22 - 27 ]. SHLE sometimes occurs in the natural history or in the treatment of certain hematological diseases, such as in tyrosine kinase inhibitor treatment for patients with MPNs, retinoic acid treatment for patients with acute promyelocytic leukemia and L-asparaginase treatment for patients with acute lymphoblastic leukemia[ 28 - 32 ].…”