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Cellular and Molecular Life Sciences :... May 2022Characterized by a surplus of whole-body adiposity, obesity is strongly associated with the prognosis of atherosclerosis, a hallmark of coronary artery disease (CAD) and... (Review)
Review
Characterized by a surplus of whole-body adiposity, obesity is strongly associated with the prognosis of atherosclerosis, a hallmark of coronary artery disease (CAD) and the major contributor to cardiovascular disease (CVD) mortality. Adipose tissue serves a primary role as a lipid-storage organ, secreting cytokines known as adipokines that affect whole-body metabolism, inflammation, and endocrine functions. Emerging evidence suggests that adipokines can play important roles in atherosclerosis development, progression, as well as regression. Here, we review the versatile functions of various adipokines in atherosclerosis and divide these respective functions into three major groups: protective, deteriorative, and undefined. The protective adipokines represented here are adiponectin, fibroblast growth factor 21 (FGF-21), C1q tumor necrosis factor-related protein 9 (CTRP9), and progranulin, while the deteriorative adipokines listed include leptin, chemerin, resistin, Interleukin- 6 (IL-6), and more, with additional adipokines that have unclear roles denoted as undefined adipokines. Comprehensively categorizing adipokines in the context of atherosclerosis can help elucidate the various pathways involved and potentially pave novel therapeutic approaches to treat CVDs.
Topics: Adipokines; Adiponectin; Adiposity; Atherosclerosis; Cardiovascular Diseases; Humans; Interleukin-6; Leptin; Obesity
PubMed: 35503385
DOI: 10.1007/s00018-022-04286-2 -
Journal of Lipid Research Oct 2019The breakthrough discoveries of leptin and adiponectin more than two decades ago led to a widespread recognition of adipose tissue as an endocrine organ. Many more... (Review)
Review
The breakthrough discoveries of leptin and adiponectin more than two decades ago led to a widespread recognition of adipose tissue as an endocrine organ. Many more adipose tissue-secreted signaling mediators (adipokines) have been identified since then, and much has been learned about how adipose tissue communicates with other organs of the body to maintain systemic homeostasis. Beyond proteins, additional factors, such as lipids, metabolites, noncoding RNAs, and extracellular vesicles (EVs), released by adipose tissue participate in this process. Here, we review the diverse signaling mediators and mechanisms adipose tissue utilizes to relay information to other organs. We discuss recently identified adipokines (proteins, lipids, and metabolites) and briefly outline the contributions of noncoding RNAs and EVs to the ever-increasing complexities of adipose tissue inter-organ communication. We conclude by reflecting on central aspects of adipokine biology, namely, the contribution of distinct adipose tissue depots and cell types to adipokine secretion, the phenomenon of adipokine resistance, and the capacity of adipose tissue to act both as a source and sink of signaling mediators.
Topics: Adiponectin; Adipose Tissue; Animals; Humans; Leptin; Lipid Metabolism; Signal Transduction
PubMed: 31209153
DOI: 10.1194/jlr.R094060 -
Clinical Science (London, England :... Mar 2021The global obesity epidemic is a major contributor to chronic disease and disability in the world today. Since the discovery of leptin in 1994, a multitude of studies... (Review)
Review
The global obesity epidemic is a major contributor to chronic disease and disability in the world today. Since the discovery of leptin in 1994, a multitude of studies have characterized the pathological changes that occur within adipose tissue in the obese state. One significant change is the dysregulation of adipokine production. Adipokines are an indispensable link between metabolism and optimal immune system function; however, their dysregulation in obesity contributes to chronic low-grade inflammation and disease pathology. Herein, I will highlight current knowledge on adipokine structure and physiological function, and focus on the known roles of these factors in the modulation of the immune response. I will also discuss adipokines in rheumatic and autoimmune diseases.
Topics: Adipokines; Adipose Tissue; Animals; Autoimmunity; Humans; Inflammation; Obesity
PubMed: 33729498
DOI: 10.1042/CS20200895 -
Molecules (Basel, Switzerland) Jan 2022Metabolic syndrome is a cluster of metabolic indicators that increase the risk of diabetes and cardiovascular diseases. Visceral obesity and factors derived from altered... (Review)
Review
Metabolic syndrome is a cluster of metabolic indicators that increase the risk of diabetes and cardiovascular diseases. Visceral obesity and factors derived from altered adipose tissue, adipokines, play critical roles in the development of metabolic syndrome. Although the adipokines leptin and adiponectin improve insulin sensitivity, others contribute to the development of glucose intolerance, including visfatin, fetuin-A, resistin, and plasminogen activator inhibitor-1 (PAI-1). Leptin and adiponectin increase fatty acid oxidation, prevent foam cell formation, and improve lipid metabolism, while visfatin, fetuin-A, PAI-1, and resistin have pro-atherogenic properties. In this review, we briefly summarize the role of various adipokines in the development of metabolic syndrome, focusing on glucose homeostasis and lipid metabolism.
Topics: Adipokines; Animals; Humans; Metabolic Syndrome
PubMed: 35056647
DOI: 10.3390/molecules27020334 -
Current Rheumatology Reports Dec 2019Osteoarthritis (OA) is an aging-associated and injury-induced joint disease characterized by cartilage degradation, bone sclerosis, and persistent low-grade inflammation... (Review)
Review
PURPOSE OF THE REVIEW
Osteoarthritis (OA) is an aging-associated and injury-induced joint disease characterized by cartilage degradation, bone sclerosis, and persistent low-grade inflammation in the joint. Aging and injury are triggers of joint pathological changes mediated by pro-inflammatory factors, some of which are secreted by white adipose tissue. Adipokines including adiponectin, leptin, resistin, chemerin, IL-6, and TNF-α are major players not only during inflammation but also in metabolic regulation of joint cells including chondrocytes, osteoblasts, osteoclasts as well as mesenchymal stem cells. The purpose of this review is to summarize the signal transduction pathways of adipokines in the articular joint to provide new information on potential targets for intervention of OA.
RECENT FINDINGS
The risk of knee osteoarthritis is associated with adipokine gene polymorphism. While the infrapatellar fat pad is a major source of adipokines in knee synovial fluid, adipocytes also accumulate in the bone marrow during aging and obesity. Adipokines can act as SASPs (senescence associated secretory phenotype factors) that participate in cellular senescence of chondrocytes, but they also regulate energy metabolism impacting bone remodeling. Thus, adipokines are closely related to the metabolic syndrome and degenerative pathological changes in cartilage and bone during OA. Modulating the effects of adipokines on different cell types in the intra-articular joint will be a promising new option for OA intervention.
Topics: Adipokines; Humans; Osteoarthritis
PubMed: 31813080
DOI: 10.1007/s11926-019-0868-z -
Nutrients Oct 2022Gestational diabetes mellitus (GDM)is one of the most common perinatal pathologies, with a prevalence of 5-20% depending on the population or diagnostic standards. It is... (Review)
Review
Gestational diabetes mellitus (GDM)is one of the most common perinatal pathologies, with a prevalence of 5-20% depending on the population or diagnostic standards. It is diagnosed when glucose intolerance is first detected during pregnancy. In the pathogenesis of GDM, genetic, environmental, and pregnancy-related factors (excessive fat storage and increased adipokine and cytokine secretion) play important roles. A growing amount of scientific data has indicated the role of gut microbiota (GM) dysbiosis in the development of glucose intolerance during pregnancy. Previous studies have indicated that, in comparison to healthy pregnant women, GDM individuals have a greater abundance of bacteria belonging to the genera , and and a lower number of bacteria belonging to the genera , and . Recently, many studies have focused on treating GDM with methods targeting GM. Several previous studies have analyzed the effect of probiotics on the course of GDM, but their data are inconclusive. In view of this state, the aim of the study was to collect and comprehensively discuss current knowledge regarding the role of probiotic supplementation in preventing and treating GDM. According to the analyzed data, probiotics have a positive influence on glycemic control and are a promising tool for lowering the frequency of GDM. However, further studies must be conducted to determine the optimal model of probiotic therapy (strain, dose, time of intervention, etc.) in pregnant women with GDM.
Topics: Pregnancy; Female; Humans; Diabetes, Gestational; Glucose Intolerance; Probiotics; Adipokines; Cytokines
PubMed: 36296986
DOI: 10.3390/nu14204303 -
The Journal of Clinical Endocrinology... May 2022Observational studies have suggested associations between adipokines and cardiovascular disease (CVD), but the roles of certain adipokines remain controversial, and...
CONTEXT
Observational studies have suggested associations between adipokines and cardiovascular disease (CVD), but the roles of certain adipokines remain controversial, and these associations have not yet been ascertained causally.
OBJECTIVE
To investigate whether circulating adipokines causally affect the risk of CVD using 2-sample Mendelian randomization (MR).
METHODS
Independent genetic variants strongly associated with adiponectin, resistin, chemerin, and retinol binding protein 4 (RBP4) were selected from public genome-wide association studies. Summary-level statistics for CVD, including coronary artery disease (CAD), myocardial infarction, atrial fibrillation (AF), heart failure (HF), and stroke and its subtypes were collected. The inverse-variance weighted and Wald ratio methods were used for the MR estimates. The MR pleiotropy residual sum and outlier, weighted median, MR-Egger, leave-one-out analysis, MR Steiger, and colocalization analyses were used in the sensitivity analysis.
RESULTS
Genetically predicted resistin levels were positively associated with AF risk (odds ratio [OR] 1.09; 95% confidence interval [CI], 1.04-1.13; P = 4.1 × 10-5), which was attenuated to null after adjusting for blood pressure. We observed suggestive associations between higher genetically predicted chemerin levels and an increased risk of CAD (OR 1.27; 95% CI, 1.01-1.60; P = 0.040), higher genetically predicted RBP4 levels and an increased risk of HF (OR 1.14; 95% CI, 1.02-1.27; P = 0.024). There was no causal association between genetically predicted adiponectin levels and CVD risk.
CONCLUSIONS
Our findings reveal the causal association between resistin and AF, probably acting through blood pressure, and suggest potential causal associations between chemerin and CAD, RBP4, and HF.
Topics: Adipokines; Adiponectin; Atrial Fibrillation; Cardiovascular Diseases; Genome-Wide Association Study; Humans; Mendelian Randomization Analysis; Polymorphism, Single Nucleotide; Resistin; Retinol-Binding Proteins, Plasma
PubMed: 35134201
DOI: 10.1210/clinem/dgac048 -
The Journal of Clinical Investigation Oct 2019Adipose tissue plays important roles in regulating whole-body energy metabolism through its storage function in white adipocytes and its dissipating function in brown... (Review)
Review
Adipose tissue plays important roles in regulating whole-body energy metabolism through its storage function in white adipocytes and its dissipating function in brown and beige adipocytes. Adipose tissue also produces a variety of secreted factors called adipocytokines, including leptin and adiponectin. Furthermore, recent studies have suggested the important roles of extracellular vesicles of endosomal origin termed exosomes, which are secreted from adipocytes and other cells in adipose tissue and influence whole-body glucose and lipid metabolism. Adiponectin is known to be a pleiotropic organ-protective protein that is exclusively produced by adipocytes and decreased in obesity. Adiponectin accumulates in tissues such as heart, muscle, and vascular endothelium through binding with T-cadherin, a glycosylphosphatidylinositol-anchored (GPI-anchored) cadherin. Recently, adiponectin was found to enhance exosome biogenesis and secretion, leading to a decrease in cellular ceramides, excess of which is known to cause insulin resistance and cardiovascular disease phenotypes. These findings support the hypothesis that adipose tissue metabolism systemically regulates exosome production and whole-body metabolism through exosomes. This review focuses on intra-adipose and interorgan communication by exosomes, adiponectin-stimulated exosome production, and their dysregulation in metabolic diseases.
Topics: Adipokines; Adiponectin; Adipose Tissue; Animals; Cadherins; Exosomes; Glucose; Humans; Lipid Metabolism; Metabolic Syndrome; Signal Transduction
PubMed: 31483293
DOI: 10.1172/JCI129193 -
International Journal of Molecular... May 2020The World Health Organization (WHO) has recognized obesity as one of the top ten threats to human health. It is estimated that the number of obese and overweight people... (Review)
Review
The World Health Organization (WHO) has recognized obesity as one of the top ten threats to human health. It is estimated that the number of obese and overweight people worldwide exceeds the number of those who are undernourished. Obesity is not only a state of abnormally increased adipose tissue in the body, but also of increased release of biologically active adipokines. Adipokines released into the circulating blood, due to their specific receptors on the surface of target cells, act as classic hormones affecting the metabolism of tissues and organs. What is more, adipokines and cytokines may decrease the insulin sensitivity of tissues and induce inflammation and development of chronic complications. Certainly, it can be stated that in an era of a global obesity pandemic, adipokines may gain more and more importance as regards their use in the diagnostic evaluation and treatment of diseases. An extensive search for materials on the role of white, brown and perivascular fatty tissue and obesity-related metabolic and chronic complications was conducted online using PubMed, the Cochrane database and Embase.
Topics: Adipokines; Animals; Humans; Inflammation; Metabolic Diseases; Obesity
PubMed: 32443588
DOI: 10.3390/ijms21103570 -
The Journal of Clinical Investigation Dec 2021Dysregulation in adipokine biosynthesis and function contributes to obesity-induced metabolic diseases. However, the identities and functions of many of the...
Dysregulation in adipokine biosynthesis and function contributes to obesity-induced metabolic diseases. However, the identities and functions of many of the obesity-induced secretory molecules remain unknown. Here, we report the identification of leucine-rich alpha-2-glycoprotein 1 (LRG1) as an obesity-associated adipokine that exacerbates high fat diet-induced hepatosteatosis and insulin resistance. Serum levels of LRG1 were markedly elevated in obese humans and mice compared with their respective controls. LRG1 deficiency in mice greatly alleviated diet-induced hepatosteatosis, obesity, and insulin resistance. Mechanistically, LRG1 bound with high selectivity to the liver and promoted hepatosteatosis by increasing de novo lipogenesis and suppressing fatty acid β-oxidation. LRG1 also inhibited hepatic insulin signaling by downregulating insulin receptor substrates 1 and 2. Our study identified LRG1 as a key molecule that mediates the crosstalk between adipocytes and hepatocytes in diet-induced hepatosteatosis and insulin resistance. Suppressing LRG1 expression and function may be a promising strategy for the treatment of obesity-related metabolic diseases.
Topics: Adipokines; Animals; Fatty Acids; Fatty Liver; Glycoproteins; Humans; Insulin Resistance; Mice; Mice, Knockout; Obesity; Oxidation-Reduction
PubMed: 34730111
DOI: 10.1172/JCI148545