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Special Issue "Adipokines"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: closed (30 June 2017)

Special Issue Editor

Guest Editor
Prof. Dr. Christa Buechler

Department of Internal Medicine I, University Hospital Regensburg, Regensburg, Germany
Website | E-Mail
Phone: +49-941-944-7009
Fax: +49-941-944-7009
Interests: adipose tissue; obesity; non-alcoholic fatty liver disease; adiponectin; chemerin

Special Issue Information

Dear Colleagues,

This Special Issue, “Adipokines”, will cover a selection of recent research topics and current review articles related to the role of adipokines in health and disease. Up-to-date review articles, commentaries and experimental papers are all welcome.

Adipokines are released from white adipose tissues and act in an autocrine, paracrine or endocrine manner. Systemic adipokine levels have emerged as promising biomarkers in various diseases. Over the past decade, associations among adipokines and obesity, cardiovascular disease, type 2 diabetes, cancer, fertility and many more have been identified. Further research has focused on the role of these proteins in rheumatoid arthritis, inflammatory bowel disease, kidney disease, chronic liver injury, systemic lupus erythematosus and asthma just to refer to few of them. There is evidence that brown adipose tissue has its own set of secreted hormones, which may be named “brown adipokines”. These factors seem to enhance energy expenditure. Adipokine receptors are less well characterized and analysis of their tissue distribution and biological activities awaits further investigation.

Prof. Dr. Christa Buechler

Guest Editor

Manuscript Submission Information

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Keywords

  • Adipocyte
  • White adipose tissue
  • Brown adipose tissue
  • Obesity
  • Inflammation
  • Metabolic diseases
  • Cancer
  • Adipokine
  • Adipokine receptor
  • Drugs

Published Papers (13 papers)

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Research

Jump to: Review

Open AccessArticle High Expression of STAT3 in Subcutaneous Adipose Tissue Associates with Cardiovascular Risk in Women with Rheumatoid Arthritis
Int. J. Mol. Sci. 2017, 18(11), 2410; https://doi.org/10.3390/ijms18112410
Received: 29 September 2017 / Revised: 7 November 2017 / Accepted: 8 November 2017 / Published: 13 November 2017
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Abstract
Despite the predominance of female patients and uncommon obesity, rheumatoid arthritis (RA) is tightly connected to increased cardiovascular morbidity. The aim of this study was to investigate transcriptional activity in the subcutaneous white adipose tissue (WAT) with respect to this disproportionate cardiovascular risk
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Despite the predominance of female patients and uncommon obesity, rheumatoid arthritis (RA) is tightly connected to increased cardiovascular morbidity. The aim of this study was to investigate transcriptional activity in the subcutaneous white adipose tissue (WAT) with respect to this disproportionate cardiovascular risk (CVR) in RA. CVR was estimated in 182 female patients, using the modified Systematic Coronary Risk Evaluation scale, and identified 93 patients with increased CVR. The overall transcriptional activity in WAT was significantly higher in patients with CVR and was presented by higher serum levels of WAT products leptin, resistin and IL-6 (all, p < 0.001). CVR was associated with high WAT-specific transcription of the signal transducer and activator of transcription 3 (STAT3) and the nuclear factor NF-kappa-B p65 subunit (RELA), and with high transcription of serine-threonine kinase B (AKT1) in leukocytes. These findings suggest Interleukin 6 (IL-6) and leptin take part in WAT-specific activation of STAT3. The binary logistic regression analysis confirmed an independent association of CVR with IL-6 in serum, and with STAT3 in WAT. The study shows an association of CVR with transcriptional activity in WAT in female RA patients. It also emphasizes the importance of STAT3 regulatory circuits for WAT-related CVR in RA. Full article
(This article belongs to the Special Issue Adipokines)
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Open AccessArticle Novel Insights into the Adipokinome of Obese and Obese/Diabetic Mouse Models
Int. J. Mol. Sci. 2017, 18(9), 1928; https://doi.org/10.3390/ijms18091928
Received: 25 July 2017 / Revised: 19 August 2017 / Accepted: 21 August 2017 / Published: 8 September 2017
Cited by 1 | PDF Full-text (6286 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
The group of adipokines comprises hundreds of biological active proteins and peptides released from adipose tissue. Alterations of those complex protein signatures are suggested to play a crucial role in the pathophysiology of multifactorial, metabolic diseases. We hypothesized that also the pathophysiology of
[...] Read more.
The group of adipokines comprises hundreds of biological active proteins and peptides released from adipose tissue. Alterations of those complex protein signatures are suggested to play a crucial role in the pathophysiology of multifactorial, metabolic diseases. We hypothesized that also the pathophysiology of type-2-diabetes is linked to the dysregulation of the adipocyte secretome. To test this, we investigated mouse models with monogenic defects in leptin signaling which are susceptible to adipositas (C57BL/6 Cg-Lepob (obob)) or adipositas with diabetes (C57BL/KS Cg-Leprdb (dbdb)) according to their genetic background. At the age of 17 weeks, visceral fat was obtained and primary murine adipocytes were isolated to harvest secretomes. Quantitative proteome analyses (LC-ESI-MS/MS) identified more than 800 potential secreted proteins. The secretome patterns revealed significant differences connected to the pathophysiology of obese mice. Pathway analyses indicated that these differences focus on exosome modelling, but failed to provide more precise specifications. To investigate the relationship of secretome data to insulin sensitivity, we examined the content of diabetogenic lipids, i.e., diacylglycerols (DAGs), identified as key players in lipid-induced insulin resistance. In contrast to obob mice, fat tissue of dbdb mice showed elevated DAG content, especially of DAG species with saturated fatty acid C16:0 and C18:0, while unsaturated fatty acid C16:1 were only changed in obob. Furthermore, DAG signatures of the models specifically correlate to secreted regulated adipokines indicating specific pathways. In conclusion, our data further support the concept that the fat tissue is an endocrine organ that releases bioactive factors corresponding to adipose tissue health status. Full article
(This article belongs to the Special Issue Adipokines)
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Open AccessArticle Leptin Receptor Gene Variant rs11804091 Is Associated with BMI and Insulin Resistance in Spanish Female Obese Children: A Case-Control Study
Int. J. Mol. Sci. 2017, 18(8), 1690; https://doi.org/10.3390/ijms18081690
Received: 11 July 2017 / Revised: 27 July 2017 / Accepted: 28 July 2017 / Published: 3 August 2017
Cited by 4 | PDF Full-text (271 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Leptin is an endocrine hormone that has a critical role in body weight homoeostasis and mediates its effects via the leptin receptor (LEPR). Common polymorphisms in the genes coding leptin receptors have been associated with metabolic abnormalities. We assessed the association of 28
[...] Read more.
Leptin is an endocrine hormone that has a critical role in body weight homoeostasis and mediates its effects via the leptin receptor (LEPR). Common polymorphisms in the genes coding leptin receptors have been associated with metabolic abnormalities. We assessed the association of 28 LEPR polymorphisms with body mass index (BMI) and their relationship with obesity-related phenotypes, inflammation and cardiovascular disease risk biomarkers. A multicentre case-control study was conducted in 522 children (286 with obesity and 236 with normal-BMI). All anthropometric, metabolic factors and biomarkers were higher in children with obesity except apolipoprotein (Apo)-AI, cholesterol, high-density lipoprotein cholesterol (HDL-c), and adiponectin, which were lower in the obesity group; and glucose, low-density lipoprotein cholesterol (LDL-c), and matrix metalloproteinase-9 that did not differ between groups. We identified the associations between rs11208659, rs11804091, rs10157275, rs9436303 and rs1627238, and BMI in the whole population, as well as the association of rs11804091, rs10157275, and rs1327118 with BMI in the female group, although only the rs11804091 remained associated after Bonferroni correction (p = 0.038). This single nucleotide polymorphisms (SNP) was also associated with insulin (p = 0.004), homeostasis model assessment for insulin resistance (HOMA-IR) (p = 0.006), quantitative insulin sensitivity check index (QUICKI) (p = 0.005) and adiponectin (p = 0.046) after adjusting for age, Tanner stage and BMI. Our results show a sex-specific association between the rs11804091 and obesity suggesting an influence of this SNP on insulin resistance. Full article
(This article belongs to the Special Issue Adipokines)
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Open AccessArticle Subcutaneous and Visceral Adipose Tissue Secretions from Extremely Obese Men and Women both Acutely Suppress Muscle Insulin Signaling
Int. J. Mol. Sci. 2017, 18(5), 959; https://doi.org/10.3390/ijms18050959
Received: 17 February 2017 / Revised: 14 April 2017 / Accepted: 21 April 2017 / Published: 2 May 2017
Cited by 2 | PDF Full-text (689 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Adipose tissue plays a key role in the development of type-2 diabetes via the secretion of adipokines. The current study investigated if secretion media derived from intact visceral (VAT) and subcutaneous (SAT) adipose tissues from extremely obese men and women differently suppressed insulin
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Adipose tissue plays a key role in the development of type-2 diabetes via the secretion of adipokines. The current study investigated if secretion media derived from intact visceral (VAT) and subcutaneous (SAT) adipose tissues from extremely obese men and women differently suppressed insulin signaling in human skeletal myotubes derived from a healthy, non-diabetic male and female donor, respectively. Adipose tissue samples were collected from men and women during laparoscopic bariatric surgery. In general, secretion media collected from both SAT and VAT depots caused impaired insulin signaling in myotubes, independent of sex. In females, this was true regardless of the protein kinase B (Akt) phosphorylation site (Akt Thr308 and Akt Ser473) assessed (p < 0.01). In males, both SAT and VAT secretion media reduced Akt Thr308 activation in insulin-stimulated myotubes compared to controls (p < 0.001); however, only the VAT secretion media impaired Akt Ser473 phosphorylation. Independent of sex, 13 out of 18 detected cytokines, chemokines, and growth factors were more abundant in VAT versus SAT secretion media (p < 0.01). Both SAT and VAT secretion media from obese men and women acutely suppress insulin signaling in myotubes, despite different secretion profiles. We propose that this crosstalk model will help to extend our understanding of the interplay between adipose and muscle, as well as the pathogenesis of type-2 diabetes. Full article
(This article belongs to the Special Issue Adipokines)
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Open AccessArticle Sex-Dependent Effects of HO-1 Deletion from Adipocytes in Mice
Int. J. Mol. Sci. 2017, 18(3), 611; https://doi.org/10.3390/ijms18030611
Received: 3 January 2017 / Revised: 8 March 2017 / Accepted: 9 March 2017 / Published: 11 March 2017
Cited by 1 | PDF Full-text (3001 KB) | HTML Full-text | XML Full-text
Abstract
Induction of heme oxygenase-1 (HO-1) has been demonstrated to decrease body weight and improve insulin sensitivity in several models of obesity in rodents. To further study the role of HO-1 in adipose tissue, we created an adipose-specific HO-1 knockout mouse model. Male and
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Induction of heme oxygenase-1 (HO-1) has been demonstrated to decrease body weight and improve insulin sensitivity in several models of obesity in rodents. To further study the role of HO-1 in adipose tissue, we created an adipose-specific HO-1 knockout mouse model. Male and female mice were fed either a control or a high-fat diet for 30 weeks. Body weights were measured weekly and body composition, fasting blood glucose and insulin levels were determined every six weeks. Adipocyte-specific knockout of HO-1 had no significant effect on body weight in mice fed a high-fat diet but increased body weight in female mice fed a normal-fat diet. Although body weights were not different in females fed a high fat diet, loss of HO-1 in adipocytes resulted in significant alterations in body composition. Adipose-specific HO-1 knockout resulted in increased fasting hyperglycemia and insulinemia in female but not male mice on both diets. Adipose-specific knockout of HO-1 resulted in a significant loss of HO activity and a decrease in the protein levels of adiponectin in adipose tissue. These results demonstrate that loss of HO-1 in adipocytes has greater effects on body fat and fasting hyperglycemia in a sex-dependent fashion and that expression of HO-1 in adipose tissue may have a greater protective role in females as compared to males. Full article
(This article belongs to the Special Issue Adipokines)
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Open AccessArticle Lunasin Attenuates Obesity-Associated Metastasis of 4T1 Breast Cancer Cell through Anti-Inflammatory Property
Int. J. Mol. Sci. 2016, 17(12), 2109; https://doi.org/10.3390/ijms17122109
Received: 18 November 2016 / Revised: 9 December 2016 / Accepted: 12 December 2016 / Published: 15 December 2016
Cited by 5 | PDF Full-text (2891 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Obesity prevalence is increasing worldwide and is accompanied by low-grade inflammation with macrophage infiltration, which is linked with a poorer breast cancer prognosis. Lunasin is a natural seed peptide with chemopreventive properties and multiple bioactivities. This is the first study to explore the
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Obesity prevalence is increasing worldwide and is accompanied by low-grade inflammation with macrophage infiltration, which is linked with a poorer breast cancer prognosis. Lunasin is a natural seed peptide with chemopreventive properties and multiple bioactivities. This is the first study to explore the chemopreventive effects of lunasin in the obesity-related breast cancer condition using 4T1 breast cancer cells, 3T3-L1 adipocytes, and conditioned media. An obesity-related environment, such as leptin-treatment or adipocyte-conditioned medium (Ad-CM), promoted 4T1 cell proliferation and metastasis. Lunasin treatment inhibited metastasis of breast cancer cells, partially through modestly inhibiting production of the angiogenesis-mediator vascular endothelial growth factor (VEGF) and significantly by inhibiting secretion in the Ad-CM condition. Subsequently, two adipocytes inflammation models, 3T3-L1 adipocytes were stimulated by tumor necrosis factor (TNF)-α, and RAW 264.7 cell-conditioned medium (RAW-CM) was used to mimic the obese microenvironment. Lunasin significantly inhibited interleukin (IL)-6 and macrophage chemoattractant protein (MCP)-1 secretion by TNF-α stimulation, and MCP-1 secretion in the RAW-CM model. This study highlights that lunasin suppressed 3T3-L1 adipocyte inflammation and inhibited 4T1 breast cancer cell migration. Interestingly, lunasin exerted more effective anti-metastasis activity in the obesity-related condition models, indicating that it possesses anti-inflammatory properties and blocks adipocyte-cancer cell cross-talk. Full article
(This article belongs to the Special Issue Adipokines)
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Review

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Open AccessReview Role of Omentin, Vaspin, Cardiotrophin-1, TWEAK and NOV/CCN3 in Obesity and Diabetes Development
Int. J. Mol. Sci. 2017, 18(8), 1770; https://doi.org/10.3390/ijms18081770
Received: 17 July 2017 / Revised: 9 August 2017 / Accepted: 10 August 2017 / Published: 15 August 2017
Cited by 3 | PDF Full-text (2892 KB) | HTML Full-text | XML Full-text
Abstract
Adipose tissue releases bioactive mediators called adipokines. This review focuses on the effects of omentin, vaspin, cardiotrophin-1, Tumor necrosis factor-like Weak Inducer of Apoptosis (TWEAK) and nephroblastoma overexpressed (NOV/CCN3) on obesity and diabetes. Omentin is produced by the stromal-vascular fraction of visceral adipose
[...] Read more.
Adipose tissue releases bioactive mediators called adipokines. This review focuses on the effects of omentin, vaspin, cardiotrophin-1, Tumor necrosis factor-like Weak Inducer of Apoptosis (TWEAK) and nephroblastoma overexpressed (NOV/CCN3) on obesity and diabetes. Omentin is produced by the stromal-vascular fraction of visceral adipose tissue. Obesity reduces omentin serum concentrations and adipose tissue secretion in adults and adolescents. This adipokine regulates insulin sensitivity, but its clinical relevance has to be confirmed. Vaspin is produced by visceral and subcutaneous adipose tissues. Vaspin levels are higher in obese subjects, as well as in subjects showing insulin resistance or type 2 diabetes. Cardiotrophin-1 is an adipokine with a similar structure as cytokines from interleukin-6 family. There is some controversy regarding the regulation of cardiotrophin-1 levels in obese -subjects, but gene expression levels of cardiotrophin-1 are down-regulated in white adipose tissue from diet-induced obese mice. It also shows anti-obesity and hypoglycemic properties. TWEAK is a potential regulator of the low-grade chronic inflammation characteristic of obesity. TWEAK levels seem not to be directly related to adiposity, and metabolic factors play a critical role in its regulation. Finally, a strong correlation has been found between plasma NOV/CCN3 concentration and fat mass. This adipokine improves insulin actions. Full article
(This article belongs to the Special Issue Adipokines)
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Open AccessReview Epigenetic Regulation of Adipokines
Int. J. Mol. Sci. 2017, 18(8), 1740; https://doi.org/10.3390/ijms18081740
Received: 7 July 2017 / Revised: 4 August 2017 / Accepted: 8 August 2017 / Published: 10 August 2017
PDF Full-text (199 KB) | HTML Full-text | XML Full-text
Abstract
Adipose tissue expansion in obesity leads to changes in the expression of adipokines, adipocyte-specific hormones that can regulate whole body energy metabolism. Epigenetic regulation of gene expression is a mechanism by which cells can alter gene expression through the modifications of DNA and
[...] Read more.
Adipose tissue expansion in obesity leads to changes in the expression of adipokines, adipocyte-specific hormones that can regulate whole body energy metabolism. Epigenetic regulation of gene expression is a mechanism by which cells can alter gene expression through the modifications of DNA and histones. Epigenetic mechanisms, such as DNA methylation and histone modifications, are intimately tied to energy metabolism due to their dependence on metabolic intermediates such as S-adenosylmethionine and acetyl-CoA. Altered expression of adipokines in obesity may be due to epigenetic changes. The goal of this review is to highlight current knowledge of epigenetic regulation of adipokines. Full article
(This article belongs to the Special Issue Adipokines)
Open AccessReview Adipokines and Non-Alcoholic Fatty Liver Disease: Multiple Interactions
Int. J. Mol. Sci. 2017, 18(8), 1649; https://doi.org/10.3390/ijms18081649
Received: 18 July 2017 / Revised: 18 July 2017 / Accepted: 26 July 2017 / Published: 29 July 2017
Cited by 15 | PDF Full-text (985 KB) | HTML Full-text | XML Full-text
Abstract
Accumulating evidence links obesity with low-grade inflammation which may originate from adipose tissue that secretes a plethora of pro- and anti-inflammatory cytokines termed adipokines. Adiponectin and leptin have evolved as crucial signals in many obesity-related pathologies including non-alcoholic fatty liver disease (NAFLD). Whereas
[...] Read more.
Accumulating evidence links obesity with low-grade inflammation which may originate from adipose tissue that secretes a plethora of pro- and anti-inflammatory cytokines termed adipokines. Adiponectin and leptin have evolved as crucial signals in many obesity-related pathologies including non-alcoholic fatty liver disease (NAFLD). Whereas adiponectin deficiency might be critically involved in the pro-inflammatory state associated with obesity and related disorders, overproduction of leptin, a rather pro-inflammatory mediator, is considered of equal relevance. An imbalanced adipokine profile in obesity consecutively contributes to metabolic inflammation in NAFLD, which is associated with a substantial risk for developing hepatocellular carcinoma (HCC) also in the non-cirrhotic stage of disease. Both adiponectin and leptin have been related to liver tumorigenesis especially in preclinical models. This review covers recent advances in our understanding of some adipokines in NAFLD and associated HCC. Full article
(This article belongs to the Special Issue Adipokines)
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Open AccessReview Obesity and Asthma: A Missing Link
Int. J. Mol. Sci. 2017, 18(7), 1490; https://doi.org/10.3390/ijms18071490
Received: 15 June 2017 / Revised: 3 July 2017 / Accepted: 8 July 2017 / Published: 11 July 2017
Cited by 3 | PDF Full-text (735 KB) | HTML Full-text | XML Full-text
Abstract
Obesity and asthma are two chronic conditions that affect millions of people. Genetic and lifestyle factors such as diet, physical activity, and early exposure to micro-organisms are important factors that may contribute to the escalating prevalence of both conditions. The prevalence of asthma
[...] Read more.
Obesity and asthma are two chronic conditions that affect millions of people. Genetic and lifestyle factors such as diet, physical activity, and early exposure to micro-organisms are important factors that may contribute to the escalating prevalence of both conditions. The prevalence of asthma is higher in obese individuals. Recently, two major phenotypes of asthma with obesity have been described: one phenotype of early-onset asthma that is aggravated by obesity, and a second phenotype of later-onset asthma that predominantly affects women. Systemic inflammation and mechanical effect, both due to the expansion of the adipose tissue, have been proposed as the main reasons for the association between obesity and asthma. However, the mechanisms involved are not yet fully understood. Moreover, it has also been suggested that insulin resistance syndrome can have a role in the association between these conditions. The intestinal microbiota is an important factor in the development of the immune system, and can be considered a link between obesity and asthma. In the obese state, higher lipopolysaccharide (LPS) serum levels as a consequence of a microbiota dysbiosis have been found. In addition, changes in microbiota composition result in a modification of carbohydrate fermentation capacity, therefore modifying short chain fatty acid (SCFA) levels. The main objective of this review is to summarize the principal findings that link obesity and asthma. Full article
(This article belongs to the Special Issue Adipokines)
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Open AccessReview Adipokines in Liver Cirrhosis
Int. J. Mol. Sci. 2017, 18(7), 1392; https://doi.org/10.3390/ijms18071392
Received: 30 May 2017 / Revised: 23 June 2017 / Accepted: 27 June 2017 / Published: 29 June 2017
Cited by 8 | PDF Full-text (1396 KB) | HTML Full-text | XML Full-text
Abstract
Liver fibrosis can progress to cirrhosis, which is considered a serious disease. The Child-Pugh score and the model of end-stage liver disease score have been established to assess residual liver function in patients with liver cirrhosis. The development of portal hypertension contributes to
[...] Read more.
Liver fibrosis can progress to cirrhosis, which is considered a serious disease. The Child-Pugh score and the model of end-stage liver disease score have been established to assess residual liver function in patients with liver cirrhosis. The development of portal hypertension contributes to ascites, variceal bleeding and further complications in these patients. A transjugular intrahepatic portosystemic shunt (TIPS) is used to lower portal pressure, which represents a major improvement in the treatment of patients. Adipokines are proteins released from adipose tissue and modulate hepatic fibrogenesis. These proteins affect various biological processes that are involved in liver function, including angiogenesis, vasodilation, inflammation and deposition of extracellular matrix proteins. The best studied adipokines are adiponectin and leptin. Adiponectin protects against hepatic inflammation and fibrogenesis, and leptin functions as a profibrogenic factor. These and other adipokines are supposed to modulate disease severity in patients with liver cirrhosis. Consequently, circulating levels of these proteins have been analyzed to identify associations with parameters of hepatic function, portal hypertension and its associated complications in patients with liver cirrhosis. This review article briefly addresses the role of adipokines in hepatitis and liver fibrosis. Here, studies having analyzed these proteins in systemic blood in cirrhotic patients are listed to identify adipokines that are comparably changed in the different cohorts of patients with liver cirrhosis. Some studies measured these proteins in systemic, hepatic and portal vein blood or after TIPS to specify the tissues contributing to circulating levels of these proteins and the effect of portal hypertension, respectively. Full article
(This article belongs to the Special Issue Adipokines)
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Open AccessReview Adiponectin, a Therapeutic Target for Obesity, Diabetes, and Endothelial Dysfunction
Int. J. Mol. Sci. 2017, 18(6), 1321; https://doi.org/10.3390/ijms18061321
Received: 7 April 2017 / Revised: 12 June 2017 / Accepted: 13 June 2017 / Published: 21 June 2017
Cited by 29 | PDF Full-text (1108 KB) | HTML Full-text | XML Full-text
Abstract
Adiponectin is the most abundant peptide secreted by adipocytes, whose reduction plays a central role in obesity-related diseases, including insulin resistance/type 2 diabetes and cardiovascular disease. In addition to adipocytes, other cell types, such as skeletal and cardiac myocytes and endothelial cells, can
[...] Read more.
Adiponectin is the most abundant peptide secreted by adipocytes, whose reduction plays a central role in obesity-related diseases, including insulin resistance/type 2 diabetes and cardiovascular disease. In addition to adipocytes, other cell types, such as skeletal and cardiac myocytes and endothelial cells, can also produce this adipocytokine. Adiponectin effects are mediated by adiponectin receptors, which occur as two isoforms (AdipoR1 and AdipoR2). Adiponectin has direct actions in liver, skeletal muscle, and the vasculature.Adiponectin exists in the circulation as varying molecular weight forms, produced by multimerization. Several endoplasmic reticulum ER-associated proteins, including ER oxidoreductase 1-α (Ero1-α), ER resident protein 44 (ERp44), disulfide-bond A oxidoreductase-like protein (DsbA-L), and glucose-regulated protein 94 (GPR94), have recently been found to be involved in the assembly and secretion of higher-order adiponectin complexes. Recent data indicate that the high-molecular weight (HMW) complexes have the predominant action in metabolic tissues. Studies have shown that adiponectin administration in humans and rodents has insulin-sensitizing, anti-atherogenic, and anti-inflammatory effects, and, in certain settings, also decreases body weight. Therefore, adiponectin replacement therapy in humans may suggest potential versatile therapeutic targets in the treatment of obesity, insulin resistance/type 2 diabetes, and atherosclerosis. The current knowledge on regulation and function of adiponectin in obesity, insulin resistance, and cardiovascular disease is summarized in this review. Full article
(This article belongs to the Special Issue Adipokines)
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Open AccessReview Effect of High Glucose Levels on White Adipose Cells and Adipokines—Fuel for the Fire
Int. J. Mol. Sci. 2017, 18(5), 944; https://doi.org/10.3390/ijms18050944
Received: 17 March 2017 / Revised: 24 April 2017 / Accepted: 26 April 2017 / Published: 29 April 2017
PDF Full-text (178 KB) | HTML Full-text | XML Full-text
Abstract
White adipocytes release adipokines that influence metabolic and vascular health. Hypertrophic obesity is associated with adipose tissue malfunctioning, leading to inflammation and insulin resistance. When pancreatic islet β cells can no longer compensate, the blood glucose concentration rises (hyperglycemia), resulting in type 2
[...] Read more.
White adipocytes release adipokines that influence metabolic and vascular health. Hypertrophic obesity is associated with adipose tissue malfunctioning, leading to inflammation and insulin resistance. When pancreatic islet β cells can no longer compensate, the blood glucose concentration rises (hyperglycemia), resulting in type 2 diabetes. Hyperglycaemia may further aggravate adipose cell dysfunction in ~90% of patients with type 2 diabetes who are obese or overweight. This review will focus on the effects of high glucose levels on human adipose cells and the regulation of adipokines. Full article
(This article belongs to the Special Issue Adipokines)
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