Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2014 Apr:1311:42-56.
doi: 10.1111/nyas.12385. Epub 2014 Mar 6.

Gastrointestinal morbidity in obesity

Andres Acosta  1 , Michael Camilleri
Affiliations
Review

Gastrointestinal morbidity in obesity

Andres Acosta et al. Ann N Y Acad Sci. 2014 Apr.

Abstract

Obesity is a complex disease that results from increased energy intake and decreased energy expenditure. The gastrointestinal system plays a key role in the pathogenesis of obesity and facilitates caloric imbalance. Changes in gastrointestinal hormones and the inhibition of mechanisms that curtail caloric intake result in weight gain. It is not clear if the gastrointestinal role in obesity is a cause or an effect of this disease. Obesity is often associated with type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD). Obesity is also associated with gastrointestinal disorders, which are more frequent and present earlier than T2DM and CVD. Diseases such as gastroesophageal reflux disease (GERD), cholelithiasis, or nonalcoholic steatohepatitis are directly related to body weight and abdominal adiposity. Our objective is to assess the role of each gastrointestinal organ in obesity and the gastrointestinal morbidity resulting in those organs from the effects of obesity.

Keywords: GERD; appetite; cancer; diarrhea; gastrointestinal; obesity.

PubMed Disclaimer

Conflict of interest statement

Disclosures: There are no conflicts of interest.

Figures

Figure 1
Figure 1
Caloric intake at maximum satiation by gender and BMI. There was higher caloric intake at maximum satiation in male subjects compared with women (left). After adjusting for differences in sex, overweight (BMI 25–30 kg/m2) and obese (BMI>30 kg/m2) (merged as “obese”) showed higher caloric intakes at maximum satiation compared with normal weight subjects, whereas underweight individuals showed lower caloric intakes. Reproduced from Delgado-Aros et al. Gastroenterology 2004;126:432–440.
Figure 2
Figure 2
Body mass index in men and women with idiopathic bile acid malabsorption and in healthy men and women shown as median, IQR, and percentile 10 and 90. The dashed line shows the upper limit of normal weight (25kg/m2). Reproduced from Sadik et al. Am J Gastroenterol 2004;99:711-718.
See this image and copyright information in PMC

References

    1. Blundell J, Gillett A. Control of food intake in the obese. Obesity research. 2001;9(Suppl 4) - PubMed
    1. Cannon WB, Washburn AL. An Explanation of Hunger1. Obesity research. 1912;1 - PubMed
    1. Hertz AF. The sensibility of the alimentary canal in health and disease. The Lancet. 1911
    1. Boring EG. The Sensations of the Alimentary Canal. The American Journal of Psychology. 1915;26
    1. Delgado-Aros S, Cremonini F, Castillo J, Chial H, Burton D, Ferber I, et al. Independent influences of body mass and gastric volumes on satiation in humans. Gastroenterology. 2004;126(2):432–40. - PubMed

Publication types

MeSH terms