Role of Obesity, Physical Exercise, Adipose Tissue-Skeletal Muscle Crosstalk and Molecular Advances in Barrett’s Esophagus and Esophageal Adenocarcinoma

Abstract

Both obesity and esophageal adenocarcinoma (EAC) rates have increased sharply in the United States and Western Europe in recent years. EAC is a classic example of obesity-related cancer where the risk of EAC increases with increasing body mass index. Pathologically altered visceral fat in obesity appears to play a key role in this process. Visceral obesity may promote EAC by directly affecting gastroesophageal reflux disease and Barrett’s esophagus (BE), as well as a less reflux-dependent effect, including the release of pro-inflammatory adipokines and insulin resistance. Deregulation of adipokine production, such as the shift to an increased amount of leptin relative to “protective” adiponectin, has been implicated in the pathogenesis of BE and EAC. This review discusses not only the epidemiology and pathophysiology of obesity in BE and EAC, but also molecular alterations at the level of mRNA and proteins associated with these esophageal pathologies and the potential role of adipokines and myokines in these disorders. Particular attention is given to discussing the possible crosstalk of adipokines and myokines during exercise. It is concluded that lifestyle interventions to increase regular physical activity could be helpful as a promising strategy for preventing the development of BE and EAC.

Analysis of Body Mass Index in Early and Middle Adulthood and Estimated Risk of Gastrointestinal Cancer

“…Transcriptomic analysis of the ColoCare Study, a prospective cohort of newly diagnosed CRCs, found enrichment of pathways, such as fibrosis and glycolytic metabolism, associated with adipose–tumor tissue crosstalk . Similar findings have been observed for noncolorectal GI cancers . Although likely not the initiator, excess adipocytes promote tumorigenesis through supplying cancer cells with much-needed nutrients and stimulation of oncogenic pathways.…”

“… 37 Similar findings have been observed for noncolorectal GI cancers. 38 , 39 , 40 Although likely not the initiator, excess adipocytes promote tumorigenesis through supplying cancer cells with much-needed nutrients and stimulation of oncogenic pathways. Therefore, cancer prevention mechanisms that target the harmful physiologic effects of obesity may work to counteract tumorigenesis.…”

Bibliometric and visual analysis of esophagogastric junction cancer research from 2002 to 2021

“…[ 12 , 38 , 39 ] Numerous studies have substantiated that obesity, especially visceral obesity, served as an independent risk factor contributing to the progression and severity of BE and GERD, which might ultimately result in EGC. [ 40 ] Recently, a growing interest is being focused on immunotherapy, targeted therapy, and neo-adjuvant chemotherapy. [ 41 ] EGC patients may not be the candidates for radical surgery owing to the advanced-stage or metastatic disease at diagnosis.…”

Efeito do treinamento concorrente na composição corporal e perfil metabólico de pessoas obesas: Uma revisão sistemática

“…No entanto, determinar a eficácia do ER é um desafio devido à dependência do corpo e peso do que a composição corporal geral em indivíduos com sobrepeso/obesidade (Da Silva et al, 2020;Batrakoulis;Fatouros, 2022), pois o ER pode resultando em aumentos de peso corporal devido ao acúmulo de massa magra (melhora da composição corporal (CC) que está altamente associada à saúde metabólica e função física versus diminuição de tecido adiposo subcutâneo principalmente), subestimando a importância desses tecidos para a saúde geral (Bilski et al, 2022;Mangano et al, 2022).…”