Obesity and Cancer Risk: Recent Review and Evidence

Basen-Engquist, Karen; Chang, Maria

doi:10.1007/s11912-010-0139-7

Cited by 383 publications

(255 citation statements)

References 34 publications

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“…4,25 Several mechanisms have been proposed to explain how obesity increases HCC risk, with the primary underlying condition being NASH. 6 We have previously shown that extended feeding of the HF-HC-HSD alone results in NASH.…”

Section: Discussionmentioning

confidence: 99%

“…2 Recently large-scale epidemiological studies have pointed out that overweight and obese individuals possess substantial increase in cancer risk. 3,4 Although the obesity-associated increase in cancer risk is dependent on the type of cancer, the largest increase is seen for HCC. 5 Several mechanisms are proposed to explain how obesity increases HCC risk, including the prevalence of type II diabetes, Non Alcoholic Steato-Hepatitis (NASH), and cellular inflammation.…”

Section: Introductionmentioning

confidence: 99%

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Hepatocellular carcinoma is accelerated by NASH involving M2 macrophage polarization mediated by hif-1αinduced IL-10

et al. 2016

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Obesity-related inflammation promotes cancer development. Tissue resident macrophages affect tumor progression and the tumor micro-environment favors polarization into alternatively activated macrophages (M2) that facilitate tumor invasiveness. Here, we dissected the role of western diet-induced NASH in inducing macrophage polarization in a carcinogen initiated model of hepatocellular carcinoma (HCC). Adult C57BL/6 male mice received diethyl nitrosamine (DEN) followed by 24 weeks of high fat-high cholesterol-high sugar diet (HF-HC-HSD). We assessed liver MRI and histology, serum ALT, AFP, liver triglycerides, and cytokines. Macrophage polarization was determined by IL-12/TNFa (M1) and CD163/ CD206 (M2) expression using flow cytometry. Role of hif-1a-induced IL-10 was dissected in hepatocyte specific hif-1aKO and hif-1adPA (over-expression) mice. The western diet-induced features of NASH and accelerated HCC development after carcinogen exposure. Liver fibrosis and serum AFP were significantly increased in DEN C HF-HC-HSD mice compared to controls. Western diet resulted in macrophage (F4/ 80 C CD11b C ) infiltration to liver and DEN C HF-HC-HSD mice showed preferential increase in M2 macrophages. Isolated hepatocytes from western diet fed mice showed significant upregulation of the hypoxia-inducible transcription factor, hif-1a, and livers from hif-1a over-expressing mice had increased proportion of M2 macrophages. Primary hepatocytes from wild-type mice treated with DEN and palmitic acid in vitro showed activation of hif-1a and induction of IL-10, a M2 polarizing cytokine. IL-10 neutralization in hepatocyte-derived culture supernatant prevented M2 macrophage polarization and silencing hif-1a in macrophages blocked their M2 polarization. Therefore, our data demonstrate that NASH accelerates HCC progression via upregulation of hif-1a mediated IL-10 polarizing M2 macrophages.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Hepatocellular carcinoma is accelerated by NASH involving M2 macrophage polarization mediated by hif-1αinduced IL-10

et al. 2016

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“…These hormones are responsible for body cell growth and division; hence, contribute to the growth of cancer cells [19]. Obese menopausal women have been found to have higher percentage of circulating estrogen that is produced from adipose tissue.…”

Section: Obesity-cancer Connectionmentioning

confidence: 99%

Obesity and Cancer: What’s the Interconnection?

Faris¹

2015

AOWMC

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Obesity is one of the most prevalent nutritional diseases, associated with chronic morbidity and mortality. Persuasive evidence indicates a striking association between obesity and incidence of common neoplasms, such as those of the esophagus, endometrium, kidney and breast in post menopause women, prostate in men, in addition to colon, rectum and bladder. Such an association has been supported by clinical and laboratory experiments on humans and animals, respectively. The findings have revealed that obesity and increased body fatness, in general and visceral adiposity, in particular, increase the vulnerability to develop different cancers. Although the impact of obesity in cancer progression differs according to the type of cancer, all the obesity-related cancers are centered around body adiposity. This review highlights the different hormonal, biochemical and molecular changes that might be involved in obesity-related cancers. Increased serum insulin, insulin-like growth factor, steroids "sex hormones" and the disturbances in adiponectin and leptin hormones are included. Biochemical and metabolic changes that mediate obesity-related carcinogenesis involving elevated oxidative stress and inflammation levels in the body and the concomitant increment in circulatory proinflammatory cytokines are discussed.

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“…Az alimentáris eredetű májkárosodásban csökkent metilpool felhívja a fi gyelmet az elhízás és a rák kialakulása közötti kapcsolatban a metilezettségi szint jelentőségére [45,46,47].…”

Section: Megbeszélésunclassified

Transmethylation and the redox homeostasis

et al. 2013

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Bevezetés: A transzmetilezés térszerkezet-módosító szubsztitúciós folyamat. Feladata az élő szervezetekben, töb-bek között, a fehérje-és génműködés szabályozása. A táplálékláncon keresztül szervezetbe juttatott metildonor vegyületek hasznosulása, illetve a könnyen mobilizálható metilpool analitikai módszerekkel nyomon követhető. Célkitűzés: A szerzők célul tűzték ki néhány növényi (búza, bab, cékla, káposzta) és állati (baromfi -és nyúlmáj) eredetű táplálék könnyen mobilizálható metilcsoportjainak koncentrációmérését, a transzmetilezés és a redox-homeosztázis kapcsolatának vizsgálatát baromfi -és nyúlmájban, valamint e paraméterek tanulmányozását kísérletes zsír-májban, patkányban. Módszer: Patkánykísérletben a tápot koleszterin, napraforgóolaj és kólsav eltérő koncentrációival dúsították. A könnyen mobilizálható metilcsoportok meghatározása túlnyomásos rétegkromatográfi ás módszerrel, a hidrogéndonor-aktivitás mérése 1,1-difenil-2-pikrilhidrazil stabil szabad gyök alkalmazásával, spektrofotometriá-san történt. Eredmények: A vizsgált növényi minták közül a legjelentősebb metilpoollal a babmagok rendelkeztek. A baromfi máj a nyúlmájnál szignifi kánsan nagyobb könnyen mobilizálható metilcsoportszintet és hidrogéndonor-aktivitást mutatott. Patkányokban, súlyos zsírmájban csökkent a hidrogéndonor-aktivitás, és szig nifi kánsan csökkent a könnyen mobilizálható metilcsoportszint. Következtetések: Az eredmények felhívják a fi gyelmet a táplálkozás jelentőségére, különösen az elhízással összefüggő megbetegedések kapcsán. Orv. Hetil., 2013, 154, 1180-1187. Kulcsszavak: transzmetilezés, redox-homeosztázis, zsírmáj, táplálkozási faktor Transmethylation and the redox homeostasisIntroduction: Transmethylation modifi es confi guration and proceeds via formaldehyde. It has a signifi cant role for example in epigenetic regulation. The whole methyl-pool can be evaluated by the measurement of bound formaldehyde. Aim: The bound formaldehyde was measured in wheat, bean, beetroot, cabbage, broiler-and rabbit liver. The relationship between transmethylation and redox homeosthasis was studied in the liver of domestic animals, and in the rat model of fatty liver. Method: The diet of rats was enriched with cholesterol, sunfl ower oil and cholic acid. The bound formaldehyde was determined by overpressured layer chromatography. The hydrogen-donating ability was measured with 1.1-diphenyl-2-picrylhydrazylt free radical using spectrophotometric measurement. Results: Beans had the most bound formaldehyde. The liver of broilers possessed signifi cantly elevated hydrogendonating ability and transmethylation ability. Rats with severe fatty liver had signifi cantly less bound formaldehyde and the hydrogen-donating ability tendentiously decreased. Conclusions: These results draw attention to the diet, especially in obesity and obesity-related diseases. Orv. Hetil., 2013, 154, 1180-1187

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Obesity and Cancer Risk: Recent Review and Evidence

Cited by 383 publications

References 34 publications

Hepatocellular carcinoma is accelerated by NASH involving M2 macrophage polarization mediated by hif-1αinduced IL-10

Hepatocellular carcinoma is accelerated by NASH involving M2 macrophage polarization mediated by hif-1αinduced IL-10

Obesity and Cancer: What’s the Interconnection?

Transmethylation and the redox homeostasis

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