Obesity as a risk factor for diseases of the digestive system

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Abstract

Currently, the global prevalence of obesity among the world’s adult population is about 650 million people, which makes it possible to consider this chronic metabolic disease as a non-infectious pandemic of the 21st century. It has been proven that obesity is associated with several gastroenterological diseases, while the mechanisms of these associations are extremely heterogeneous and multifactorial. Hypertrophy and hyperplasia of adipocytes in obesity lead to a change in the profile of adipokine production (a decrease in adiponectin, an increase in leptin), an increase in the production of pro-inflammatory cytokines (interleukin-1, 6, 8, tumor necrosis factor á), C-reactive protein, free fatty acids, as well as active forms of oxygen (superoxide radicals, H2O2). All the above induces the development of chronic slowly progressive inflammation, oxidative stress, and insulin resistance. In addition, peptides secreted by adipocytes (adiponectin, leptin, nesfatin-1 and apelin) can modulate gastrointestinal motility, acting both centrally and peripherally. The qualitative and quantitative changes in the intestinal microbiota observed in obese patients (increased Firmicutes and decreased Bacteroidetes) lead to a decrease in the production of short-chain fatty acids and an increase in the intestinal permeability due to disruption of intercellular tight junctions, which leads to increased translocation of bacteria and endotoxins into the systemic circulation. Numerous studies have demonstrated the association of obesity with diseases of the esophagus (gastroesophageal reflux disease, Barrett’s esophagus, esophageal adenocarcinoma, esophageal motility disorders), stomach (functional dyspepsia, stomach cancer), gallbladder (cholelithiasis, gallbladder cancer), pancreas (acute pancreatitis, pancreatic cancer), liver (non-alcoholic fatty liver disease, hepatocellular carcinoma), intestine (diverticular disease, irritable bowel syndrome, colorectal cancer).

About the authors

Dmitry N. Andreev

Yevdokimov Moscow State University of Medicine and Dentistry

Author for correspondence.
Email: dna-mit8@mail.ru
ORCID iD: 0000-0002-4007-7112

кандидат медицинских наук, доцент кафедры пропедевтики внутренних болезней и гастроэнтерологии

Russian Federation, Moscow

Yury A. Kucheryavyy

Ilyinsky Hospital

Email: dna-mit8@mail.ru
ORCID iD: 0000-0001-7760-2091

кандидат медицинских наук, доцент, заведующий гастроэнтерологическим отделением

Russian Federation, Krasnogorsk

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2. Fig. 1. Global prevalence of obesity (%) [6].

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3. Fig. 2. Pathophysiological mechanisms of gastroesophageal reflux disease in obese patients [33].

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4. Fig. 3. The concept of non-alcoholic fatty liver disease pathogenesis in obese individuals [56].

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5. Fig. 4. Algorithm for managing a patient with exogenous constitutional obesity (2020 Russian Association of Endocrinologists/Society for Bariatric Surgeons clinical guidelines) [74].

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6. Fig. 5. Weight loss under therapy with Mucofalk [79].

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7. Fig. 6. Relative weight loss after 6 months of therapy in obese patients with functional constipation (%) [80].

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