Function Of Adipokines Research Articles

Unique Characteristics of Adipocytes in Metabolic Health: Insights and Implications

Adipocytes secrete a wide range of bioactive peptides known as adipokines. These factors play a crucial role in the complex network of metabolic control that connects adipose tissue activity with systemic metabolic balance. The intricacy of adipokine signalling networks and their relationships with other bodily metabolic regulators is also highlighted in this study. Although adipokines are necessary for healthy metabolism, the pathophysiology of various metabolic illnesses, such as obesity, type 2 diabetes, and cardiovascular diseases, are associated with their dysregulation. We explored the effects of changes in adipokine function and levels that affect various disorders, providing a detailed picture of the pathophysiology. This review also delves into the potential of adipokine as a metabolic illness biomarker, including its prognostic and diagnostic potential. Moreover, it assesses the potential therapeutic benefits of regulating adipokine activity and explores present and upcoming approaches to target these molecules to enhance metabolic health. Overall, This study emphasizes the many functions of adipokines in several metabolic processes, such as insulin sensitivity, lipid metabolism, glucose regulation, and inflammation. Additionally, it offers a comprehensive and insightful understanding of adipokines, emphasizing their pivotal role in metabolic well-being and disease.

A Review on Role of Different Adipokines in Gestational Diabetes

Adipokines are cell-signaling molecules produced by the adipose tissue that play functional roles in energy or metabolic status of the body, inflammation, obesity, gestational diabetes etc. Adipokines come in several forms, including adiponectin, leptin, chemeein, resistin, and nicotinamide phosphoribosyl transferase. The hormone adiponectin is primarily recognised for its anti- inflammatory and insulin-sensitizing properties. Through its anti-inflammatory, anti-fibrotic, and antioxidant properties, the adipocyte-secreted hormone adiponectin regulates lipid metabolism, insulin sensitivity, blood sugar levels, and adipocyte function. The hormone leptin, which is released from adipose tissue (body fat), aids the body in long-term maintenance of a healthy weight. In order to prevent the body from producing the hunger response when it doesn't need energy. White adipocytes release resistin, a hormone high in cysteine. Insulin resistance is influenced by resistin. Adipocytes secrete a protein called chemerin, which has endocrine functions in metabolism and immunity as well as autocrine/paracrine effects on adipose formation and function. Due to significantly greater oestrogen levels, there is an increase in insulin sensitivity in the first and second trimesters. Increased insulin resistance and decreased sensitivity are caused by a number of antagonistic hormones, particularly placental lactogen, leptin, progesterone, prolactin, and cortisol in the late second and early third trimester. In addition to outlining their mechanisms of action in the development of gestational diabetes, this review paper attempts to summarise the functions of adipokines in the induction of insulin resistance during pregnancy.

The Role of Adipokines in the Pathologies of the Central Nervous System.

Adipokines are protein hormones secreted by adipose tissue in response to disruptions in physiological homeostasis within the body's systems. The regulatory functions of adipokines within the central nervous system (CNS) are multifaceted and intricate, and they have been identified in a number of pathologies. Therefore, specific adipokines have the potential to be used as biomarkers for screening purposes in neurological dysfunctions. The systematic review presented herein focuses on the analysis of the functions of various adipokines in the pathogenesis of CNS diseases. Thirteen proteins were selected for analysis through scientific databases. It was found that these proteins can be identified within the cerebrospinal fluid either by their ability to modify their molecular complex and cross the blood-brain barrier or by being endogenously produced within the CNS itself. As a result, this can correlate with their measurability during pathological processes, including Alzheimer's disease, amyotrophic lateral sclerosis, multiple sclerosis, depression, or brain tumors.

Regulation and function of adiponectin in the intestinal epithelial cells in response to Trichinella spiralis infection

Besides metabolic homeostasis regulation, adipokines are recently emerged as important players in regulating immunity and inflammation. Helminth infection has known to modulate circulating adipokine secretion; however, the regulation and function of adipokines in response to helminth infection is still unclear. Here, we investigated the regulation and function of adiponectin during T. spiralis infection. While there was no change in circulating level of adiponectin, we found an increased adiponectin, but not leptin expression in the small intestine. Interestingly, the intestinal adiponectin expression was strongly associated with the expression of epithelial cell-derived cytokines IL-25, IL-33, and TSLP following infection. Indeed, mice deficiency of IL-25 receptor exhibited no intestinal adiponectin induction upon helminth infection. Interestingly, IL-25-induced adiponectin modulated intestinal epithelial cell responses by enhancing occludin and CCL17 expression. Using LPS-induced intestinal epithelial barrier dysfunctions in a Caco-2 cell monolayer model, adiponectin pretreatment enhanced a Transepithelial electrical resistance (TEER) and occludin expression. More importantly, adiponectin pretreatment of Caco2 cells prevented T. spiralis larval invasion in vitro and its administration during infection enhanced intestinal IL-13 secretion and worm expulsion in vivo. Altogether, our data suggest that intestinal adiponectin expression induced by helminth infection through the regulation of IL-25 promotes worm clearance and intestinal barrier function.

Relationship between chronic obstructive pulmonary disease and adiponectin concentrations: An updated meta-analysis and single-cell RNA sequencing.

Adipose tissue, being an organ of the endocrine system, can influence the severity of chronic obstructive pulmonary disease (COPD). Even though several inflammatory markers can potentially significantly influence lung function, the precise function of adipokines, like adiponectin, in COPD is still disputed. To analyze the association of COPD with adiponectin concentrations, a meta-analysis of the most recent literature and single-cell sequencing data were conducted. Studies in Embase, PubMed, Cochrane Library, and Web of Science were browsed to obtain relevant data, which were then assessed with the aid of R 4.1.3 and STATA 11.0 software. Standardized mean differences and correlation coefficients aided the analysis of effect values. Moreover, a single-cell sequencing GSE136831 dataset was retrieved to ascertain the mRNA expression of adiponectin gene (ADIPOQ) in the lung tissue of COPD patients to confirm the difference in the expression of adiponectin between the case and control groups. This meta-analysis comprised 18 publications involving 24 studies. The overall combined data established the concentration of plasma/serum adiponectin as significantly higher in patients with COPD compared to healthy subjects. Subgroup analyses based on disease status, specimen type, ethnicity, study design method, measurement method, and age of COPD patients demonstrated that all patients with COPD had elevated levels of adiponectin compared to healthy controls. When subgroup analysis was performed for gender alone, the results depicted that male COPD patients had significantly higher adiponectin than healthy males, while female patients of COPD had elevated adiponectin compared to healthy females. Furthermore, it was found that plasma/serum adiponectin appeared to be positively correlated with tumor necrosis factor-α, and it was negatively correlated with FEV1% and FEV1/FVC. The results of single-cell sequencing data suggested that ADIPOQ mRNA was mainly expressed in alveolar epithelial cells, and the level of ADIPOQ mRNA was higher in lung tissues of patients with COPD than in lung tissues of healthy subjects. This meta-analysis suggests that the levels of plasma/serum adiponectin are significantly elevated in patients with COPD versus controls. Tumor necrosis factor-α, FEV1/FVC, and FEV1% may all be associated with the concentrations of adiponectin.

Adipokines in Periodontal disease – Culprits or Accomplice?

Periodontitis is a disease of periodontium resulting from pathogenic microorganisms combined with other risk factors. For many years, the relationship of obesity with periodontal disease has been debated. Recently, obesity is considered a risk factor for periodontitis. The pathomechanistic association studies have shown a link between adipose tissue secreted adipokines and periodontal disease, although the inherent mechanisms are obscure. Thus, this review aims to get an overview of the association between adipokines and periodontal disease. Adipokines, bioactive molecules secreted by adipose tissue, regulate energy outflow and insulin sensitivity apart from modulation of inflammation and healing. Obesity causes chronic low-grade inflammation and increases adipokines. Recent studies have also shown that adipokines, such as leptin, adiponectin, and visfatin, could play a role in periodontal disease progression and may be used as biomarkers. They increase the production of pro-inflammatory factors, creating a hyperinflammatory state that affects systemic diseases and enhances the risk for periodontitis and compromises healing post periodontal therapy. Understanding the function of adipokines may better help us interpret the triad of obesity with periodontitis and type 2 diabetes. Moreover, periodontal disease treatment may imply positive effects on the overall health of the individual.

Adipoquinas, envejecimiento y daño vascular

The main physiologic function of adipokines on the energy metabolism and the cardiovascular homeostasis, among others, are well known. In the last years, our laboratory is providing increasing evidence about the possible role of adipokines as mediators of vascular damage, by inducing different pro-inflammatory and pro-senescent mechanisms. The secretion of adipokines like visfatin or dipeptidylpeptidase-4 (DPP4) by adipose tissue, particularly by the visceral fat, is enhanced in obese and type 2 diabetic patients. Both adipokines are enzymes metabolically active that can induce the activation of specific receptors, namely type 4 “toll like receptors” (TLR4) for visfatin and “protease activated receptor 2” (PAR2) for DPP4. Stimulation of such receptors is triggering well known pro-inflammatory and pro-senescent mechanisms, like the nuclear transcription factor-κB (NF-κB) or the inflammasome NLRP3 (“nucleotide-binding, leucine-rich-repeat, pyrin domain containing 3”), a cell structure that transforms the immature forms of classic cytokines in their active derivates, interleukin-1β (IL-1β) or interleukin 18 (IL-18). It is worth to note that these classic cytokines are the final effectors for the harmful effects of the adipokines and its blockade can be a very relevant therapeutic approach. In our experiments, the specific antagonism of IL-1 receptors with anakinra prevents the inflammatory and senescent effects evoked by visfatin and DPP4. Moreover, this finding is in agreement with data from other researchers, as well as with the results of the CANTOS clinical trial, which demonstrate a very important cardioprotective cardiovascular effect mediated by the anti-inflammatory effect of the monoclonal antibody canakinumab. On the other hand, we have also provided experimental evidence about possible vasculopotective adipokines, such angiotensin-(1-7), which is able to induce, through activation of Mas receptors, the expression of klotho protein and the activation of antioxidant pathways, like the well known Nrf2-HO-1 (“nuclear factor erythroid-2 y hemoygenase-1”).

The Role of Adipokines in Inflammatory Mechanisms of Obesity

Adipokines are currently widely studied cellular signaling proteins produced by adipose tissue and involved in various processes, including inflammation; energy and appetite modulation; lipid and glucose metabolism; insulin sensitivity; endothelial cell functioning; angiogenesis; the regulation of blood pressure; and hemostasis. The current review attempted to highlight the key functions of adipokines in the inflammatory mechanisms of obesity, its complications, and its associated diseases. An extensive search for materials on the role of adipokines in the pathogenesis of obesity was conducted online using the PubMed and Scopus databases until October 2022.

Adipokines as Immune Cell Modulators in Multiple Sclerosis

Multiple sclerosis (MS), a chronic inflammatory and demyelinating disease of the central nervous system (CNS), is a major clinical and societal problem, which has a tremendous impact on the life of patients and their proxies. Current immunomodulatory and anti-inflammatory therapies prove to be relatively effective; however, they fail to concomitantly stop ongoing neurological deterioration and do not reverse acquired disability. The proportion to which genetic and environmental factors contribute to the etiology of MS is still incompletely understood; however, a recent association between MS etiology and obesity was shown, with obesity greatly increasing the risk of developing MS. An altered balance of adipokines, which are white adipose tissue (WAT) hormones, plays an important role in the low-grade chronic inflammation during obesity by their pervasive modification of local and systemic inflammation. Vice versa, inflammatory factors secreted by immune cells affect adipokine function. To explore the role of adipokines in MS pathology, we will here review the reciprocal effects of adipokines and immune cells and summarize alterations in adipokine levels in MS patient cohorts. Finally, we will discuss proof-of-concept studies demonstrating the therapeutic potential of adipokines to target both neuroinflammation and neurodegeneration processes in MS.

Melanoma Progression under Obesity: Focus on Adipokines.

Simple SummaryObesity is a rapidly growing public health problem and the reason for numerous diseases in the human body, including cancer. This article reviews the current knowledge of the effect of molecules secreted by adipose tissue-adipokines on melanoma progression. We also discuss the role of these factors as markers of incidence, metastasis, and melanoma patient survival. Understanding the functions of adipokines will lead to knowledge of whether and how obesity promotes melanoma growth.Obesity is a growing problem in the world and is one of the risk factors of various cancers. Among these cancers is melanoma, which accounts for the majority of skin tumor deaths. Current studies are looking for a correlation between obesity and melanoma. They suspect that a potential cause of its development is connected to the biology of adipokines, active molecules secreted by adipose tissue. Under physiological conditions, adipokines control many processes, including lipid and glucose homeostasis, insulin sensitivity, angiogenesis, and inflammations. However, when there is an increased amount of fat in the body, their secretion is dysregulated. This article reviews the current knowledge of the effect of adipokines on melanoma growth. This work focuses on the molecular pathways by which adipose tissue secreted molecules modify the angiogenesis, migration, invasion, proliferation, and death of melanoma cells. We also discuss the role of these factors as markers of incidence, metastasis, and melanoma patient survival. Understanding the functions of adipokines will lead to knowledge of whether and how obesity promotes melanoma growth. Further studies may contribute to the innovations of therapies and the use of adipokines as predictive and/or prognostic biomarkers.

The pathophysiological role of adipokines in the development of bronchial asthma combined with obesity

The combined course of bronchial asthma (BA) and obesity is one of the urgent medical and social problems that requires a comprehensive and careful study in connection with a decrease in the quality of life of such patients, an increase in the frequency, duration of hospitalization and a high economic burden for the state as a whole. The relationship between BA and obesity is now confirmed by numerous studies, at the same time, despite the variability of the proposed mechanisms of pathogenetic effects of obesity on asthma, metabolic aspects of the relationship of these diseases need further study. Adipose tissue hormones are responsible for the energy homeostasis of the body therefore, excessive accumulation of adipose tissue is accompanied by the development of an imbalance in metabolic processes in various organs and tissues. Due to the emergence of new scientific data on the role and function of adipokines in the body, metabolic effects of adipokines are considered in the focus of their pathophysiological association with obesity and asthma. This literary review highlights the current understanding of the role of metabolic effects of the most studied adipokines (resistin, retinol-binding protein, leptin and adiponectin) in the development of obesity and BA. Gender and age-dependent features of adipokine levels in BA and obesity are described. Data on the confirmed role of adiponectin and leptin in the progression of BA combined with obesity are presented. It has been shown that the role of resistin and retinol-binding protein in the development of BA combined with obesity has not been studied. It is demonstrated that further study of metabolic activity of adipokines in BA is an actual and perspective direction of researches which will allow to develop new diagnostic and therapeutic strategies in patients with BA with obesity.

Emerging functions of adipokines in linking the development of obesity and cardiovascular diseases.

Increasing evidence shows that obesity is the critical factor in shaping cardio-metabolic phenotypes. However, the pathogenic mechanisms remain incompletely clarified. According to the published reports, adipose tissue communicates with several diverse organs, such as heart, lungs, and kidneys through the secretion of various cytokines named adipokines. The adipocytes isolated from obese mice or humans are dysfunctional with aberrant production of pro-inflammatory adipokines, which subsequently induce both acute and chronic inflammatory reaction and facilitate the process of cardio-metabolic disorder complications. Furthermore, the microenvironment within adipose tissue under obese status also influence the secretion of adipokines. Recently, given that several important adipokines have been completely researched and causally involved in various diseases, we could make a conclusion that adipokines play an essential role in modulating the development of cardio-metabolic disorder diseases, whereas several novel adipokines continue to be explored and elucidated. In the present review, we summarized the current knowledge of the microenvironment of adipose tissue and the published mechanisms whereby adipocytes affects obesity and cardiovascular diseases. On the other hand, we also provide the evidence to elucidate the functions of adipokines in controlling and regulating the inflammatory reactions which contribute to obesity and cardiovascular disease.

Coenzyme Q10 Supplementation Improves Adipokine Levels and Alleviates Inflammation and Lipid Peroxidation in Conditions of Metabolic Syndrome: A Meta-Analysis of Randomized Controlled Trials.

Evidence from randomized controlled trials (RCTs) suggests that coenzyme Q10 (CoQ10) can regulate adipokine levels to impact inflammation and oxidative stress in conditions of metabolic syndrome. Here, prominent electronic databases such as MEDLINE, Cochrane Library, and EMBASE were searched for eligible RCTs reporting on any correlation between adipokine levels and modulation of inflammation and oxidative stress in individuals with metabolic syndrome taking CoQ10. The risk of bias was assessed using the modified Black and Downs checklist, while the Grading of Recommendations Assessment, Development and Evaluation (GRADE) tool was used to evaluate the quality of evidence. Results from the current meta-analysis, involving 318 participants, showed that CoQ10 supplementation in individuals with metabolic syndrome increased adiponectin levels when compared to those on placebo (SMD: 1.44 [95% CI: −0.13, 3.00]; I2 = 96%, p < 0.00001). Moreover, CoQ10 supplementation significantly lowered inflammation markers in individuals with metabolic syndrome in comparison to those on placebo (SMD: −0.31 [95% CI: −0.54, −0.08]; I2 = 51%, p = 0.07). Such benefits with CoQ10 supplementation were related to its ameliorative effects on lipid peroxidation by reducing malondialdehyde levels, concomitant to improving glucose control and liver function. The overall findings suggest that optimal regulation of adipokine function is crucial for the beneficial effects of CoQ10 in improving metabolic health.

Research progress on the role of adipokines in intervertebral disc degeneration

To review the research progress of the role and mechanism of adipokines in intervertebral disc degeneration (IVDD) in recent years. The domestic and foreign literature related to adipokines in the process of IVDD was extensively reviewed. The types and functions of adipokines, the role and mechanism in the process of IVDD, and the application prospects of intervertebral disc biotherapy were reviewed. As a kind of bioactive substance secreted by adipose tissue, adipokine plays an important role in bone and joint diseases, metabolic diseases, and breast cancer. During IVDD, most adipokines can activate multiple signaling pathways by binding to autoreceptors, cause the proliferation and apoptosis of cells and proinflammatory and anti-inflammatory factors parasecretions in the intervertebral disc, and lead to imbalance of intradiscal metabolism and establishment of the initial inflammatory environment, and finally cause the IVDD. Adipokines, as a biologically active substance with metabolic and immunomodulatory functions, play important roles in the occurrence, development, and biological treatment of IVDD.

Epigenetics and In Utero Acquired Predisposition to Metabolic Disease.

Epidemiological evidence has shown an association between prenatal malnutrition and a higher risk of developing metabolic disease in adult life. An inadequate intrauterine milieu affects both growth and development, leading to a permanent programming of endocrine and metabolic functions. Programming may be due to the epigenetic modification of genes implicated in the regulation of key metabolic mechanisms, including DNA methylation, histone modifications, and microRNAs (miRNAs). The expression of miRNAs in organs that play a key role in metabolism is influenced by in utero programming, as demonstrated by both experimental and human studies. miRNAs modulate multiple pathways such as insulin signaling, immune responses, adipokine function, lipid metabolism, and food intake. Liver is one of the main target organs of programming, undergoing structural, functional, and epigenetic changes following the exposure to a suboptimal intrauterine environment. The focus of this review is to provide an overview of the effects of exposure to an adverse in utero milieu on epigenome with a focus on the molecular mechanisms involved in liver programming.

Interplay of adipokines in the pathogenesis of essential hypertension: A comparative cross-sectional in Ghana

BackgroundThe renin-angiotensin-system (RAS), endothelial dysfunction and sympathetic nervous system are mechanistic risk factors of hypertension. The study sought to elucidate the interplay of adipokines in the pathogenesis of essential hypertension. MethodologyThis comparative cross-sectional study recruited 200 confirmed hypertensive patients from the KATH and 50 age-matched normotensives. Participants’ blood pressures, anthropometric and socio-demographic information were voluntarily obtained. Serum levels of adiponectin, leptin and resistin of the participants were quantified using the ELISA. Renal function, lipid profile and glycemic status of all subjects were also analyzed. ResultsHypertensive patients showed a significantly higher anthropometric indices of adiposity compared to normotensives, CI (p < 0.0001), BAI (p < 0.0001) and AVI (p = 0.002). Adiponectin levels (p < 0.0001) were significantly lower in the hypertensive relative to the normotensives. Furthermore, significantly higher concentrations of serum leptin (p = 0.016) and the leptin-adiponectin ratio (p = 0.001) were observed among the hypertensive compared to the normotensives. The study further observed a direct association between serum leptin and weight (r = 0.111, p = 0.022), BMI (r = 0.129, p = 0.009) and WHtR (r = 0.098, p = 0.045) but inverse relationship with height (r = −0.134, p = 0.006) among the hypertensive. Serum leptin has a significant negative correlation with HDL-C among the hypertensive (r = −0.174, p = 0.013). The fully aOR for hypertension as predicted by resistin and adiponectin were 1.12 (95% Cl, 1.02–1.25); p = 0.019) and 0.93 (95% Cl, 0.91–0.95); p = 0.0001) respectively. ConclusionWe found that elevations in serum levels of leptin and resistin, and low levels of adiponectin may play a role in the pathogenesis of essential hypertension. Therefore, adipokines may offer themselves as potential indices for early and accurate detection of high blood pressure. At the same time our present results also confirm the conclusions with respect to correlation of leptin and obesity. Further longitudinal studies in a larger population are warranted to investigate the physiological and pathological functions of adipokines in hypertension.

Collagen overlays can inhibit leptin and adiponectin secretion but not lipid accumulation in adipocytes.

BackgroundWhite adipose tissue (WAT) is essential for energy storage as well as being an active endocrine organ. The secretion of adipokines by adipocytes can affect whole body metabolism, appetite, and contribute to overall health. WAT is comprised of lipid-laden mature adipocytes, as well as immune cells, endothelial cells, pre-adipocytes, and adipose-derived stem cells. In addition, the presence of extracellular matrix (ECM) proteins in WAT can actively influence adipocyte differentiation, growth, and function. Type I collagen is an abundant fibrous ECM protein in WAT that is secreted by developing adipocytes. However, the extent and overall effect of Type I collagen on adipokine secretion in mature adipocytes when added exogenously has not been established.MethodsWe characterized the effects of Type I collagen overlays prepared using two different buffers on adipocyte physiology and function when added at different times during differentiation. In addition, we compared the effect of collagen overlays when adipocytes were cultured on two different tissue culture plastics that have different adherent capabilities. Triglyceride accumulation was analyzed to measure adipocyte physiology, and leptin and adiponectin secretion was determined to analyze effects on adipokine secretion.ResultsWe found that collagen overlays, particularly when added during the early differentiation stage, impaired adipokine secretion from mature adipocytes. Collagen prepared using PBS had a greater suppression of leptin than adiponectin while collagen prepared using HANKS buffer suppressed the secretion of both adipokines. The use of CellBind plates further suppressed leptin secretion. Triglyceride accumulation was not substantially impacted with any of the collagen overlays.DiscussionAdipokine secretion can be selectively altered by collagen overlays. Thus, it is feasible to selectively manipulate the secretion of adipokines by adipocytes in vitro by altering the composition or timing of collagen overlays. The use of this technique could be applied to studies of adipokine function and secretion in vitro as well as having potential therapeutic implications to specifically alter adipocyte functionality in vivo.

Relationship of circulating chemerin and omentin levels with Th17 and Th9 cell immune responses in patients with asthma

ABSTRACTObjective: Adipokines are correlated with immune responses in asthma, but data on the roles of chemerin and omentin in asthma are limited. This study explored the relationship of chemerin and omentin levels with Th17 and Th9 cells in asthma. Methods: Seventy-six asthmatics were divided into intermittent-to-mild persistent (n = 28), moderate persistent (n = 26) and severe persistent (n = 22) and were enrolled in the study. Additionally, 20 healthy subjects were enrolled as controls. Clinical characteristics of the subjects, the Asthma Control Test, lung function, fractional exhaled nitric oxide score, and plasma chemerin and omentin levels were evaluated, and the percentages of Th17 and Th9 cells were determined by flow cytometry. Results: The percentages of Th17 and Th9 cells were higher in the moderate-to-severe persistent asthmatics than in the intermittent-to-mild persistent asthmatics or healthy controls (p < 0.05). The severe persistent asthma group had a higher chemerin level but lower omentin levels than the control group (p < 0.05). Chemerin levels were positively correlated with Th17 and Th9 cell percentages, while omentin levels were negatively correlated with Th17 and Th9 cell percentages (p < 0.01). Conclusions: The regulatory functions of adipokines on immune responses may be associated with pathogenesis and processes of asthma.

Metrnl: a secreted protein with new emerging functions.

Secreted proteins play critical roles in physiological and pathological processes and can be used as biomarkers and therapies for aging and disease. Metrnl is a novel secreted protein homologous to the neurotrophin Metrn. But this protein, unlike Metrn that is mainly expressed in the brain, shows a relatively wider distribution in the body with high levels of expression in white adipose tissue and barrier tissues. This protein plays important roles in neural development, white adipose browning and insulin sensitization. Based on its expression and distinct functions, this protein is also called Cometin, Subfatin and Interleukin 39, which refer to its neurotrophic effect, adipokine function and the possible action as a cytokine, respectively. The spectrum of Metrnl functions remains to be determined, and the mechanisms of Metrnl action need to be elucidated. In this review, we focus on the discovery, structural characteristics, expression pattern and physiological functions of Metrnl, which will assist in developing this protein as a new therapeutic target or agent.

Editorial: Control of Adipocyte Differentiation and Metabolism.

EDITORIAL article Front. Endocrinol., 28 August 2015Sec. Experimental Endocrinology Volume 6 - 2015 | https://doi.org/10.3389/fendo.2015.00132