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Digestive System Diseases

Digestive System and Liver · NLM MeSH · updated 2026-11-04 · version 1

Citations verified against PubMedNot yet clinician-reviewed9 referencesApproximately 3 min read

Diseases in any part of the gastrointestinal tract or the accessory organs (liver; biliary tract; pancreas).

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

Definition and research guide

This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.

Content available: 3 complete abstracts (629 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.

Definition

Diseases in any part of the gastrointestinal tract or the accessory organs (liver; biliary tract; pancreas).

Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.

Also known as: Digestive System Disease; Digestive System Disorders; Digestive System Disorder; System Disorders, Digestive; Hepatobiliary Disorders; Hepatobiliary Disorder; Hepatobiliary Diseases; Hepatobiliary Disease.

Where it fits in the MeSH classification

Narrower topics
Biliary Tract Diseases; Digestive System Abnormalities; Digestive System Fistula; Digestive System Neoplasms; Gastrointestinal Diseases; Liver Diseases; Pancreatic Diseases; Peritoneal Diseases

Related concepts

  • Gastrointestinal Tract
  • Liver
  • Biliary Tract
  • Pancreas

Research landscape

PubMed indexes 2,157,314 records tagged with the MeSH heading “Digestive System Diseases” (counts retrieved 2026-11-04). 426,539 of them (19.8%) were published from 2020 onward, and the busiest period so far is through 1999 with 798,740 records.

Reviews account for 269,125 records (12.5%) and meta-analyses for 25,558. Randomized controlled trials number 44,636 (2.1%) as a share of all records on the topic.

PubMed records by publication periodthrough 1999: 798,740 records; 2000-2009: 376,678 records; 2010-2019: 555,357 records; 2020 onward: 426,539 records798,740through 1999376,6782000-2009555,3572010-2019426,5392020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 1999798,740
2000-2009376,678
2010-2019555,357
2020 onward426,539
Share of records by publication typeReviews: 12.5 percent; Meta-analyses: 1.2 percent; Randomized controlled trials: 2.1 percentReviews12.5% (269,125)Meta-analyses1.2% (25,558)Randomized controlled trials2.1% (44,636)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 2,157,314 PubMed records
TypeRecordsShare
Reviews269,12512.5%
Meta-analyses25,5581.2%
Randomized controlled trials44,6362.1%

Method: PubMed query "Digestive System Diseases"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.

Reading the evidence in digestive system and liver

Gut and liver research ranges from laboratory studies of the microbiome to large trials of drugs and surgery. Symptoms such as pain, reflux or bowel change are reported by patients and overlap between conditions, and diet and microbiome studies are mostly observational. Check whether the study measured symptoms, tissue findings or long-term outcomes, how the diagnosis was made and how long people were followed. Nothing here replaces advice from a qualified clinician.

Evidence from open-access studies

These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.

Study comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
Momordica charantia Attenuates Hepatic Steatosis in High-Fat, High-Sucrose Diet-Induced Obese Mice
Woo HM, Park SY, Jo YH, Lee SJ, Yeon SH, Han HS, et al.
2026Research article
Design not recorded in structured metadata
1cc by
PMID 42929325 · DOI · PMC13700938
Selective AUTAC-mediated ATP7B degradation unlocks cuproptosis vulnerability in pancreatic ductal adenocarcinoma
Zhang Z, Li M, Feng J, Li JA, Zhang L
2026Research article
Design not recorded in structured metadata
0cc by
PMID 42947336 · DOI · PMC13714097
Disparities in screening participation and stage at diagnosis for breast and bowel cancers among individuals with pre-existing mental health disorders: A population-based study
Wang YH, Aggarwal A, Davies EA
2026Research article
Design not recorded in structured metadata
0cc by
PMID 42945295 · DOI · PMC13712726

Momordica charantia Attenuates Hepatic Steatosis in High-Fat, High-Sucrose Diet-Induced Obese Mice [1]

Research article Woo HM, Park SY, Jo YH, Lee SJ, Yeon SH, Han HS, et al. · · 2026 · cited 1 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
High-fat, high-sucrose (HFHS) diet consumption is a major contributor to obesity and liver-related metabolic disorders.
Closing excerpt
Collectively, the present findings suggest that MC may influence metabolic responses associated with chronic consumption of a HFHS diet.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (236 words)

High-fat, high-sucrose (HFHS) diet consumption is a major contributor to obesity and liver-related metabolic disorders. Momordica charantia ethanolic extract powder (MC), derived from a traditional climbing plant, has been shown to exert multiple biological activities, including exhibiting antidiabetic, antioxidant, and antiinflammatory activities. Building on these properties, the present study investigated the potential effects of MC on hepatic lipid metabolism and obesity-related parameters in mice fed a HFHS diet. Male C57BL/6J mice (6 weeks old) were fed an HFHS diet for 4 weeks and subsequently divided into four dietary groups, receiving either continued HFHS, Cissus quadrangularis (CQ; positive control), MC 125 (125 mg/kg), or MC 250 (250 mg/kg) for an additional 12 weeks. Compared with the HFHS group, MC supplementation was associated with lower body weight gain, hepatic lipid accumulation, and epididymal adipocyte size. Histological findings were consistent with these changes in adipose tissue. At the molecular level, MC supplementation was associated with altered hepatic expression of genes involved in lipid metabolism, including decreased expression of the lipogenesis-related genes SREBP-1c, ACC, FAS, and SCD1, as well as alterations in C/EBPα and PPARγ expression. In addition, the expression of fibrosis-related genes Col1α1 and αSMA was decreased in the MC-supplemented groups. These findings suggest that MC supplementation may modulate hepatic lipid metabolism- and fibrosis-related gene expression in HFHS diet-fed mice. Collectively, the present findings suggest that MC may influence metabolic responses associated with chronic consumption of a HFHS diet.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42929325 · DOI · PMC13700938

Selective AUTAC-mediated ATP7B degradation unlocks cuproptosis vulnerability in pancreatic ductal adenocarcinoma [2]

Research article Zhang Z, Li M, Feng J, Li JA, Zhang L · · 2026

Abstract reading summary — source excerpts
Opening excerpt
Cuproptosis arises from mitochondrial copper overload, yet how tumour cells evade this metabolic vulnerability remains unclear.
Closing excerpt
ATAUTAC offers a promising avenue for precision therapy in PDAC and other refractory malignancies.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (154 words)

Cuproptosis arises from mitochondrial copper overload, yet how tumour cells evade this metabolic vulnerability remains unclear. We identify ATP7B as the central barrier to cuproptosis in pancreatic ductal adenocarcinoma (PDAC). ATP7B is aberrantly upregulated in PDAC and predicts poor prognosis. Its depletion increases intracellular copper, activates FDX1, DLAT/DLST lipoylation, disrupts tricarboxylic acid (TCA) metabolism, and reinstates cuproptosis in vitro and in vivo. Mechanistically, ATP7B undergoes ZBTB10-driven K63-linked ubiquitination, recognized by NBR1 for selective autophagic degradation. Leveraging this, we developed an ATP7B-targeting autophagy-targeting chimera (ATAUTAC) that promotes ATP7B clearance, amplifies copper-driven mitochondrial metabolic perturbations, triggers cuproptosis, and inhibits tumour growth with favourable tolerability. Notably, ATAUTAC sensitizes PDAC to gemcitabine, overcoming resistance by exposing latent metabolic fragility. These findings establish ATP7B as a mechanistic hub of cuproptosis tolerance and demonstrate that autophagy-based ATP7B degradation is a druggable strategy for copper-dependent tumour eradication. ATAUTAC offers a promising avenue for precision therapy in PDAC and other refractory malignancies.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42947336 · DOI · PMC13714097

Disparities in screening participation and stage at diagnosis for breast and bowel cancers among individuals with pre-existing mental health disorders: A population-based study [3]

Research article Wang YH, Aggarwal A, Davies EA · · 2026

Abstract reading summary — source excerpts
Opening excerpt
People with pre-existing mental health disorders (PMHD) often have lower cancer screening uptake and later-stage diagnoses.
Closing excerpt
Targeted interventions, procedural simplifications for self-administered tests, and multidisciplinary person-centred care models, may be needed to ensure health equity.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (239 words)

People with pre-existing mental health disorders (PMHD) often have lower cancer screening uptake and later-stage diagnoses. It remains unclear whether these disparities persist within highly accessible universal healthcare systems without strict gatekeeping. We simultaneously investigated the associations between PMHD and both screening participation and stage at diagnosis of breast and bowel cancers within the Taiwan health service. Using nationwide National Health Insurance and Cancer Registry data covering over 99% of the population, we compared outcomes between individuals with and without PMHD. Propensity score matching was applied for the screening cohort. Adjusted odds ratios were estimated using logistic regression, with subgroup analyses for severe PMHD. Overall, PMHD was associated with higher screening participation (adjusted odds ratios [aOR]: breast = 1.04, bowel = 1.12) and reduced odds of metastatic disease at diagnosis (breast = 0.72, bowel = 0.93), although the magnitude of these associations was modest, particularly for bowel cancer. Conversely, individuals with severe PMHD had significantly lower odds of screening (breast = 0.81, bowel = 0.88) despite high outpatient use. Furthermore, while the severe group retained reduced odds of metastatic breast cancer at diagnosis (aOR = 0.79), they showed no staging advantage for bowel cancer. While Taiwan's highly accessible universal healthcare system may contribute to a surveillance effect benefiting the general PMHD population, significant disparities persist for individuals with severe illnesses. Targeted interventions, procedural simplifications for self-administered tests, and multidisciplinary person-centred care models, may be needed to ensure health equity.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42945295 · DOI · PMC13712726

Key reviews and meta-analyses

The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.

  • Research article Global Prevalence, Incidence, and Outcomes of Coexisting MASLD and Chronic Kidney Disease: A Meta-Analysis [4]
    Kueh MTW, Yeo JKW, Chen Y, Chua NYZ, Koh HL, Khaw SP, et al. · Liver Int · 2026 · cited 10 times (Europe PMC)
  • Research article High-intensity interval training and moderate-intensity continuous training are effective, feasible, and safe for patients with metabolic dysfunction-associated steatotic liver disease (MASLD): A systematic review and meta-analysis [5]
    Wang B, Zeng X, Deng H, Qiu B, Xu K, Tao M, et al. · Metabolism · 2026 · cited 5 times (Europe PMC)
  • Research article Meta-Analysis: Crohn's Disease Exclusion Diet for Induction and Maintenance in Crohn's Disease [6]
    Batra G, Shukla A, Chatterjee A, Chandnani S, Singh A, Yadav DP, et al. · Aliment Pharmacol Ther · 2026 · cited 3 times (Europe PMC)
  • Research article Meta-analysis reveals microbiome signatures for colorectal cancer that are universal across age groups and sequencing methods [7]
    Pekel S, Karcher N, Essex M, Springer F, Romano S, Ducarmon QR, et al. · Cell Host Microbe · 2026 · cited 3 times (Europe PMC)
  • Research article Incidence of Cirrhosis in Fibrotic Metabolic Dysfunction-Associated Steatohepatitis: A Meta-Analysis of Placebo Arms from Randomized Clinical Trials [8]
    Khalil SM, Al-Sharif L, Diaz I, Souza M · Dig Dis Sci · 2026 · cited 2 times (Europe PMC)
  • Research article Meta-Analysis: Prevalence of Non-Helicobacter pylori, Non-NSAID Peptic Ulcer Disease [9]
    Watanabe J, Sekiguchi H, Kanno T, Misawa K, Sato S, Yuan Y, et al. · Aliment Pharmacol Ther · 2026 · cited 2 times (Europe PMC)

References

  1. Woo HM, Park SY, Jo YH, Lee SJ, Yeon SH, Han HS, et al.. Momordica charantia Attenuates Hepatic Steatosis in High-Fat, High-Sucrose Diet-Induced Obese Mice. . 2026. PMID 42929325 · DOI · PMC13700938
  2. Zhang Z, Li M, Feng J, Li JA, Zhang L. Selective AUTAC-mediated ATP7B degradation unlocks cuproptosis vulnerability in pancreatic ductal adenocarcinoma. . 2026. PMID 42947336 · DOI · PMC13714097
  3. Wang YH, Aggarwal A, Davies EA. Disparities in screening participation and stage at diagnosis for breast and bowel cancers among individuals with pre-existing mental health disorders: A population-based study. . 2026. PMID 42945295 · DOI · PMC13712726
  4. Kueh MTW, Yeo JKW, Chen Y, Chua NYZ, Koh HL, Khaw SP, et al.. Global Prevalence, Incidence, and Outcomes of Coexisting MASLD and Chronic Kidney Disease: A Meta-Analysis. Liver Int. 2026. PMID 42347761 · DOI
  5. Wang B, Zeng X, Deng H, Qiu B, Xu K, Tao M, et al.. High-intensity interval training and moderate-intensity continuous training are effective, feasible, and safe for patients with metabolic dysfunction-associated steatotic liver disease (MASLD): A systematic review and meta-analysis. Metabolism. 2026. PMID 42297097 · DOI
  6. Batra G, Shukla A, Chatterjee A, Chandnani S, Singh A, Yadav DP, et al.. Meta-Analysis: Crohn's Disease Exclusion Diet for Induction and Maintenance in Crohn's Disease. Aliment Pharmacol Ther. 2026. PMID 42437372 · DOI · PMC13511444
  7. Pekel S, Karcher N, Essex M, Springer F, Romano S, Ducarmon QR, et al.. Meta-analysis reveals microbiome signatures for colorectal cancer that are universal across age groups and sequencing methods. Cell Host Microbe. 2026. PMID 42341762 · DOI
  8. Khalil SM, Al-Sharif L, Diaz I, Souza M. Incidence of Cirrhosis in Fibrotic Metabolic Dysfunction-Associated Steatohepatitis: A Meta-Analysis of Placebo Arms from Randomized Clinical Trials. Dig Dis Sci. 2026. PMID 42315723 · DOI
  9. Watanabe J, Sekiguchi H, Kanno T, Misawa K, Sato S, Yuan Y, et al.. Meta-Analysis: Prevalence of Non-Helicobacter pylori, Non-NSAID Peptic Ulcer Disease. Aliment Pharmacol Ther. 2026. PMID 42572812 · DOI · PMC13603966

About this article

Sources
NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
Verification
Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
Review state
automated source verified; no human expert review has been recorded yet.
Version
1, last updated 2026-11-04.

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EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.

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At a glance

2,157,314
PubMed records on this heading
20%
published since 2020
269,125
review articles
44,636
randomized trials
9
verified references below

Counts come from PubMed on 2026-11-04; they show how much has been written, not how strong the evidence is.

Related topics See all →

  • Digestive SystemAnatomy and Physiology
  • Gastrointestinal TractAnatomy and Physiology
  • Biliary Tract DiseasesDigestive System and Liver
  • DiverticulumDigestive System and Liver
  • HematemesisDigestive System and Liver

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