Obesity and Gastroesophageal Reflux Disease

El–Serag, Hashem B.; Thrift, Aaron P.

doi:10.1002/9781119599692.ch36

Cited by 6 publications

(3 citation statements)

References 67 publications

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“…Moreover, the prevalence of GERD is proportional to the severity of obesity [ 106 ]. The prevalence of GERD symptoms in patients with morbid obesity reaches 50% [ 107 ]. Successful weight loss and the therapy to reduce the visceral adipose tissue have been shown to significantly reduce GERD symptoms [ 108 , 109 , 110 , 111 , 112 , 113 ].…”

Section: The Role Of Obesity In Be and Eac Developmentmentioning

confidence: 99%

“…It is not excluded that adipokines released by adipose tissue may influence the development and severity of GERD [ 107 ]. Increased leptin and leptin receptor (ObR) levels and decreased APN levels were reported in obese patients with GERD [ 129 , 130 , 131 , 132 ], and increased leptin levels, widely considered as a marker of obesity, have been associated with frequent GERD symptoms [ 133 ] and clinical and endoscopic severity of GERD [ 130 ].…”

Section: The Role Of Obesity In Be and Eac Developmentmentioning

confidence: 99%

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

Bilski

Pinkas

Wójcik

et al. 2022

IJMS

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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.

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Section: The Role Of Obesity In Be and Eac Developmentmentioning

confidence: 99%

Section: The Role Of Obesity In Be and Eac Developmentmentioning

confidence: 99%

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

Bilski

Pinkas

Wójcik

et al. 2022

IJMS

View full text Add to dashboard Cite

show abstract

“…[1] An undesirable hallmark of obesity is the development of a chronic inflammatory state that can exacerbate various human diseases. [2] For instance, inflammation of the gastrointestinal (GI) tract can increase the risk of non-alcoholic fatty liver disease, [3] gastroesophageal reflux, [4] gallstones, [5] and colorectal cancer. [6] Inflammation that is linked to obesity is a complex process that results from the interaction between various pathways including nitric oxide (NO) signalling and the endocannabinoid system (ECS).…”

Section: Introductionmentioning

confidence: 99%

Activity‐based Photoacoustic Probes Reveal Elevated Intestinal MGL and FAAH Activity in a Murine Model of Obesity

et al. 2022

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Obesity is a chronic health condition characterized by the accumulation of excessive body fat which can lead to and exacerbate cardiovascular disease, type-II diabetes, high blood pressure, and cancer through systemic inflammation. Unfortunately, visualizing key mediators of the inflammatory response, such as monoacylglycerol lipase (MGL) and fatty acid amide hydrolase (FAAH), in a selective manner is a profound challenge owing to an overlapping substrate scope that involves arachidonic acid (AA). Specifically, these enzymes work in concert to generate AA, which in the context of obesity, has been implicated to control appetite and energy metabolism. In this study, we developed the first selective activity-based sensing probes to detect MGL (PA-HD-MGL) and FAAH (PA-HD-FAAH) activity via photoacoustic imaging. Activation of PA-HD-MGL and PA-HD-FAAH by their target enzymes resulted in 1.74-fold and 1.59-fold signal enhancements, respectively. Due to their exceptional selectivity profiles and deep-tissue photoacoustic imaging capabilities, these probes were employed to measure MGL and FAAH activity in a murine model of obesity. Contrary to conflicting reports suggesting levels of MGL can be attenuated or elevated, our results support the latter. Indeed, we discovered a marked increase of both targets in the gastrointestinal tract. These key findings set the stage to uncover the role of the endocannabinoid pathway in obesity-mediated inflammation.

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Epidemiology, Microbiome, and Risk Factors Involved in Carcinogenesis of Esophagus, Gastric, and Intestine

Chew,

Yim,

Ali

et al. 2024

Gastrointestinal Oncology ‐ a Critical Multidisciplinary Team Approach 2e

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Obesity and Gastroesophageal Reflux Disease

Cited by 6 publications

References 67 publications

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

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

Activity‐based Photoacoustic Probes Reveal Elevated Intestinal MGL and FAAH Activity in a Murine Model of Obesity

Epidemiology, Microbiome, and Risk Factors Involved in Carcinogenesis of Esophagus, Gastric, and Intestine

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