Did you mean: adypokine
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European Journal of Clinical... Sep 2018Obesity, a worldwide epidemic, confers increased risk for multiple serious conditions, including type 2 diabetes, cardiovascular diseases, nonalcoholic fatty liver... (Review)
Review
Obesity, a worldwide epidemic, confers increased risk for multiple serious conditions, including type 2 diabetes, cardiovascular diseases, nonalcoholic fatty liver disease and cancer. Adipose tissue is considered one of the largest endocrine organs in the body as well as an active tissue for cellular reactions and metabolic homeostasis rather than an inert tissue for energy storage. The functional pleiotropism of adipose tissue relies on its ability to synthesize and release a large number of hormones, cytokines, extracellular matrix proteins and growth and vasoactive factors, collectively termed adipokines that influence a variety of physiological and pathophysiological processes. In the obese state, excessive visceral fat accumulation causes adipose tissue dysfunctionality that strongly contributes to the onset of obesity-related comorbidities. The mechanisms underlying adipose tissue dysfunction include adipocyte hypertrophy and hyperplasia, increased inflammation, impaired extracellular matrix remodelling and fibrosis together with an altered secretion of adipokines. This review describes how adipose tissue becomes inflamed in obesity and summarizes key players and molecular mechanisms involved in adipose inflammation.
Topics: Adipokines; Adipose Tissue; Humans; Inflammation; Intra-Abdominal Fat; Obesity
PubMed: 29995306
DOI: 10.1111/eci.12997 -
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 -
Molecular and Cellular Endocrinology Aug 2021Under conditions of nutritional and environmental stress, organismal homeostasis is preserved through inter-communication between multiple organs. To do so, higher... (Review)
Review
Under conditions of nutritional and environmental stress, organismal homeostasis is preserved through inter-communication between multiple organs. To do so, higher organisms have developed a system of interorgan communication through which one tissue can affect the metabolism, activity or fate of remote organs, tissues or cells. In this review, we discuss the latest findings emphasizing Drosophila melanogaster as a powerful model organism to study these interactions and may constitute one of the best documented examples depicting the long-distance communication between organs. In flies, the adipose tissue appears to be one of the main organizing centers for the regulation of insect development and behavior: it senses nutritional and hormonal signals and in turn, orchestrates the release of appropriate adipokines. We discuss the nature and the role of recently uncovered adipokines, their regulations by external cues, their secretory routes and their modes of action to adjust developmental growth and timing accordingly. These findings have the potential for identification of candidate factors and signaling pathways that mediate conserved interorgan crosstalk.
Topics: Adipokines; Animals; Behavior, Animal; Drosophila Proteins; Drosophila melanogaster; Fat Body; Gene Expression Regulation; Homeostasis; Models, Animal
PubMed: 34082046
DOI: 10.1016/j.mce.2021.111339 -
Seminars in Ophthalmology Oct 2023Adiponectin has also been associated with diabetic retinopathy, a diabetic microvascular complication. However, the mechanism of action of adiponectin in retinopathy is... (Review)
Review
PURPOSE
Adiponectin has also been associated with diabetic retinopathy, a diabetic microvascular complication. However, the mechanism of action of adiponectin in retinopathy is still under investigation. This review summarizes emerging evidence on the association with diabetic retinopathy in type 2 diabetes.
METHODS
We reviwed papers from 2004 to 2022 and included studies related to retinopathy and its association with blood and intraocular adiponectin in type 2 diabetes.
RESULTS
Most of the studies analyzed in this review suggested an association between the diabetic retinopathy progression and intraocular, serum, or plasma adiponectin levels. Increased levels of adiponectin contributed to the development of the disease in diabetic patients. In a minority of studies, it was indicated an inversely proportional relationship between adiponectin concentration and diabetic retinopathy severity.
CONCLUSION
The high levels of adiponectin in diabetic patients may be related to the decrease in renal clearance. Under this situation, if the predominant isoform is globular adiponectin, this may explain the retinopathy progression, considering a pro-inflammatory response induced by this isoform. However, the actions of adiponectin in diabetic retinopathy pathophysiology are still controversial.
Topics: Humans; Diabetic Retinopathy; Adiponectin; Diabetes Mellitus, Type 2; Adipokines
PubMed: 37157861
DOI: 10.1080/08820538.2023.2205929 -
International Journal of... 2021We performed a systematic literature review to summarize the underlying pathogenic mechanisms by which adipokines influence rheumatological diseases and the resulting... (Review)
Review
We performed a systematic literature review to summarize the underlying pathogenic mechanisms by which adipokines influence rheumatological diseases and the resulting clinical manifestations. Increasing evidence display that numerous adipokines may significantly influence the development or clinical course of various rheumatological diseases. Despite the normal anti- or pro-inflammatory role of the cytokines, the serum level varies enormously in various rheumatological diseases. The expression of high levels of pro-inflammatory cytokines such as leptin or visfatin, respectively in systemic lupus erythematosus and in rheumatoid arthritis, represents a negative prognostic factor; other adipokines such as adiponectin, broadly known for their anti-inflammatory effects, showed a correlation with disease activity in rheumatoid arthritis. In the near future pro-inflammatory cytokines may represent a potential therapeutic target to restrain the severity of rheumatological diseases. Further studies on adipokines may provide important information on the pathogenesis of these diseases, which are not yet fully understood. The mechanisms by which adipokines induce, worsen, or suppress inflammatory and degenerative musculoskeletal pathologies and their clinical significance will be discussed in this review.
Topics: Adipokines; Animals; Humans; Inflammation; Musculoskeletal Diseases
PubMed: 33983056
DOI: 10.1177/20587384211015034 -
International Journal of Molecular... Aug 2019Rheumatic diseases encompass a diverse group of chronic disorders that commonly affect musculoskeletal structures. Osteoarthritis (OA) and rheumatoid arthritis (RA) are... (Review)
Review
Rheumatic diseases encompass a diverse group of chronic disorders that commonly affect musculoskeletal structures. Osteoarthritis (OA) and rheumatoid arthritis (RA) are the two most common, leading to considerable functional limitations and irreversible disability when patients are unsuccessfully treated. Although the specific causes of many rheumatic conditions remain unknown, it is generally accepted that immune mechanisms and/or uncontrolled inflammatory responses are involved in their etiology and symptomatology. In this regard, the bidirectional communication between neuroendocrine and immune system has been demonstrated to provide a homeostatic network that is involved in several pathological conditions. Adipokines represent a wide variety of bioactive, immune and inflammatory mediators mainly released by adipocytes that act as signal molecules in the neuroendocrine-immune interactions. Adipokines can also be synthesized by synoviocytes, osteoclasts, osteoblasts, chondrocytes and inflammatory cells in the joint microenvironment, showing potent modulatory properties on different effector cells in OA and RA pathogenesis. Effects of adiponectin, leptin, resistin and visfatin on local and systemic inflammation are broadly described. However, more recently, other adipokines, such as progranulin, chemerin, lipocalin-2, vaspin, omentin-1 and nesfatin, have been recognized to display immunomodulatory actions in rheumatic diseases. This review highlights the latest relevant findings on the role of the adipokine network in the pathophysiology of OA and RA.
Topics: Adipokines; Animals; Arthritis, Rheumatoid; Biomarkers; Disease Susceptibility; Gene Expression Regulation; Humans; Leptin; Nicotinamide Phosphoribosyltransferase; Resistin; Signal Transduction; T-Lymphocyte Subsets
PubMed: 31443349
DOI: 10.3390/ijms20174091 -
International Journal of Molecular... Dec 2020Inflammatory colon diseases, which are a global health concern, include a variety of gastrointestinal tract disorders, such as inflammatory bowel disease and colon... (Review)
Review
Inflammatory colon diseases, which are a global health concern, include a variety of gastrointestinal tract disorders, such as inflammatory bowel disease and colon cancer. The pathogenesis of these colon disorders involves immune alterations with the pronounced infiltration of innate and adaptive immune cells into the intestines and the augmented expression of mucosal pro-inflammatory cytokines stimulated by commensal microbiota. Epidemiological studies during the past half century have shown that the proportion of obese people in a population is associated with the incidence and pathogenesis of gastrointestinal tract disorders. The advancement of understanding of the immunological basis of colon disease has shown that adipocyte-derived biologically active substances (adipokines) modulate the role of innate and adaptive immune cells in the progress of intestinal inflammation. The biomedical significance in immunological homeostasis of adipokines, including adiponectin, leptin, apelin and resistin, is clear. In this review, we highlight the existing literature on the effect and contribution of adipokines to the regulation of immunological homeostasis in inflammatory colon diseases and discuss their crucial roles in disease etiology and pathogenesis, as well as the implications of these results for new therapies in these disorders.
Topics: Adipokines; Adipose Tissue; Animals; Biomarkers; Disease Susceptibility; Homeostasis; Humans; Immune System; Immunomodulation; Inflammatory Bowel Diseases
PubMed: 33334069
DOI: 10.3390/ijms21249564 -
International Journal of Molecular... Sep 2019Chemerin is widely recognized as an adipokine, with diverse biological roles in cellular differentiation and metabolism, as well as a leukocyte chemoattractant. Research... (Review)
Review
Chemerin is widely recognized as an adipokine, with diverse biological roles in cellular differentiation and metabolism, as well as a leukocyte chemoattractant. Research investigating the role of chemerin in the obesity-cancer relationship has provided evidence both for pro- and anti-cancer effects. The tumor-promoting effects of chemerin primarily involve direct effects on migration, invasion, and metastasis as well as growth and proliferation of cancer cells. Chemerin can also promote tumor growth via the recruitment of tumor-supporting mesenchymal stromal cells and stimulation of angiogenesis pathways in endothelial cells. In contrast, the majority of evidence supports that the tumor-suppressing effects of chemerin are immune-mediated and result in a shift from immunosuppressive to immunogenic cell populations within the tumor microenvironment. Systemic chemerin and chemerin produced within the tumor microenvironment may contribute to these effects via signaling through CMKLR1 (chemerin), GPR1 (chemerin), and CCLR2 on target cells. As such, inhibition or activation of chemerin signaling could be beneficial as a therapeutic approach depending on the type of cancer. Additional studies are required to determine if obesity influences cancer initiation or progression through increased adipose tissue production of chemerin and/or altered chemerin processing that leads to changes in chemerin signaling in the tumor microenvironment.
Topics: Adipokines; Animals; Biomarkers; Chemokines; Disease Susceptibility; Humans; Immunomodulation; Neoplasms; Obesity; Organ Specificity; Protein Binding; Signal Transduction
PubMed: 31561459
DOI: 10.3390/ijms20194778 -
Current Opinion in Pharmacology Jun 2020Both skeletal muscle and adipose tissue are considered as endocrine organs due to their ability to produce and secrete several bioactive peptides (e.g. myokines and... (Review)
Review
Both skeletal muscle and adipose tissue are considered as endocrine organs due to their ability to produce and secrete several bioactive peptides (e.g. myokines and adipokines). Those bioactive molecules are well known for their capacity to influence whole-body homeostasis and alterations in their production/secretion are contributing to the development of various metabolic disorders. While it is well accepted that changes in the composition and functionality of the gut microbiota are associated with the onset of several pathological disorders (e.g. obesity, diabetes, and cancer), its contribution to the regulation of the myokine-adipokine profile and function remains largely unknown. This review will focus on myokines and adipokines with a special interest on their interaction with the gut microbiota.
Topics: Adipokines; Adipose Tissue; Animals; Exercise; Gastrointestinal Microbiome; Humans; Muscle, Skeletal; Muscle, Smooth; Myocardium
PubMed: 32388413
DOI: 10.1016/j.coph.2020.03.006 -
Endocrinology, Diabetes & Metabolism May 2023Adipose tissue is the source of a broad array of signalling molecules (adipokines), which mediate interorgan communication and regulate metabolic homeostasis.... (Review)
Review
INTRODUCTION
Adipose tissue is the source of a broad array of signalling molecules (adipokines), which mediate interorgan communication and regulate metabolic homeostasis. Alterations in adipokine levels have been causally implicated in various metabolic disorders, including changes in bone mass. Osteoporosis is the commonest progressive metabolic bone disease, characterized by elevated risk of fragility fractures as a result of a reduced bone mass and microarchitectural deterioration. The effects of different adipokines on bone mass have been studied in an attempt to identify novel modulators of bone mass or diagnostic biomarkers of osteoporosis.
METHODS
In this review, we sought to aggregate and assess evidence from independent studies that quantify specific adipokines and their effect on bone mineral density (BMD).
RESULTS
A literature search identified 57 articles that explored associations between different adipokines and BMD. Adiponectin and leptin were the most frequently studied adipokines, with most studies demonstrating that adiponectin levels are associated with decreased BMD at the lumbar spine and femoral neck. Conversely, leptin levels are associated with increased BMD at these sites. However, extensive heterogeneity with regards to sample size, characteristics of study subjects, ethnicity, as well as direction and magnitude of effect at specific skeletal anatomical sites was identified. The broad degree of conflicting findings reported in this study can be attributed several factors. These include differences in study design and ascertainment criteria, the analytic challenges of quantifying specific adipokines and their isoforms, pre-analytical variables (in particular patient preparation) and confounding effects of co-existing disease.
CONCLUSIONS
This review highlights the biological relevance of adipokines in bone metabolism and reinforces the need for longitudinal research to elucidate the causal relationship of adipokines on bone mass.
Topics: Humans; Adipokines; Bone Density; Leptin; Adiponectin; Osteoporosis
PubMed: 36759562
DOI: 10.1002/edm2.408