ArticleProbiotics and antimicrobial proteins2026
Lactobacillus rhamnosus GG Supernatant Improves GLP-1 Secretion Through Attenuating L Cell Lipotoxicity and Modulating Gut Microbiota in Obesity.
Article in Probiotics and antimicrobial proteins, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Effects of Wilac D001 (Journal of microbiology and biotechnology · 2026Trial
- Reframing obesity through the gut microbiota: functional dysbiosis and metabolic disease.Current opinion in clinical nutrition and metabolic care · 2026Review
- Improving Lipid Profiles ThroughFoods (Basel, Switzerland) · 2026Review
- Article
- Gut Microbial Metabolites of Tryptophan Augment Enteroendocrine Cell Differentiation in Human Colonic Organoids: Therapeutic Potential for Dysregulated GLP1 Secretion in Obesity.International journal of molecular sciences · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Obesity is associated with decreased secretion of glucagon-like peptide-1 (GLP-1), which may result from lipotoxic damage to L cells caused by elevated levels of free fatty acids (FFAs). Although the probiotic Lactobacillus rhamnosus GG (LGG) exhibits anti-apoptotic properties, its potential to protect L cells from lipotoxic damage remains uncertain. This study investigated the impact of LGG supernatant (LGGs) on NCI-H716 cells treated with palmitic acid (PA) to mimic lipotoxic injury, focusing on cell apoptosis and function. Transcriptome sequencing was used to explore the mechanism of the action of LGGs. Additionally, the effects of LGGs on body weight, glucose tolerance, GLP-1 secretion, and gut microbiota were assessed in a diet-induced obese mouse model. PA induced L cell apoptosis and decreased the level of prohormone convertase 1 (PC1) in a concentration- and time-dependent manner, leading to intracellular accumulation of proglucagon (GCG). LGGs significantly restored PA-induced downregulation of PC1, GCG accumulation, and cell apoptosis, mainly by inhibiting endoplasmic reticulum stress and downregulating the ATF3/Chop pathway. Overexpression of Chop or ATF3 partially reversed the protective effect of LGGs. Additionally, in the mouse model, LGGs improved obesity, insulin resistance, and glucose tolerance, and restored GLP-1 secretion, which may be related to LGGs' inhibition of the ATF3/Chop pathway in L cells, regulation of gut microbiota composition, and enhancement of short-chain fatty acid production. Overall, LGGs can ameliorate high-fat diet-induced impairment of GLP-1 secretion by inhibiting lipotoxicity-mediated damage through the ATF3/Chop pathway and modulating the gut microbiota.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.