Barb D, Williams CJ, Neuwirth AK, Mantzoros CSAdiponectin in relation to malignancies: a review of existing basic research and clinical evidence. Am J Clin Nutr 86(3): s858-s866

Division of Endocrinology, Diabetes and Metabolism and Disease, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
American Journal of Clinical Nutrition (Impact Factor: 6.92). 10/2007; 86(3):s858-66.
Source: PubMed

ABSTRACT Adiponectin, an adipocyte-secreted hormone that plays an important role in diabetes and cardiovascular disease, may also be of importance in the development and progression of several malignancies. Circulating adiponectin concentrations, which are determined mainly by genetic factors, nutrition, and adiposity, are lower in patients with breast, endometrial, prostate, and colon cancer. It has thus been proposed that adiponectin may be a biological link between obesity (especially central obesity) and increased cancer risk. Adiponectin may influence cancer risk through its well-recognized effects on insulin resistance, but it is also plausible that adiponectin acts on tumor cells directly. Several cancer cell types express adiponectin receptors that may mediate the effects of adiponectin on cellular proliferation. Herein, we review recent evidence supporting a role of serum adiponectin concentrations as a novel risk factor and possible diagnostic marker for obesity-related malignancies, including cancers of the breast, endometrium, colon, and prostate. Further studies are needed to fully elucidate the potential role of adiponectin in cancer diagnostics and therapeutics.

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    • "This interaction is essential to verify its biological activity. Adiponectin is expressed as a single subunit but circulates in plasma or serum in four isoform states [21] (Fig. 1): a simple trimer complex (90 kDa), a low molecular-weight (LMW; 180 kDa), complex of two trimers, a high molecular-weight (HMW; 360– 400 kDa), complex of up to six trimers and a globular form of adiponectin that also exists in plasma [15]. These forms of adiponectin may show divergent biological roles during the activation of downstream signaling pathways, which may define their eventual roles in tumor progression. "
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    ABSTRACT: Adiponectin is produced in the white adipose tissue and is known to have anti-metabolic and anti-inflammatory properties. Serum/plasma adiponectin levels depend on diet, physical activity, and inheritance. Epidemiologic observations suggest a potential link between obesity and gastrointestinal malignancies. Low levels of adiponectin, which are known to occur in obesity, may contribute to the high incidence of cancer in this population. This review discusses the biochemical and molecular evidence regarding the relationship between adiponectin and gastrointestinal carcinogenesis and provides several future perspectives on the role of adiponectin as a target for prevention and therapy.
    Cytokine & Growth Factor Reviews 06/2014; 26(1). DOI:10.1016/j.cytogfr.2014.06.007 · 6.54 Impact Factor
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    • "This hormone also plays an important role in the secretion of estrogen and insulin-like growth factor (IGF), which are important cancer risk factors [25]. Studies indicate that cancer cells express adiponectin receptors thus attaching adiponectin to its receptors may limit the proliferation of cancer cells [18] [26]. Since obesity and insulin resistance are risk factors of cancer, adiponectin may act as an anticancer agent specially in breast cancer due to its significant effect on obesity and insulin resistance [15]. "
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    ABSTRACT: Background. Adiponectin, an adipokine secreted from adipose tissue, has antiobesity, anti-insulin resistance, and anticancer roles. The present study aimed to review the epidemiologic evidence about the association between adiponectin and cancers. Method. We searched in PubMed from 2002 to October 2011 by using the following key words: cancer, malignancy, cell proliferation, and adiponectin. Finally, 45 articles were recruited to review in the present paper. Findings. Several findings suggested inverse association between concentration of hormone and breast cancer risk. Low levels of adiponectin increase the risk of endometrial cancer in women. Adiponectin levels were significantly associated with prostate cancer in men. It seems that there is an inverse relationship between levels of adiponectin or its gene and colorectal cancer. Significant association between hormone and pancreatic cancer was found. Conclusion. Several findings suggested the negative correlation between adiponectin and risk of cancers. This relationship was more elucidated by the correlation between the hormone with obesity and insulin resistance. Suppression of growth and proliferation of cancer cells by adiponectin were explained via several mechanisms.
    11/2012; 2012:982769. DOI:10.5402/2012/982769
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    • "The relationship of leptin/ adiponectin with oncogenesis and cancer proliferation is not fully elucidated. However, accumulating clinical and experimental evidence supports a role of these adipokines in the development and progression of several cancers including melanoma and colon cancer (Gogas et al., 2008; Barb et al., 2007) via either a direct influence on cellular proliferation and/or indirect effects on inflammation and angiogenesis (Fujisawa et al., 2008; Brandon et al., 2009). We also observed that leptin significantly enhanced both B16 melanoma and MC38 colon cancer cell growth in culture while in contrast, adiponectin significantly inhibited tumor cell growth in vitro (data not shown). "
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    ABSTRACT: Cancer is influenced by its microenvironment, yet broader, environmental effects also play a role but remain poorly defined. We report here that mice living in an enriched housing environment show reduced tumor growth and increased remission. We found this effect in melanoma and colon cancer models, and that it was not caused by physical activity alone. Serum from animals held in an enriched environment (EE) inhibited cancer proliferation in vitro and was markedly lower in leptin. Hypothalamic brain-derived neurotrophic factor (BDNF) was selectively upregulated by EE, and its genetic overexpression reduced tumor burden, whereas BDNF knockdown blocked the effect of EE. Mechanistically, we show that hypothalamic BDNF downregulated leptin production in adipocytes via sympathoneural beta-adrenergic signaling. These results suggest that genetic or environmental activation of this BDNF/leptin axis may have therapeutic significance for cancer.
    Cell 07/2010; 142(1):52-64. DOI:10.1016/j.cell.2010.05.029 · 33.12 Impact Factor
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