Adiponectin Levels and Risk of Type 2 Diabetes

Li, Shanshan; Shin, Hyun Joon; Ding, Eric L.; Dam, Rob M. van

doi:10.1001/jama.2009.976

Cited by 882 publications

(557 citation statements)

References 42 publications

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“…Consistent with this, analysis of plasma adiponectin complexes in CML patients, before and after 3 months of imatinib therapy, revealed a significant increase in the level of HMW complexes . In humans, adiponectin levels correlate negatively with insulin resistance and metabolic syndrome, with low adiponectin levels being associated with a higher risk of type 2 diabetes (Li et al 2009). Thiazolidinedione compounds, a class of anti-diabetic drugs that improve systemic insulin sensitivity, are thought to work, at least in part, by promoting the formation of small adipocytes that secrete high levels of HMW adiponectin , Phillips et al 2003, Nawrocki et al 2006.…”

Section: Imatinib Promotes Adipogenesis S Fitter and Others 235mentioning

confidence: 99%

Suppression of PDGF-induced PI3 kinase activity by imatinib promotes adipogenesis and adiponectin secretion

Fitter¹,

Vandyke²,

Gronthos³

et al. 2012

Journal of Molecular Endocrinology

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Improved glucose and lipid metabolism is a unique side effect of imatinib therapy in some chronic myeloid leukaemia (CML) patients. We recently reported that plasma levels of adiponectin, an important regulator of insulin sensitivity, are elevated following imatinib therapy in CML patients, which could account for these improved metabolic outcomes. Adiponectin is secreted exclusively from adipocytes, suggesting that imatinib modulates adiponectin levels directly, by transcriptional upregulation of adiponectin in pre-existing adipocytes, and/or indirectly, by stimulating adipogenesis. In this report, we have demonstrated that imatinib promotes adipogenic differentiation of human mesenchymal stromal cells (MSCs), which in turn secrete high-molecular-weight adiponectin. Conversely, imatinib does not stimulate adiponectin secretion from mature adipocytes. We hypothesise that inhibition of PDGFRa (PDGFRA) and PDGFRb (PDGFRB) is the mechanism by which imatinib promotes adipogenesis. Supporting this, functional blocking antibodies to PDGFR promote adipogenesis and adiponectin secretion in MSC cultures. We have shown that imatinib is a potent inhibitor of PDGF-induced PI3 kinase activation and, using a PI3 kinase p110a-specific inhibitor (PIK-75), we have demonstrated that suppression of this pathway recapitulates the effects of imatinib on MSC differentiation. Furthermore, using mitogens that activate the PI3 kinase pathway, or MSCs expressing constitutively activated Akt, we have shown that activation of the PI3 kinase pathway negates the pro-adipogenic effects of imatinib. Taken together, our results suggest that imatinib increases plasma adiponectin levels by promoting adipogenesis through the suppression of PI3 kinase signalling downstream of PDGFR.

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Section: Imatinib Promotes Adipogenesis S Fitter and Others 235mentioning

confidence: 99%

Suppression of PDGF-induced PI3 kinase activity by imatinib promotes adipogenesis and adiponectin secretion

Fitter¹,

Vandyke²,

Gronthos³

et al. 2012

Journal of Molecular Endocrinology

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“…Risk of T2DM appeared to decrease with increasing adiponectin levels. Currently, adiponectin is one of the strongest biochemical predictors of T2DM [116]. In this study, diabetic patients showed significantly decreased serum adiponectin levels compared to the controls.…”

Section: Resultsmentioning

confidence: 50%

Exploration of the Relationship between Adipocytokines, Tradition Risk Markers, Nontraditional Risk Markers and Anthropometric Measurements in T2DM Patients

Al-Sowayan¹

2015

JBiSE

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Obesity is commonly associated with type 2 diabetes and vascular disease. Changes in body composition in the obese state lead to a dysregulation of secretion of adipocyte-secreted hormones known as adipokines. The current study aimed to assess the relative physiological correlation of adipocytokines with immunity in urban Saudi patients. The serum adipocytokine (leptin, adiponectin, resistin, visfatin and apelin), metabolic parameters (insulin, fasting glucose, HbA1c % (Glycated Hemoglobin) immunological indices (IgG, IgA, IgM and IgE) and complement factors (C3, C4) in different metabolic disorders states such as obesity and T2DM (Type 2 Diabetes Mellitus) were determined. A total 100 adult male subjects were enrolled including 30 healthy that served as a control, 25 Glucophage treated T2DM, 22 overweight (Body Mass Index (BMI) ≥ 25 -29.99) and 23 obese (BMI ≥ 30) patients. The current results showed that serum adipocytokines status has altered in obesity and treated T2DM compared to healthy individuals. In addition to HbA1c %, serum visfatin was also the prominent biomarker adipokine in treated T2DM while leptin was the highest in obese (BMI ≥ 30). These metabolic disorders did not affect serum levels of the assessed immunity indices. Current knowledge suggests that adipokines provide potential therapeutic targets against type 2 diabetes and vascular disease. This study provides a strong association between adipocytokine and IR (Insulin Resistance). With the increasing epidemic of obesity and T2DM in Saudi Arabia, these adipocytokine markers that integrate metabolic and inflammatory signals may play important roles in the treatment and prevention of obesity and diabetes as well as planning of therapeutic strategies and the early detection of diabetes.N. S. Al-Sowayan 185

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“…Adiponectin affects the gluconeogenesis process and fatty acid oxidation through 5' adenosine monophosphate-activated protein kinase (AMP)-dependent protein kinase and peroxisome proliferator-activated receptor (PPAR) in the liver. Moreover, it increases glucose uptake in the peripheral tissues and stimulates insulin secretion, ultimately leading to a regulation of the body's energy (25). The interaction between adiponectin and adapter proteins, such as adaptor protein containing PH domain, phosphotyrosinebinding domain, and leucine zipper, is important in the adiponectin signaling pathway and for an increase in insulin sensitivity (26).…”

Section: Effect On Adiponectin Releasingmentioning

confidence: 99%

Effect and Mechanism of Herbal Ingredients in Improving Diabetes Mellitus Complications

Ebrahimi

Shirali

Afrisham

2016

Jundishapur J Nat Pharm Prod

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Context: Diabetes mellitus is the most common endocrine disease worldwide and its prevalence is increasing. The development of drugs with fewer side-effects is required when treating this disease. Thus, the objective of this study was to evaluate the use of traditional medicine and medicinal plants in this regard. The various mechanisms by which isolated extracts and herbal compounds exert their effects on different diabetes mellitus factors was investigated. Evidence Acquisition: Databases such as PubMed, Science Direct, and Web of Science (from 1990 until the present) were searched, using a detailed list of terms related to the effects and mechanism of herbal ingredients on diabetes mellitus complications. Results:The presence of secondary metabolites, such as phenols, flavonoids and alkaloids in plants, have been used as a source of medication for the treatment of many diseases, including diabetes mellitus. Following an extensive review of the literature, it was found that the secondary metabolites of plants have a wide range of anti-diabetic effects. Conclusions: Plant compounds should be isolated and their effects on diabetes mellitus and its complications examined in order to treatment for diabetes mellitus.

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Adiponectin Levels and Risk of Type 2 Diabetes

Cited by 882 publications

References 42 publications

Suppression of PDGF-induced PI3 kinase activity by imatinib promotes adipogenesis and adiponectin secretion

Suppression of PDGF-induced PI3 kinase activity by imatinib promotes adipogenesis and adiponectin secretion

Exploration of the Relationship between Adipocytokines, Tradition Risk Markers, Nontraditional Risk Markers and Anthropometric Measurements in T2DM Patients

Effect and Mechanism of Herbal Ingredients in Improving Diabetes Mellitus Complications

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