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To our knowledge, this study is the first to provide direct evidence of an association between visceral adiposity and colorectal cancer risk.
Our data indicate age-dependent differences in the relationship between visceral adiposity and brain changes, in particular respecting the cerebellum's structure and connectivity.
In HIV-infected men and women, with or without lipodystrophy, the normal negative relationship between visceral adiposity and adiponectin was maintained [ 30, 36, 37, 41].
Though we used waist circumference as a surrogate measure of visceral adiposity, our findings are consistent with those of Hanley et al who reported an inverse correlation between visceral adiposity and adiponectin in African Americans but not Mexican Americans [ 31].
Whilst further work is required to fully elucidate the link between visceral adiposity and altered mitochondrial function and metabolism in EAC, this study suggests a novel cellular mechanism by which excess adipose tissue may promote and drive carcinogenesis in EAC.
In conclusion, we found a negative correlation between visceral adiposity and cerebellar structure as well as functional connectivity in 20-year-old to 45-year-old subjects which differed significantly compared to 65-year-old to 70-year-old individuals.
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Associations between visceral adiposity, insulin resistance, and comorbidities have been demonstrated across most age groups and ethnicities.
The linkage between dysfunctional visceral adiposity and CV disease has been proven; however, the best way to measure visceral adiposity in chronic kidney disease (CKD) and dialysis patients remains inconclusive [ 8].
The insulin hypothesis has been proposed to explain the association between obesity or visceral adiposity and colorectal cancer (12, 13).
Studies of Japanese immigrants and their offspring in the United States have, however, demonstrated the complex interplay between lifestyle factors promoting visceral adiposity and insulin resistance, and unmasking impaired beta-cell function in genetically susceptible individuals [ 20].
Epidemiological studies demonstrate a strong relationship between body mass index (BMI), measures of visceral adiposity and risk of oesophageal and gastro-oesophageal junctional adenocarcinoma and leptin receptor is expressed in the majority of gastro-oesophageal adenocarcinomas (Abnet et al, 2008; Howard et al, 2010).
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