Potential Role Of Adiponectin Research Articles

Erratum: Addendum: Metabolic Syndrome, and Particularly the Hypertriglyceridemic-Waist Phenotype, Increases Breast Cancer Risk, and Adiponectin Is a Potential Mechanism: A Case-Control Study in Chinese Women.

[This corrects the article DOI: 10.3389/fendo.2019.00905.].

Role of Adiponectin in prostate cancer.

ABSTRACTObesity is defined as a chronic and excessive growth of adipose tissue. It has been associated with a high risk for development and progression of obesity-associated malignancies, while adipokines may mediate this association. Adiponectin is an adipose tissue-derived adipokines, with significant anti-diabetic, anti-inflammatory, anti-atherosclerotic and anti-proliferative properties. Plasma adiponectin levels are decreased in obese individuals, and this feature is closely correlated with development of several metabolic, immunological and neoplastic diseases. Recent studies have shown that prostate cancer patients have lower serum adiponectin levels and decreased expression of adiponectin receptors in tumor tissues, which suggests plasma adiponectin level is a risk factor for prostate cancer. Furthermore, exogenous adiponectin has exhibited therapeutic potential in animal models. In this review, we focus on the potential role of adiponectin and the underlying mechanism of adiponectin in the development and progression of prostate cancer. Exploring the signaling pathways linking adiponectin with tumorigenesis might provide a potential target for therapy.

Clinical and Humoral Determinants of Congestion in Heart Failure: Potential Role of Adiponectin

Background: Some patients with heart failure (HF) are more prone to systemic congestion than others. The goal of this study was to identify clinical and humoral factors linked to congestion and its prognostic impact in HF patients. Methods: A total of 371 advanced HF patients underwent physical examination, echocardiography, right heart catheterization, blood samplings, and Minnesota Living with HF Questionnaire. Subjects were followed-up for adverse events (death, urgent transplantation, or assist device implantation without heart transplantation). Results: Thirty-one percent of patients were classified as prone to congestion. During a median follow-up of 1,093 days, 159 (43%) patients had an adverse event. In the Cox analysis, the congestion-prone (CP) status was associated with a 43% higher event risk. The CP status was strongly (p ˂ 0.001) associated with body weight loss, right ventricular dysfunction (RVD), dilated inferior vena cava (IVC), diuretics, and beta-blockers prescription and the majority of tested hormones in the univariate analysis. In the multivariate analysis, the only independent variables associated with the CP status were adiponectin, albumin, IVC diameter, and RVD. Adiponectin by itself was predictive of adverse events. In a multivariate model, CP status was no longer predictive of adverse events, in contrast to adiponectin. Conclusions: CP patients experienced more severe symptoms and had shorter survival. Potential role of adiponectin, a new independent predictor of CP status, should be further examined.

Exercise augments the modulatory effects of vitamin E on pre-diabetes-induced aortopathy: a potential role of adiponectin

Background: We tested the hypothesis that vitamin E may protect against pre-diabetes-induced aortic injury (aortopathy), and exercise can augment the action of vitamin E.Material and methods: Rats were either fed with a high fat and fructose diet (HFD) (model group) or a standard laboratory chow (control group) for 15 weeks before being sacrificed. The three protective groups were treated with vitamin E (HFD + Vit E), swimming exercises (HFD + Ex), and vitamin E plus swimming exercises (HFD + VitE + Ex), respectively.Results: Aortopathy was developed in the model group as demonstrated by substantial tissue ultrastructural alterations, which were partially protected by vitamin E and effectively protected with vitamin E plus swim exercise. Also, swimming exercises significantly (p < .05) increased the modulatory effects of vitamin E on dyslipidemia, insulin resistance, blood pressure, oxidative stress, inflammation, leptin, and adiponectin, except coagulation and thrombosis.Conclusions: Swim exercise augments the protective effects of vitamin E in a pre-diabetic animal model.

Adiponectin, Leptin, IGF-1, and Tumor Necrosis Factor Alpha As Potential Serum Biomarkers for Non-Invasive Diagnosis of Colorectal Adenoma in African Americans.

The potential role of adiponectin, leptin, IGF-1, and tumor necrosis factor alpha (TNF-α) as biomarkers in colorectal adenoma is not clear. Therefore, we aimed to investigate the blood serum levels of these biomarkers in colorectal adenoma. The case–control study consisted of serum from 180 African American patients with colon adenoma (cases) and 198 healthy African Americans (controls) at Howard University Hospital. We used ELISA for adiponectin, leptin, IGF-1, and TNF-α detection and quantification. Statistical analysis was performed by t-test and multivariate logistic regression. The respective differences in median leptin, adiponectin, IGF-1, and TNF-α levels between control and case groups (13.9 vs. 16.4), (11.3 vs. 46.0), (4.5 vs. 12.9), and (71.4 vs. 130.8) were statistically significant (P < 0.05). In a multivariate model, the odds ratio for adiponectin, TNF-α, and IGF-1 were 2.0 (95% CI = 1.6–2.5; P < 0.001), 1.5 (95% CI = 1.5(1.1–2.0); P = 0.004), and 1.6 (95% CI = 1.3–2.0; P < 0.001), respectively. There was a positive correlation between serum adiponectin and IGF-1 concentrations with age (r = 0.17, P < 0.001 and r = 0.13, P = 0.009), TNF-α, IGF-1, and leptin concentration with body mass index (BMI) (r = 0.44, P < 0.001; r = 0.11, P = 0.03; and r = 0.48, P < 0.001), respectively. Also, there was a negative correlation between adiponectin and leptin concentrations with BMI (r = −0.40, P < 0.001), respectively. These data support the hypothesis that adiponectin, IGF-1, and TNF-α high levels correlate with higher risk of colon adenoma and can thus be used for colorectal adenomas risk assessment.

Abstract 3130: Adiponectin, Leptin, IGF1 and TNFα serum biomarker as noninvasive diagnosis of colon adenoma

Abstract Background and Aim: The potential role of Adiponectin, Leptin, IGF1 and TNFα as biomarker in colon adenoma has not been studied. Therefore, we investigated the blood serum levels of these biomarkers in colorectal adenoma. Method: The case-control study consisted of 198 African American patients with colon adenoma (cases) and 198 healthy individuals (controls) at Howard University Hospital. We used Elisa for biomarkers detection. Statistical analysis was performed by t-test and multivariate logistic regression. Results: The differences in median leptin, Adiponectin, IGF1 and TNFα levels between control and case groups (6.7 vs.16.4), (11.3 vs.46.0), (4.5 vs.12.9) and (71.4 vs. 130.8) were statistically significant (p&amp;lt;0.05), respectively. In a multivariate model, the odds ratio (ORs) for Adiponectin, TNFα and IGF1 were 2.0 (95% CI = 1.6-2.5; P≤0.001), 1.5 (95% CI = 1.5- 2.0; P 0.004) and 1.6 (95% CI = 1.3-2.0; P≤ 0.001), respectively. There were positive correlations between serum Adiponectin and IGF1 concentrations with age (r = 0.17, P≤ 0.001 and r = 0.13, P = 0.009), also between TNFα, IGF1 and Leptin concentration with Body Mass Index (BMI) (r = 0.44, P≤ 0.001 and r = 0.11, P = 0.03; r = 0.48, P≤0.001), respectively. There was a negative correlation between Adiponectin concentration and BMI (r = -0.40, P≤0.001), respectively. Conclusion: These data support the hypothesis that serum Adiponectin, IGF1 and TNFα are risk biomarkers for noninvasive detection of colorectal adenomas. Citation Format: Hassan Ashktorab, Akbar Soleimani, Alexandra Nichols, Komal Sodhi, Lakshmi Kannan, Laiyemo Adeyinka, Mehdi Nouraie, Hassan Brim. Adiponectin, Leptin, IGF1 and TNFα serum biomarker as noninvasive diagnosis of colon adenoma. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3130.

Abstract 480: Exacerbation of Arterial Stiffness in Obese Adiponectin Deficient Mice

Background and Objective: Arterial stiffness is recognized as being an independent predictor of incipient vascular disease associated with obesity and metabolic syndrome. In obese subjects, the decrease in the plasma level of adiponectin, an anti-diabetic and anti-atherogenic adipokine, is well known. Hence the aim of our study was to examine the effect of loss of adiponectin on the development of arterial stiffness in response to a high fat diet. Methods and Results: Male 8-week old adiponectin knockout (APN KO) and C57BL/6 (control) mice were fed a high fat diet (60% Calories from fat) for 12 weeks to induce obesity and insulin resistance (n=10/group). APN KO and C57BL/6 mice were fed a low fat diet (10% Calories from fat) and used as lean controls (n=10/group). After 12 weeks on the high fat diet, the APN KO mice weighed significantly more than the C57BL/6 mice (45.1±1.3 g vs 40.1±1.1 g, p=0.0008) but there was no difference in the final weights between genotypes fed the low fat diet. APN KO mice on both high and low fat diets for 12 weeks developed insulin resistance as measured by oral glucose tolerance test (Area under curve (AUC) mmol/L х min = 437±70 and 438±57) as compared to the C57BL/6 mice fed low or high fat diets (AUC mmol/L х min = 251±27 and 245±43). Arterial stiffness was determined by Doppler pulse wave velocity analysis of the femoral artery. Pulse wave velocity was increased in APN KO mice fed a high fat diet relative to those fed the low fat diet (12.56±0.78 cm/s vs 9.47±0.95 cm/s, p=0.0035; n=8-10). Pulse wave velocity was not different between C57BL/6 control mice on the low or high fat diets (10.63±0.73 cm/s and 10.86±0.50 cm/s), thus revealing that only mice deficient in adiponectin developed arterial stiffness in response to high fat diet. Conclusions: Potentiation of the vascular stiffness in diet-induced obese APN KO mice indicates that adiponectin has a role in modulating vascular structure and the APN KO mouse models the vascular changes that occur in human obesity and metabolic disorders. Morphometric analysis of the aortic tissues for vessel thickness and expression of extracellular proteins will further validate the potential role of adiponectin on the maintenance of arterial elasticity in addition to its known effect on eNOS mediated vasoprotection.

Prediagnostic plasma adiponectin and survival among patients with colorectal cancer.

526 Background: Adiponectin is a hormone secreted by adipose tissue and has been demonstrated to possess anticarcinogenic, anti-inflammatory and insulin-sensitizing effects. Circulating adiponectin has been shown to be inversely associated with the risk of colorectal cancer (CRC) in prospective studies. However, the association of prediagnostic adiponectin with survival among patients with established colorectal cancer is unclear. Methods: We conducted a prospective study of 621 incident colorectal cancer cases from the Nurses’ Health Study and Health Professionals Follow-up Study to evaluate the association between prediagnostic plasma adiponectin and mortality. Plasma adiponectin levels were determined by enzyme-linked immunosorbent assay from ALPCO Diagnostics. The interbatch coefficient of variation from quality control samples randomly interspersed among the case samples was 8.6%. We examined the associations between quartiles of plasma adiponectin and mortality using a Cox proportional hazards model adjusted for established and putative risk factors. All statistical tests were two sided. Results: After a median follow-up of 9 years, there were 267 (43%) total deaths and 130 (21%) CRC deaths in the total study cohort. Compared with patients in the lowest quartile of adiponectin, patients in the highest quartile had a multivariate hazard ratio (HR) for CRC-specific mortality of 2.70 [95% confidence interval (CI), 1.54-4.75; Ptrend = 0.001]. The corresponding multivariate HR for overall mortality was 1.64 (95% CI, 1.14-2.36; Ptrend = 0.007). These associations were reasonably consistent in analyses according to subgroups defined by age, gender, body mass index, stage, grade and site of primary cancer. Similar results were yielded after excluding patients diagnosed within 4 years of blood collection (Ptrend = 0.027). Conclusions: Prediagnostic adiponectin is associated with an increased risk of colorectal cancer- specific and overall mortality. Further studies are needed to elucidate the mechanistic basis for these findings and determine the potential role of adiponectin as a prognostic marker in colorectal cancer.

The potential role of adiponectin- and resistin-like peptides in the regulation of lipid levels in the hemolymph of over-wintering adult females of Osmia bicornis

The presence and potential role of adiponectin- and resistin-like peptides in mobilizing free lipids of hemolymph during over-wintering was studied in females of the European solitary red mason bee Osmia bicornis L. (Hymenoptera: Megachilidae). The levels of both peptides (as demonstrated both by RIA/ELISA and Western blots) were highest in fat body tissue homogenates during early pre-wintering (September) followed by a gradual and significant decline during wintering and post-wintering months (November–March). There was a gradual reduction of the lipid levels in hemolymph and adiponectin-like and resistin-like peptide content in fat body. Thus, the total lipid content in hemolymph and the adiponectin-like and resistin-like peptides in fat body homogenates was positively correlated. Our experiments also demonstrated that injections of various concentrations of fat body extracts as well as various doses of adiponectin and resistin increased the lipid levels in hemolymph in O. bicornis females at the three different periods of over-wintering time. In particular, injections of fat body extract and adiponectin resulted in the strongest mobilization of lipids especially in the first two periods of over-wintering: pre-wintering and wintering. Resistin also elicited an increase of lipid levels in hemolymph, but its effectiveness was lower compared to fat body extract and adiponectin. Taken together, our results strongly suggest the presence of adiponectin-like and resistin-like peptides in the fat body of O. bicornis and postulate a dynamic physiological role for these peptides during the process of over-wintering.

Adiponectin in Diabetes Mellitus

Adiponectin represents one of the most abundant and well-studied adipokines that has been implicated as a major protective factor against the adverse metabolic and cardiovascular consequences of obesity. The main insulin-sensitizing action of adiponectin results from decrease in hepatic gluconeogenesis and increase in muscle glucose transport and, secondly from enhancement of energy consumption and fatty acid oxidation in peripheral tissues with the aim of increasing ATP production. Besides these effects, the potential role of adiponectin on insulin secretion, as well as on energy expenditure, through central action, has also been investigated. Accumulating evidence from clinical, experimental animal and genetic studies support a close association between hypoadiponectinemia and insulin resistance/ type 2 diabetes. The question that arises is whether hypoadiponectinemia is the result of insulin resistance/type 2 diabetes or the cause of this disorder. Based on the observation that various drug classes exert beneficial effects on insulin resistance partly by increasing plasma adiponectin levels, it could hypothesized that substances that enhance or mimic adiponectin to activate its receptors and/or postreceptor signaling pathway may be a promising therapeutic strategy in the prevention and treatment of diabetes. However, many questions need to be addressed before adiponectin can be used as a potent therapeutic target.

Adiponectin and breast cancer

Adiponectin, an adipose tissue-derived hormone, has been studied intensively for the past decade because of its anti-inflammatory, anti-atherogenic, and anti-diabetic properties. Recent advances suggest that adiponectin also plays an important role in the development and progression of various cancers, especially obesity-related cancers. In this review, the authors focus on the potential role of adiponectin in breast cancer, an obesity- and endocrine-associated tumor. Epidemiological studies have shown that plasma adiponectin level is a risk factor for breast cancer in post-menopausal women. Adiponectin and its receptors are expressed on both breast cancer line cells and tumor tissues. Furthermore, exogenous adiponectin has exhibited therapeutic potential in animal models. Underlying mechanisms include the inhibition of cell proliferation and promotion of apoptosis, the regulation of tumorigenic-related factors, and the suppression of angiogenesis. The signaling pathways linking adiponectin with tumorigenesis might provide potential drug targets for the future. However, more convincing evidence is needed to fully elucidate the exact role of adiponectin in breast cancer, since both its beneficial effects and possible mechanisms remain controversial.

Abstract A123: Common polymorphisms in adiponectin and adiponectin receptor genes and prostate cancer survival

Abstract Background: Adiponectin, an adipokine with anti-inflammatory and insulin-sensitizing properties, is inversely associated with adiposity. Our group previously showed that high circulating levels of adiponectin were inversely associated with prostate cancer (PCa) risk and progression. Moreover, four polymorphisms in ADIPOQ, a gene encoding adiponectin, were significantly associated with overall PCa risk, two of which were also associated with plasma adiponectin levels. However, the role of genetic variation in ADIPOQ and the adiponectin receptor genes ADIPOR1 and ADIPOR2 in PCa progression remains unknown. We related polymorphisms in ADIPOQ, ADIPOR1, and ADIPOR2 to PCa survival, ADIPOR2 expression, and a biomarker of proliferation. Methods: Using genotype data from 1286 cases from the Physicians' Health Study, we evaluated 29 common SNPs in ADIPOQ, ADIPOR1 and ADIPOR2 with the development of lethal PCa, defined as progression to bony metastases or PCa-specific death, during 25 years of follow-up. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (95% CIs). We assumed a codominant genotype model and assessed the association between each genotype and PCa survival by a p-value from a likelihood ratio test comparing models with and without the heterozygote and rare homozygote indicator variables. Using ANOVA, we also evaluated each genotype with tumor expression of ki67 (n=203), a marker of cellular proliferation, and ADIPOR2 (n=180) for a subset of cases. Results: Two polymorphisms, one in ADIPOR1 and one in ADIPOR2, were significantly associated with time to lethal PCa. Compared to wildtype homozygotes for ADIPOR1 SNP rs16850799, the HRs for lethal PCa were 1.1 (95% CI: 0.8, 1.6) for heterozygotes and 2.5 (95% CI: 1.4, 4.4) for rare homozygotes (p=0.02). The variant allele for rs16850799 was also associated with increased cellular proliferation in prostate tumors (p=0.004). For ADIPOR2 rs1044471, the HRs compared to wildtype homozygotes were 0.6 (95% CI: 0.4, 0.9) for heterozygotes and 0.9 (95% CI: 0.6, 1.3) for rare homozygotes (p=0.03). The variant allele for rs1044471 was associated with lower expression levels of ADIPOR2 (p=0.03). Conclusions: Of 29 SNPs evaluated in ADIPOQ, ADIPOR1 and ADIPOR2, we found two polymorphic loci (ADIPOR1 rs16850799 and ADIPOR2 rs1044471) to be associated with PCa progression and death. Variant allele carriers of the rs16850799 polymorphism in ADIPOR1 were more likely to develop lethal PCa and exhibited phenotypic changes consistent with disease aggressiveness in their tumors. Variant allele status in ADIPOR2 rs1044471 predicted ADIPOR2 expression levels. None of the four SNPs in ADIPOQ that we previously found to be associated with PCa risk were associated with time to lethal PCa. Our work suggests a potential role of adiponectin and its receptors in mediating the association between obesity and aggressive PCa. Citation Information: Cancer Prev Res 2010;3(1 Suppl):A123.

Adiponectin action from head to toe

Adiponectin, the most abundant protein secreted by white adipose tissue, is known for its involvement in obesity-related disorders such as insulin resistance, type 2 diabetes mellitus and atherosclerosis. Moreover, modulation of the circulating adiponectin concentration is observed in pathologies that are more or less obesity-related, such as cancer and rheumatoid arthritis. The wide distribution of adiponectin receptors in various organs and tissues suggests that adiponectin has pleiotropic effects on numerous physiological processes. Besides its well-known insulin-sensitizing, anti-inflammatory and antiatherosclerotic properties, accumulating evidence suggests that adiponectin may also have anticancer properties and be cardioprotective. A beneficial effect of adiponectin on female reproductive function was also suggested. Since adiponectin has numerous beneficial biological functions, its use as a therapeutic agent has been suggested. However, the use of adiponectin or its receptors as therapeutic targets is complicated by the presence of different adiponectin oligomeric isoforms and production sites, by multiple receptors with differing affinities for adiponectin isoforms, and by cell-type-specific effects in different tissues. In this review, we discuss the known and potential roles of adiponectin in various tissues and pathologies. The therapeutic promise of administration of adiponectin and the use of its circulating levels as a diagnostic biomarker are further discussed based on the latest experimental studies.

Review: Adiponectin for prediction of cardiovascular risk?

Adiponectin is an endogenous insulin-sensitising and anti-inflammatory hormone, released by the adipose tissue. Because of its in vitro effects on endothelial cells, macrophages and vascular smooth muscle cells, adiponectin is thought to have anti-atherogenic properties. Moreover, findings from the Health Professionals Follow-up Studies and other cohort studies, mainly in male populations, suggest that adiponectin may be an independent predictor for cardiovascular risk. This, however, was not confirmed by subsequent studies that included female subjects, different ethnicities and patients with established coronary artery disease. The present article briefly summarises recent findings regarding the potential role of adiponectin as a predictor of risk and its biological role. Br J Diabetes Vasc Dis 2009;9: 150—154

Associations of Serum Adiponectin with Skeletal Muscle Morphology and Insulin Sensitivity

Skeletal muscle morphology and function are strongly associated with insulin sensitivity. The objective of the study was to test the hypothesis that circulating adiponectin is associated with skeletal muscle morphology and that adiponectin mediates the relation of muscle morphology to insulin sensitivity. This was a cross-sectional investigation of 461 men aged 71 yr, participants of the community-based Uppsala Longitudinal Study of Adult Men study. Measures included serum adiponectin, insulin sensitivity measured with euglycemic insulin clamp technique, and capillary density and muscle fiber composition determined from vastus lateralis muscle biopsies. In multivariable linear regression models (adjusting for age, physical activity, fasting glucose, and pharmacological treatment for diabetes), serum adiponectin levels rose with increasing capillary density (beta, 0.30 per 50 capillaries per square millimeter increase; P = 0.041) and higher proportion of type I muscle fibers (beta, 0.27 per 10% increase; P = 0.036) but declined with a higher proportion of type IIb fibers (beta, -0.39 per 10% increase; P = 0.014). Using bootstrap methods to examine the potential role of adiponectin in associations between muscle morphology and insulin sensitivity and the associations of capillary density (beta difference, 0.041; 95% confidence interval 0.001, 0.085) and proportion of type IIb muscle fibers (beta difference, -0.053; 95% confidence interval -0.107, -0.002) with insulin sensitivity were significantly attenuated when adiponectin was included in the models. Circulating adiponectin concentrations were higher with increasing skeletal muscle capillary density and in individuals with higher proportion of slow oxidative muscle fibers. Furthermore, our results indicate that adiponectin could be a partial mediator of the relations between skeletal muscle morphology and insulin sensitivity.

Adiponectin inhibits steatotic CD95/Fas up-regulation by hepatocytes: Therapeutic implications for hepatitis C

Steatosis may trigger hepatocytes to up-regulate CD95/Fas thereby increasing susceptibility to apoptosis, inflammation and fibrosis. We investigated this concept and potential roles of adiponectin and its receptors (AdipoR1; AdipoR2) in chronically HCV-infected patients. In 98 HCV+ patients and 20 controls, sera were tested for HCV genotypes, FFAs, adiponectin and the M30 apoptosis indicator, and biopsies were evaluated for steatosis/inflammation/fibrosis, CD95/Fas (mRNA/protein), adiponectin (mRNA/protein), AdipoR1/-R2 (mRNA) and M30 (protein). We also questioned whether adiponectin protects HepG2 hepatoblastoma cells from FFA-triggered CD95/Fas up-regulation and apoptosis. Patients [HCV clades 1 (78%), 2 (3%) and 3 (19%)] revealed increased FFA and adiponectin serum levels (p = .005). Hepatocyte CD95/Fas up-regulation correlated with steatosis, inflammation and fibrosis (p = .004). Advanced fibrosis correlated significantly (p = .05) with serum M30. Liver adiponectin correlated with steatosis (p = .016), CD95/Fas (p < .001) and inflammation/fibrosis. Hepatocyte AdipoR2 mRNA specifically correlated with serum adiponectin and steatosis (p = .003), while hepatocyte AdipoR1 mRNA dropped in pronounced fibrosis (p = .060). Finally, adiponectin protected HepG2 cells from FFA-triggered CD95/Fas expression and induction of apoptosis (p = .0396). In chronic HCV infection, steatosis up-regulates hepatocyte CD95/Fas and thus increases apoptosis, which facilitates inflammation and fibrosis. The physiologic countermeasure of adiponectin up-regulation may offer clues for future therapeutic intervention.

Adiponectin: a link between obesity and cancer

Adiponectin, an insulin-sensitising hormone produced by adipocytes, has direct antidiabetic, antiatherogenic, anti-inflammatory and antiangiogenic properties. Circulating adiponectin levels are lower in obesity, a disease state that is associated with certain malignancies. Recently, accumulating evidence suggests that adiponectin may have an important protective role in carcinogenesis. There is also evidence that at least some, if not most, cancer cell types express adiponectin receptors; thus adiponectin may act on tumour cells directly by binding and activating adiponectin receptors and downstream signalling pathways. Through its antiangiogenic properties, and also possibly through other mechanisms regulating cell proliferation discussed in this review, adiponectin may prove to be an effective novel anticancer agent. Large association and prospective studies to assess adiponectin levels in relation to risk from cancer, as well as mechanistic studies to prove adiponectin’s role in the development of malignancies, and interventional trials to address potential roles of adiponectin in cancer pathogenesis and therapeutics are needed.

The potential role of adiponectin in driving arthritis

The potential role of adiponectin in driving arthritis