Resistin levelispositively correlated with thrombotic complications in Southern Chinese metabolic syndrome patients

Fang, Weili; Zhang, Q.; Peng, Yongbo; Chen, M.; Lin, Xu; Wu, Jing; Cai, Chengfu; Mei, Yifang; Jin, Hua

doi:10.1007/bf03347059

Cited by 21 publications

(21 citation statements)

References 33 publications

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“…Recenty, resistin was shown to induce a procoagulant state in HUVECs by inducing both the expression of tissue factor (TF) and the activity of factor Xa [34]. Correlative observations made in metabolic syndrome cohorts showed that resistin is strongly associated with hypercoagulative and hypofibrinolitic activities [35]. It seems that inflammation-associated increases in the release of resistin into circulation might contribute to the prothrombotic state observed under diabetic conditions.…”

Section: Discussionmentioning

confidence: 99%

Molecular signature of adipose tissue in patients with both Non-Alcoholic Fatty Liver Disease (NAFLD) and Polycystic Ovarian Syndrome (PCOS)

et al. 2013

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BackgroundPolycystic ovarian syndrome (PCOS) is one of the most common reproductive disorders with strong association with both insulin resistance and non-alcoholic fatty liver disease (NAFLD). To untangle the complex relationship between PCOS and NAFLD, we analyzed serum biomarkers of apoptosis, some adipokines and mRNA profiles in the visceral adipose tissue of obese patients with NAFLD who were also diagnosed with PCOS and compared to a group with NAFLD only.MethodsWe included patients with biopsy-proven NAFLD and PCOS (N = 12) and BMI-matched biopsy-proven NAFLD patients without PCOS (N = 12). Expression levels of individual mRNAs and soluble serum biomarkers were compared by non-parametric Mann–Whitney test. The analysis also included Spearman rank correlation tests and multiple regression analysis. For co-correlated genes, the factor analysis was performed.ResultsThe total serum levels of apoptotic biomarker M30 were significantly elevated in PCOS patients with liver steatosis as compared to non-PCOS NAFLD controls (P < 0.02), pointing that androgen-dependent proapoptotic PCOS environment that may directly contribute to NAFLD progression in these patients. Similarly, hyperandrogenism may explain the observed PCOS-specific decrease (P < 0.04) in adipose LDLR mRNA expression that may be connected to the proneness of PCOS patients to NAFLD. The levels of mRNA encoding angiogenesis-associated GSK-3B interacting protein ninein were also significantly increased in the adipose tissue of NAFLD patients with PCOS (P < 0.007). Furthermore, the levels of resistin positively correlated with expression levels of LDLR and prothrombin time (PT).ConclusionAn androgen-dependent proapoptotic PCOS environment may directly contribute to NAFLD progression in these patients. Hyperandrogenism may explain an observed decrease in adipose LDLR mRNA expression. An inflammation-associated increase in the release of resistin into circulation might contribute to the prothrombotic state observed under conditions associated with insulin resistance, including PCOS. The studies of larger cohorts of NAFLD with and without PCOS patients are needed to further assess these potential interactions.

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Section: Discussionmentioning

confidence: 99%

Molecular signature of adipose tissue in patients with both Non-Alcoholic Fatty Liver Disease (NAFLD) and Polycystic Ovarian Syndrome (PCOS)

et al. 2013

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“…108 In chondrocytes, resistin up-regulated several cytokines and chemokines (TNF-a, IL-6, and IL-12), through NF-kB and CCAAT/enhancer-binding protein (C/EBP)b. 109 Moreover, low shear stress modulated resistin-induced COX-2 expression in human OA chondrocytes 110 via NF-kB, cAMP response element binding protein (CREB), AMPK, and SIRT1, indicating the interplay between mechanical shear stress and resistin activity. 110 Mechanical stretch also regulated the resistin expression in vascular smooth muscle cells 111 and cardiomyocytes.…”

Section: Resistinmentioning

confidence: 99%

“…Resistin stimulated osteoblast proliferation and its expression is augmented during osteoclast differentiation, through protein kinase C (PKC) and protein kinase A (PKA) signaling pathways . In chondrocytes, resistin up‐regulated several cytokines and chemokines (TNF‐α, IL‐6, and IL‐12), through NF‐κB and CCAAT/enhancer‐binding protein (C/EBP)β . Moreover, low shear stress modulated resistin‐induced COX‐2 expression in human OA chondrocytes via NF‐κB, cAMP response element binding protein (CREB), AMPK, and SIRT1, indicating the interplay between mechanical shear stress and resistin activity .…”

Section: Resistinmentioning

confidence: 99%

Biomechanics, obesity, and osteoarthritis. The role of adipokines: When the levee breaks

Francisco

Pérez

Pino

et al. 2017

Journal Orthopaedic Research

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Osteoarthritis is a high-incidence painful and debilitating disease characterized by progressive degeneration of articular joints, which indicates a breakdown in joint homeostasis favoring catabolic processes. Biomechanical loading, associated with inflammatory and metabolic imbalances of joint, strongly contributes to the initiation and progression of the disease. Obesity is a primary risk factor for disease onset, and mechanical factors increased the risk for disease progression. Moreover, inflammatory mediators, in particular, adipose tissue-derived cytokines (better known as adipokines) play a critical role linking obesity and osteoarthritis. The present article summarizes the knowledge about the role of adipokines in cartilage and bone function, highlighting their contribution to the imbalance of joint homeostasis and, consequently, pathogenesis of osteoarthritis. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:594-604, 2018.

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“…In a recent clinical study, the serum resistin level of 90 patients with the MetS was determined and compared with serum levels of mediators of thrombosis (Fang et al ., 2011). It was determined that the average level of resistin in MetS patients with or without acute myocardial or cerebral infarction was significantly higher than that of the control patients.…”

Section: Resistin and Thrombosismentioning

confidence: 99%

Resistin: functional roles and therapeutic considerations for cardiovascular disease

Jamaluddin

Weakley

Yao

et al. 2012

British J Pharmacology

408

304

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Resistin, originally described as an adipocyte‐specific hormone, has been suggested to be an important link between obesity, insulin resistance and diabetes. Although its expression was initially defined in adipocytes, significant levels of resistin expression in humans are mainly found in mononuclear leukocytes, macrophages, spleen and bone marrow cells. Increasing evidence indicates that resistin plays important regulatory roles apart from its role in insulin resistance and diabetes in a variety of biological processes: atherosclerosis and cardiovascular disease (CVD), non‐alcoholic fatty liver disease, autoimmune disease, malignancy, asthma, inflammatory bowel disease and chronic kidney disease. As CVD accounts for a significant amount of morbidity and mortality in patients with diabetes and without diabetes, it is important to understand the role that adipokines such as resistin play in the cardiovascular system. Evidence suggests that resistin is involved in pathological processes leading to CVD including inflammation, endothelial dysfunction, thrombosis, angiogenesis and smooth muscle cell dysfunction. The modes of action and signalling pathways whereby resistin interacts with its target cells are beginning to be understood. In this review, the current knowledge about the functions and pathophysiological implications of resistin in CVD development is summarized; clinical translations, therapeutic considerations and future directions in the field of resistin research are discussed. LINKED ARTICLES This article is part of a themed section on Fat and Vascular Responsiveness. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2012.165.issue-3

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Resistin levelispositively correlated with thrombotic complications in Southern Chinese metabolic syndrome patients

Abstract: In patients with MetS, resistin is strongly associated with hypercoagulative and hypofibrinolitic activities. Moreover, resistin may induce thrombotic complications via mediating the lipoprotein metabolism and stimulating inflammation.

Cited by 21 publications

References 33 publications

Molecular signature of adipose tissue in patients with both Non-Alcoholic Fatty Liver Disease (NAFLD) and Polycystic Ovarian Syndrome (PCOS)

Molecular signature of adipose tissue in patients with both Non-Alcoholic Fatty Liver Disease (NAFLD) and Polycystic Ovarian Syndrome (PCOS)

Biomechanics, obesity, and osteoarthritis. The role of adipokines: When the levee breaks

Resistin: functional roles and therapeutic considerations for cardiovascular disease

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