Associations between leptin and adiponectin receptor upregulation, visceral obesity and tumour stage in oesophageal and junctional adenocarcinoma

Howard, Julia; Beddy, Peter; Ennis, Darren; Keogan, Mary T.; Pidgeon, Graham P.; Reynolds, John V.

doi:10.1002/bjs.7072

Cited by 82 publications

(64 citation statements)

References 45 publications

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“…The WC association with OAC was not attenuated when adjusted for BMI, adding to the evidence that abdominal fat is more important than just excess weight [O'Doherty et al 2012;MacInnis et al 2006;Corley et al 2007a]. Patients with OAC were also found to have significantly more VAT on CT compared with controls [Beddy et al 2010]. In a meta-analysis including data from six studies, when compared with normal body habitus, central adiposity was associated with higher risk of OAC (aOR 2.51; 95% CI 1.54-4.06) [Singh et al 2013b].…”

Section: Obesity and Oacmentioning

confidence: 84%

The role of obesity in oesophageal cancer development

Long

Beales

2014

Therap Adv Gastroenterol

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Abstract:The incidence of oesophageal adenocarcinoma has increased dramatically in the developed world in the last half century. Over approximately the same period there has been an increase in the prevalence of obesity. Multiple epidemiological studies and metaanalyses have confirmed that obesity, especially abdominal, visceral obesity, is a risk factor for gastro-oesophageal reflux, Barrett's oesophagus and oesophageal adenocarcinoma. Although visceral obesity enhances gastro-oesophageal reflux, the available data also show that visceral obesity increases the risk of Barrett's oesophagus and adenocarcinoma via reflux-independent mechanisms. Several possible mechanisms could link obesity with the risk of oesophageal adenocarcinoma in addition to mechanical effects increasing reflux. These include reduced gastric Helicobacter pylori infection, altered intestinal microbiome, factors related to lifestyle, the metabolic syndrome and associated low-grade inflammation induced by obesity and the secretion of mediators by adipocytes which may directly influence the oesophageal epithelium. Of these adipocyte-derived mediators, increased leptin levels have been independently associated with progression to oesophageal adenocarcinoma and in laboratory studies leptin enhances malignant behaviours in cell lines. Adiponectin is also secreted by adipocytes and levels decline with obesity: decreased serum adiponectin levels are associated with malignant progression in Barrett's oesophagus and experimentally adiponectin exerts anticancer effects in Barrett's cell lines and inhibits growth factor signalling. At present there are no proven chemopreventative interventions that may reduce the incidence of obesity-associated oesophageal cancer: observational studies suggest that the combined use of a statin and aspirin or another cyclo-oxygenase inhibitor is associated with a significantly reduced cancer incidence in patients with Barrett's oesophagus.

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Section: Obesity and Oacmentioning

confidence: 84%

The role of obesity in oesophageal cancer development

Long

Beales

2014

Therap Adv Gastroenterol

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“…Moreover, antiproliferative effects of phytoestrogens have been found in certain cell lines, including esophageal cancer cells [7,18,19]. Lignans can reduce expression of leptin and stimulate the expression of adiponectin [20], both of which in turn are inversely associated with the risk of adenocarcinoma of esophagus and gastroesophageal junction [21][22][23]. Taken together, these findings indicate that lignans have the potential to prevent esophageal cancer [24].…”

Section: Introductionmentioning

confidence: 99%

Dietary intake of lignans and risk of adenocarcinoma of the esophagus and gastroesophageal junction

Lin

Yngve

Lagergren

et al. 2012

Cancer Causes Control

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“…A number of in-vitro studies of adipokines have shown them to effect cellular proliferation, apoptosis, angiogenesis and inflammation [25-28]. In patients with OA there is obesity-associated upregulation of the leptin receptor (ObR) and adiponectin receptor 2 (AdipR2) [29]. Leptin and adiponectin have been shown to be associated with the risk of BO suggesting that adipokines may have a role in BO and OA [17, 30].…”

Section: Discussionmentioning

confidence: 99%

Total body fat and the risk of Barrett's oesophagus – A bioelectrical impedance study

Kendall

Macdonald

Prins

et al. 2014

Cancer Epidemiology

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Background Body mass index is associated with the risk of Barrett's oesophagus (BO). It is uncertain whether this is related to total body fat or other factors that correlate with body mass index. We aimed to quantify the association between total body fat (measured by bioelectrical impedance) and risk of BO and examine if this association was modified by gastro-oesophageal reflux (GOR) and abdominal obesity. Methods In 2007-9, we surveyed 235 cases (69% Males, Mean age 62.1 years) and 244 age and sex matched population controls from a population based case-control study of BO. We conducted structured interviews, standard anthropometry and bioimpedance analysis of total body fat. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using multivariable logistic regression analysis. Results There was a significantly increased risk of BO among those in the highest tertile of total body fat weight (OR 2.01; 95%CI 1.26-3.21) and total body fat percentage (OR 1.86; 95%CI 1.10-3.15). These risks were largely attenuated after adjustment for GOR and waist circumference. There was a significantly increased risk of BO among those in the highest tertile of waist circumference (OR 2.21; 95%CI 1.39-3.51) and this was minimally attenuated after adjustment for total body fat and moderately attenuated after adjustment for GOR. Conclusions Total body fat is associated with an increased risk of BO but this appears to be mediated via both abdominal obesity and GOR. These findings provide evidence that abdominal obesity is more important than total body fat in the development of BO.

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Associations between leptin and adiponectin receptor upregulation, visceral obesity and tumour stage in oesophageal and junctional adenocarcinoma

Abstract: Obesity is associated with upregulated ObR and AdipR2 expression in oesophageal adenocarcinoma. The association of ObR and AdipR2 with tumour stage suggest that pathways involving adipocytokines affect tumour biology.

Cited by 82 publications

References 45 publications

The role of obesity in oesophageal cancer development

The role of obesity in oesophageal cancer development

Dietary intake of lignans and risk of adenocarcinoma of the esophagus and gastroesophageal junction

Total body fat and the risk of Barrett's oesophagus – A bioelectrical impedance study

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