全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...
ISRN Oncology  2012 

Serum Adiponectin Level and Different Kinds of Cancer: A Review of Recent Evidence

DOI: 10.5402/2012/982769

Full-Text   Cite this paper   Add to My Lib

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. 1. Introduction Obesity, influenced by environmental and genetic factors, is one of the important factors in the etiology of metabolic syndrome, cardiovascular disease (CVD), and cancer [1–3]. Obesity is related to increased level of inflammatory markers such as CRP (C-reactive protein) that are associated with metabolic syndrome [4]. According to evidence of 2005, 937 and 396 million people around the world were obese and overweight, respectively [5]. Obesity is significantly correlated with an increase in dietary energy density and also it can elevate the risk of CVD and metabolic syndrome [6, 7]. Adherence to the healthy dietary pattern [8] and high intake of fruits and vegetables [9] are inversely related to metabolic syndrome. Moreover, the consumption of plant proteins, such as beans, drives a significant reduction in the inflammatory markers such as CRP, while meat consumption can increase inflammatory markers in bloodstream [10, 11]. Dietary intakes have major role in controlling the inflammation and also weight management [12]. Obesity increases the risk of cancer. A study showed that the risk of cancer in obese women is 50% more than women with normal weight [13]. According to published studies, obesity, inflammation, insulin resistance, metabolic syndrome, cardiovascular disease, and cancer are significantly associated

References

[1]  Y. F. Tian, C. H. Chu, M. H. Wu et al., “Anthropometric measures, plasma adiponectin, and breast cancer risk,” Endocrine-Related Cancer, vol. 14, no. 3, pp. 669–677, 2007.
[2]  J. H. Kang, B. Y. Yu, and D. S. Youn, “Relationship of serum adiponectin and resistin levels with breast cancer risk,” Journal of Korean Medical Science, vol. 22, no. 1, pp. 117–121, 2007.
[3]  A. Esmaillzadeh and L. Azadbakht, “Major dietary patterns in relation to general obesity and central adiposity among Iranian women,” Journal of Nutrition, vol. 138, no. 2, pp. 358–363, 2008.
[4]  K. F. Hilpert, P. M. Kris-Etherton, and S. G. West, “Lipid response to a low-fat diet with or without soy is modified by C-reactive protein status in moderately hypercholesterolemic adults,” Journal of Nutrition, vol. 135, no. 5, pp. 1075–1079, 2005.
[5]  F. Hosseinpanah, M. Barzin, P. S. Eskandary, P. Mirmiran, and F. Azizi, “Trends of obesity and abdominal obesity in Tehranian adults: a cohort study,” BMC Public Health, vol. 9, article 426, 2009.
[6]  A. Esmaillzadeh, H. Khosravi Boroujeni, and L. Azadbakht, “Consumption of energy-dense diets in relation to cardiometabolic abnormalities among Iranian women,” Public Health Nutrition, vol. 19, pp. 1–8, 2011.
[7]  A. Esmaillzadeh and L. Azadbakht, “Dietary energy density and the metabolic syndrome among Iranian women,” European Journal of Clinical Nutrition, vol. 65, no. 5, pp. 598–605, 2011.
[8]  A. Esmaillzadeh, M. Kimiagar, Y. Mehrabi, L. Azadbakht, F. B. Hu, and W. C. Willett, “Dietary patterns, insulin resistance, and prevalence of the metabolic syndrome in women,” American Journal of Clinical Nutrition, vol. 85, no. 3, pp. 910–918, 2007.
[9]  A. Esmaillzadeh, M. Kimiagar, Y. Mehrabi, L. Azadbakht, F. B. Hu, and W. C. Willett, “Fruit and vegetable intakes, C-reactive protein, and the metabolic syndrome,” American Journal of Clinical Nutrition, vol. 84, no. 6, pp. 1489–1497, 2006.
[10]  A. Esmaillzadeh and L. Azadbakht, “Legume consumption is inversely associated with serum concentrations of adhesion molecules and inflammatory biomarkers among Iranian women,” Journal of Nutrition, vol. 142, pp. 334–339, 2012.
[11]  L. Azadbakht and A. Esmaillzadeh, “Red meat intake is associated with metabolic syndrome and the plasma c-reactive protein concentration in women,” Journal of Nutrition, vol. 139, no. 2, pp. 335–339, 2009.
[12]  L. Azadbakht, P. J. Surkan, A. Esmaillzadeh, and W. C. Willett, “The dietary approaches to stop hypertension eating plan affects C-reactive protein, coagulation abnormalities, and hepatic function tests among type 2 diabetic patients,” Journal of Nutrition, vol. 141, no. 6, pp. 1083–1088, 2011.
[13]  E. E. Calle and R. Kaaks, “Overweight, obesity and cancer: epidemiological evidence and proposed mechanisms,” Nature Reviews Cancer, vol. 4, no. 8, pp. 579–591, 2004.
[14]  L. Otvos Jr., E. Haspinger, F. L. Russa, et al., “Design and development of a peptide-based adiponectin receptor agonist for cancer treatment,” BMC Biotechnology, vol. 11, article 90, 2011.
[15]  I. Kelesidis, T. Kelesidis, and C. S. Mantzoros, “Adiponectin and cancer: a systematic review,” British Journal of Cancer, vol. 94, no. 9, pp. 1221–1225, 2006.
[16]  M. E. Grossmann, K. J. Nkhata, N. K. Mizuno, A. Ray, and M. P. Cleary, “Effects of adiponectin on breast cancer cell growth and signaling,” British Journal of Cancer, vol. 98, no. 2, pp. 370–379, 2008.
[17]  T. Jardé, F. Caldefie-Chézet, N. Goncalves-Mendes et al., “Involvement of adiponectin and leptin in breast cancer: clinical and in vitro studies,” Endocrine-Related Cancer, vol. 16, no. 4, pp. 1197–1210, 2009.
[18]  D. Barb, C. J. Williams, A. K. Neuwirth, and C. S. Mantzoros, “Adiponectin in relation to malignancies: a review of existing basic research and clinical evidence,” American Journal of Clinical Nutrition, vol. 86, no. 3, pp. S858–S866, 2007.
[19]  S. Shahar, R. M. Salleh, A. R. Ghazali, P. B. Koon, and W. N. Wan Mohamud, “Roles of adiposity, lifetime physical activity and serum adiponectin in occurrence of breast cancer among Malaysian women in Klang Valley,” Asian Pacific Journal of Cancer Prevention, vol. 11, no. 1, pp. 61–66, 2010.
[20]  Y. Miyoshi, T. Funahashi, S. Kihara et al., “Association of serum adiponectin levels with breast cancer risk,” Clinical Cancer Research, vol. 9, no. 15, pp. 5699–5704, 2003.
[21]  Y. M. Liu, J. M. Lacorte, N. Viguerie et al., “Adiponectin gene expression in subcutaneous adipose tissue of obese women in response to short-term very low calorie diet and refeeding,” Journal of Clinical Endocrinology and Metabolism, vol. 88, no. 12, pp. 5881–5886, 2003.
[22]  M. Cnop, P. J. Havel, K. M. Utzschneider et al., “Relationship of adiponectin to body fat distribution, insulin sensitivity and plasma lipoproteins: evidence for independent roles of age and sex,” Diabetologia, vol. 46, no. 4, pp. 459–469, 2003.
[23]  A. Xu, K. W. Chan, R. L. C. Hoo et al., “Testosterone selectively reduces the high molecular weight form of adiponectin by inhibiting its secretion from adipocytes,” Journal of Biological Chemistry, vol. 280, no. 18, pp. 18073–18080, 2005.
[24]  N. Bansal, V. Charlton-Menys, P. Pemberton et al., “Adiponectin in umbilical cord blood is inversely related to low-density lipoprotein cholesterol but not ethnicity,” Journal of Clinical Endocrinology and Metabolism, vol. 91, no. 6, pp. 2244–2249, 2006.
[25]  V. G. Kaklamani, M. Sadim, A. Hsi et al., “Variants of the adiponectin and adiponectin receptor 1 genes and breast cancer risk,” Cancer Research, vol. 68, no. 9, pp. 3178–3184, 2008.
[26]  A. K?rner, K. Pazaitou-Panayiotou, T. Kelesidis et al., “Total and high-molecular-weight adiponectin in breast cancer: in vitro and in vivo studies,” Journal of Clinical Endocrinology and Metabolism, vol. 92, no. 3, pp. 1041–1048, 2007.
[27]  C. Mantzoros, E. Petridou, N. Dessypris et al., “Adiponectin and breast cancer risk,” Journal of Clinical Endocrinology and Metabolism, vol. 89, no. 3, pp. 1102–1107, 2004.
[28]  K. Michalakis, C. J. Williams, N. Mitsiades et al., “Serum adiponectin concentrations and tissue expression of adiponectin receptors are reduced in patients with prostate cancer: a case control study,” Cancer Epidemiology Biomarkers and Prevention, vol. 16, no. 2, pp. 308–313, 2007.
[29]  A. E. Cust, R. Kaaks, C. Friedenreich et al., “Plasma adiponectin levels and endometrial cancer risk in pre- and postmenopausal women,” Journal of Clinical Endocrinology and Metabolism, vol. 92, no. 1, pp. 255–263, 2007.
[30]  S. Otake, H. Takeda, S. Fujishima et al., “Decreased levels of plasma adiponectin associated with increased risk of colorectal cancer,” World Journal of Gastroenterology, vol. 16, no. 10, pp. 1252–1257, 2010.
[31]  S. S. Tworoger, A. H. Eliassen, T. Kelesidis et al., “Plasma adiponectin concentrations and risk of incident breast cancer,” Journal of Clinical Endocrinology and Metabolism, vol. 92, no. 4, pp. 1510–1516, 2007.
[32]  O. Treeck, C. Lattrich, I. Juhasz-Boess, S. Buchholz, G. Pfeiler, and O. Ortmann, “Adiponectin differentially affects gene expression in human mammary epithelial and breast cancer cells,” British Journal of Cancer, vol. 99, no. 8, pp. 1246–1250, 2008.
[33]  L. Dal Maso, L. S. A. Augustin, A. Karalis et al., “Circulating adiponectin and endometrial cancer risk,” Journal of Clinical Endocrinology and Metabolism, vol. 89, no. 3, pp. 1160–1163, 2004.
[34]  P. T. Soliman, D. Wu, G. Tortolero-Luna et al., “Association between adiponectin, insulin resistance, and endometrial cancer,” Cancer, vol. 106, no. 11, pp. 2376–2381, 2006.
[35]  E. Petridou, C. Mantzoros, N. Dessypris et al., “Clinical case seminar - Plasma adiponectin concentrations in relation to endometrial cancer: a case-control study in Greece,” Journal of Clinical Endocrinology and Metabolism, vol. 88, no. 3, pp. 993–997, 2003.
[36]  B. He, Y. Pan, Y. Zhang et al., “Effects of genetic variations in the Adiponectin pathway genes on the risk of colorectal cancer in the Chinese population,” BMC Medical Genetics, vol. 12, article 94, 2011.
[37]  J. L. Beebe-Dimmer, K. A. Zuhlke, A. M. Ray, E. M. Lange, and K. A. Cooney, “Genetic variation in adiponectin (ADIPOQ) and the type 1 receptor (ADIPOR1), obesity and prostate cancer in African Americans,” Prostate Cancer and Prostatic Diseases, vol. 13, no. 4, pp. 362–368, 2010.
[38]  A. Y?ld?r?m, M. Bilici, K. ?ayir, V. Yanmaz, S. Yildirim, and S. B. Tekin, “Serum adiponectin levels in patients with esophageal cancer,” Japanese Journal of Clinical Oncology, vol. 39, no. 2, pp. 92–96, 2009.
[39]  S. Goktas, M. I. Yilmaz, K. Caglar, A. Sonmez, S. Kilic, and S. Bedir, “Prostate cancer and adiponectin,” Urology, vol. 65, no. 6, pp. 1168–1172, 2005.
[40]  V. G. Kaklamani, K. B. Wisinski, M. Sadim et al., “Variants of the adiponectin (ADIPOQ) and adiponectin receptor 1 (ADIPOR1) genes and colorectal cancer risk,” Journal of the American Medical Association, vol. 300, no. 13, pp. 1523–1531, 2008.
[41]  R. Z. Stolzenberg-Solomon, S. Weinstein, M. Pollak et al., “Prediagnostic adiponectin concentrations and pancreatic cancer risk in male smokers,” American Journal of Epidemiology, vol. 168, no. 9, pp. 1047–1055, 2008.
[42]  J. M. Schenk, A. R. Kristal, M. L. Neuhouser et al., “Serum adiponectin, C-peptide and leptin and risk of symptomatic benign prostatic hyperplasia: results from the prostate cancer prevention trial,” Prostate, vol. 69, no. 12, pp. 1303–1311, 2009.
[43]  H. Li, M. J. Stampfer, L. Mucci et al., “A 25-year prospective study of plasma adiponectin and leptin concentrations and prostate cancer risk and survival,” Clinical Chemistry, vol. 56, no. 1, pp. 34–43, 2010.
[44]  D. Housa, Z. Vernerova, J. Heracek, et al., “Adiponectin as a potential marker of prostate cancer progression: studies in organ-confined and locally advanced prostate cancer,” Physiological Research, vol. 57, pp. 451–458, 2008.
[45]  J. D. Bub, T. Miyazaki, and Y. Iwamoto, “Adiponectin as a growth inhibitor in prostate cancer cells,” Biochemical and Biophysical Research Communications, vol. 340, no. 4, pp. 1158–1166, 2006.
[46]  C. M. L. Fontana, M. E. M. Artola, N. D. M. Monaco, et al., “Influence of leptin and adiponectin on prostate cancer,” Archivos Espa?oles de Urología, vol. 62, pp. 103–108, 2009.
[47]  E. K. Wei, E. Giovannucci, C. S. Fuchs, W. C. Willett, and C. S. Mantzoros, “Low plasma adiponectin levels and risk of colorectal cancer in men: a prospective study,” Journal of the National Cancer Institute, vol. 97, no. 22, pp. 1688–1694, 2005.
[48]  A. Lukanova, S. S?derberg, R. Kaaks, E. Jellum, and P. Stattin, “Serum adiponectin is not associated with risk of colorectal cancer,” Cancer Epidemiology Biomarkers and Prevention, vol. 15, no. 2, pp. 401–402, 2006.
[49]  I. Wolf, S. Sadetzki, H. Kanely et al., “Adiponectin, ghrelin, and leptin in cancer cachexia in breast and colon cancer patients,” Cancer, vol. 106, no. 4, pp. 966–973, 2006.
[50]  L. Liu, R. Zhong, S. Wei, et al., “Interactions between genetic variants in the adiponectin, adiponectin receptor 1 and environmental factors on the risk of colorectal cancer,” PLoS ONE, vol. 6, Article ID e27301, 2011.
[51]  L. G. Carvajal-Carmona, S. Spain, D. Kerr, R. Houlston, J. B. Cazier, and I. Tomlinson, “Common variation at the adiponectin locus is not associated with colorectal cancer risk in the UK,” Human Molecular Genetics, vol. 18, no. 10, pp. 1889–1892, 2009.
[52]  M. Dalamaga, I. Migdalis, J. L. Fargnoli et al., “Pancreatic cancer expresses adiponectin receptors and is associated with hypoleptinemia and hyperadiponectinemia: a case-control study,” Cancer Causes and Control, vol. 20, no. 5, pp. 625–633, 2009.
[53]  M. C. Chang, Y. T. Chang, T. C. Su et al., “Adiponectin as a potential differential marker to distinguish pancreatic cancer and chronic pancreatitis,” Pancreas, vol. 35, no. 1, pp. 16–21, 2007.
[54]  C. Weyer, T. Funahashi, S. Tanaka et al., “Hypoadiponectinemia in obesity and type 2 diabetes: close association with insulin resistance and hyperinsulinemia,” Journal of Clinical Endocrinology and Metabolism, vol. 86, no. 5, pp. 1930–1935, 2001.
[55]  R. E. Bachelder, M. A. Wendt, and A. M. Mercurio, “Vascular endothelial growth factor promotes breast carcinoma invasion in an autocrine manner by regulating the chemokine receptor CXCR4,” Cancer Research, vol. 62, no. 24, pp. 7203–7206, 2002.
[56]  E. Mueller, P. Sarraf, P. Tontonoz et al., “Terminal differentiation of human breast cancer through PPARγ,” Molecular Cell, vol. 1, no. 3, pp. 465–470, 1998.
[57]  Y. Miyazaki, A. Mahankali, E. Wajcberg, M. Bajaj, L. J. Mandarino, and R. A. DeFronzo, “Effect of pioglitazone on circulating adipocytokine levels and insulin sensitivity in type 2 diabetic patients,” Journal of Clinical Endocrinology and Metabolism, vol. 89, no. 9, pp. 4312–4319, 2004.
[58]  F. Jaleel, A. Jaleel, J. Aftab, and M. A. Rahman, “Relationship between adiponectin, glycemic control and blood lipids in diabetic type 2 postmenopausal women with and without complication of ischemic heart disease,” Clinica Chimica Acta, vol. 370, no. 1-2, pp. 76–81, 2006.
[59]  S. E. Hankinson, W. C. Willett, J. E. Manson et al., “Alcohol, height, and adiposity in relation to estrogen and prolactin levels in postmenopausal women,” Journal of the National Cancer Institute, vol. 87, no. 17, pp. 1297–1302, 1995.
[60]  M. N. Dieudonne, M. Bussiere, E. Dos Santos, M. C. Leneveu, Y. Giudicelli, and R. Pecquery, “Adiponectin mediates antiproliferative and apoptotic responses in human MCF7 breast cancer cells,” Biochemical and Biophysical Research Communications, vol. 345, no. 1, pp. 271–279, 2006.
[61]  D. Barb, A. Neuwirth, C. S. Mantzoros, and S. P. Balk, “Adiponectin signals in prostate cancer cells through Akt to activate the mammalian target of rapamycin pathway,” Endocrine-Related Cancer, vol. 14, no. 4, pp. 995–1005, 2007.
[62]  Y. J. Jeong, J. G. Bong, S. H. Park, J. H. Choi, and H. K. Oh, “Expression of leptin, leptin receptor, adiponectin, and adiponectin receptor in ductal carcinoma in situ and invasive breast cancer,” Journal of Breast Cancer, vol. 14, no. 2, pp. 96–103, 2011.
[63]  X. Xiang, A. K. Saha, R. Wen, N. B. Ruderman, and Z. Luo, “AMP-activated protein kinase activators can inhibit the growth of prostate cancer cells by multiple mechanisms,” Biochemical and Biophysical Research Communications, vol. 321, no. 1, pp. 161–167, 2004.
[64]  N. Yamaguchi, J. G. M. Argueta, Y. Masuhiro et al., “Adiponectin inhibits Toll-like receptor family-induced signaling,” FEBS Letters, vol. 579, no. 30, pp. 6821–6826, 2005.
[65]  T. Fujisawa, H. Endo, A. Tomimoto et al., “Adiponectin suppresses colorectal carcinogenesis under the high-fat diet condition,” Gut, vol. 57, no. 11, pp. 1531–1538, 2008.
[66]  T. Kadowaki, T. Yamauchi, N. Kubota, K. Hara, K. Ueki, and K. Tobe, “Adiponectin and adiponectin receptors in insulin resistance, diabetes, and the metabolic syndrome,” Journal of Clinical Investigation, vol. 116, no. 7, pp. 1784–1792, 2006.
[67]  R. Tsukinoki, K. Morimoto, and K. Nakayama, “Association between lifestyle factors and plasma adiponectin levels in Japanese men,” Lipids in Health and Disease, vol. 4, article 27, 2005.
[68]  J. L. Fargnoli, T. T. Fung, D. M. Olenczuk, J. P. Chamberland, F. B. Hu, and C. S. Mantzoros, “Adherence to healthy eating patterns is associated with higher circulating total and high-molecular-weight adiponectin and lower resistin concentrations in women from the Nurses' Health Study,” American Journal of Clinical Nutrition, vol. 88, no. 5, pp. 1213–1224, 2008.
[69]  Y. Nakamura, H. Ueshima, N. Okuda et al., “Relation of dietary and other lifestyle traits to difference in serum adiponectin concentration of Japanese in Japan and Hawaii: the INTERLIPID Study,” American Journal of Clinical Nutrition, vol. 88, no. 2, pp. 424–430, 2008.
[70]  C. S. Mantzoros, C. J. Williams, J. E. Manson, J. B. Meigs, and F. B. Hu, “Adherence to the Mediterranean dietary pattern is positively associated with plasma adiponectin concentrations in diabetic women,” American Journal of Clinical Nutrition, vol. 84, no. 2, pp. 328–335, 2006.
[71]  M. H. Rokling-Andersen, J. E. Reseland, M. B. Veier?d et al., “Effects of long-term exercise and diet intervention on plasma adipokine concentrations,” American Journal of Clinical Nutrition, vol. 86, no. 5, pp. 1293–1301, 2007.
[72]  Z. Kovacova, M. Vitkova, M. Kovacikova et al., “Secretion of adiponectin multimeric complexes from adipose tissue explants is not modified by very low calorie diet,” European Journal of Endocrinology, vol. 160, no. 4, pp. 585–592, 2009.
[73]  K. Shinmura, K. Tamaki, K. Saito, Y. Nakano, T. Tobe, and R. Bolli, “Cardioprotective effects of short-term caloric restriction are mediated by adiponectin via activation of AMP-activated protein kinase,” Circulation, vol. 116, no. 24, pp. 2809–2817, 2007.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133