Depletion of Short-Chain Fatty Acid-Producing Commensals in Gastric Cancer Is Not Detectably Modified by Type 2 Diabetes or Tumor Characteristics
4 affiliations
- 1Department of Food and Nutrition, Changwon National University, Changwon 51140, Republic of Korea
- 2Interdisciplinary Program in Senior Human Ecology, Changwon National University, Changwon 51140, Republic of Korea
- 3Department of Surgery, Gyeongsang National University School of Medicine and Gyeongsang National University Changwon Hospital, Changwon 51472, Republic of Korea
- 4Department of Nutritional Services, Gyeongsang National University Changwon Hospital, Changwon 51472, Republic of Korea
Abstract
Background/Objectives: Gastric cancer (GC) is associated with depletion of short-chain fatty acid (SCFA)-producing gut commensals, and the same taxa are consistently reduced in type 2 diabetes (T2D). Co-existing metabolic disease might therefore be expected to compound GC-associated dysbiosis, but this has not been examined within a single cohort alongside tumor characteristics. Methods: Fecal microbiota of 97 Korean adults (63 with GC, 34 controls) were profiled by 16S rRNA gene sequencing. Composition, α-diversity, and β-diversity were compared between groups, and within the GC cohort by T2D status, H. pylori status, tumor stage, and lesion location. The summed relative abundance of significantly depleted SCFA-producing genera was analyzed as an aggregate measure of SCFA-producer abundance. Comparisons used Mann–Whitney U tests with Benjamini–Hochberg correction; community-level differences were tested by PERMANOVA. Results: SCFA-producer abundance fell from 26.7 ± 16.9% of the fecal community in controls to 6.6 ± 8.3% in patients with GC (p < 0.001; Cliff’s δ = +0.76, 95% CI +0.61 to +0.89). Enriched genera were predominantly oral and opportunistic, accompanied by expansion of Proteobacteria. Community-level separation was confirmed by PERMANOVA (R2 = 0.088, p = 0.001) with homogeneous dispersions. Within the GC cohort, SCFA-producer abundance did not differ by T2D status, H. pylori status, tumor stage, or lesion location (p = 0.125–0.332), though confidence intervals were wide. Conclusions: Depletion of SCFA-producing commensals in gastric cancer extends across the guild rather than individual genera and was not detectably modified by co-existing T2D or tumor characteristics. Within the limits of this cohort, the signature therefore appears to reflect the presence of disease rather than its clinical or metabolic heterogeneity.
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BibTeX
@article{gu2026depletion,
title = {{Depletion of Short-Chain Fatty Acid-Producing Commensals in Gastric Cancer Is Not Detectably Modified by Type 2 Diabetes or Tumor Characteristics}},
author = {Da-Hye Gu and Amara Zulfiqar and Sang-Ho Jeong and Hyun-Hi Kang and Hyun-Young Joo and Jung-Eun Yim},
journal = {Metabolites},
year = {2026},
month = sep,
doi = {10.3390/metabo16100738},
url = {https://www.mdpi.com/2218-1989/16/10/738},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Depletion of Short-Chain Fatty Acid-Producing Commensals in Gastric Cancer Is Not Detectably Modified by Type 2 Diabetes or Tumor Characteristics
AU - Da-Hye Gu
AU - Amara Zulfiqar
AU - Sang-Ho Jeong
AU - Hyun-Hi Kang
AU - Hyun-Young Joo
AU - Jung-Eun Yim
PY - 2026
DA - 2026/09/30
JO - Metabolites
DO - 10.3390/metabo16100738
UR - https://www.mdpi.com/2218-1989/16/10/738
AB - Background/Objectives: Gastric cancer (GC) is associated with depletion of short-chain fatty acid (SCFA)-producing gut commensals, and the same taxa are consistently reduced in type 2 diabetes (T2D). Co-existing metabolic disease might therefore be expected to compound GC-associated dysbiosis, but this has not been examined within a single cohort alongside tumor characteristics. Methods: Fecal microbiota of 97 Korean adults (63 with GC, 34 controls) were profiled by 16S rRNA gene sequencing. Composition, α-diversity, and β-diversity were compared between groups, and within the GC cohort by T2D status, H. pylori status, tumor stage, and lesion location. The summed relative abundance of significantly depleted SCFA-producing genera was analyzed as an aggregate measure of SCFA-producer abundance. Comparisons used Mann–Whitney U tests with Benjamini–Hochberg correction; community-level differences were tested by PERMANOVA. Results: SCFA-producer abundance fell from 26.7 ± 16.9% of the fecal community in controls to 6.6 ± 8.3% in patients with GC (p < 0.001; Cliff’s δ = +0.76, 95% CI +0.61 to +0.89). Enriched genera were predominantly oral and opportunistic, accompanied by expansion of Proteobacteria. Community-level separation was confirmed by PERMANOVA (R2 = 0.088, p = 0.001) with homogeneous dispersions. Within the GC cohort, SCFA-producer abundance did not differ by T2D status, H. pylori status, tumor stage, or lesion location (p = 0.125–0.332), though confidence intervals were wide. Conclusions: Depletion of SCFA-producing commensals in gastric cancer extends across the guild rather than individual genera and was not detectably modified by co-existing T2D or tumor characteristics. Within the limits of this cohort, the signature therefore appears to reflect the presence of disease rather than its clinical or metabolic heterogeneity.
SN - 2218-1989
ER -