Limosilactobacillus reuteri ameliorates diet-associated metabolic dysfunction in PCOS-like rats: associations with intestinal lipid remodeling and GPR120-related regulation
4 affiliations
- 1Department of Reproductive Medicine, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
- 2Shanghai Key Laboratory for Assisted Reproduction and Reproductive Genetics, Shanghai, China
- 3State Key Laboratory of Reproductive Medicine and Offspring Health, Center for Reproductive Medicine, Institute of Women, Children and Reproductive Health, Shandong University, Jinan, Shandong, China
- 4National Research Center for Assisted Reproductive Technology and Reproductive Genetics, Shandong University, Jinan, Shandong, China
Abstract
BackgroundPolycystic ovary syndrome (PCOS) is a common endocrine-metabolic disorder frequently accompanied by dyslipidemia. However, the relationships among Limosilactobacillus reuteri (L. reuteri) supplementation, gut microbiota-associated lipid remodeling, and PCOS-related metabolic dysfunction remain unclear.MethodsA high-fat diet combined with dehydroepiandrosterone-induced PCOS-like rat model (HFHA) was established to evaluate the effects of L. reuteri supplementation. Gut microbiota composition, lipidomic profiles, jejunal GPR120/PPARγ-related molecular markers, and fatty-acid transporter expression were assessed. Potential GPR120-associated involvement was pharmacologically evaluated using AH-7614, with complementary experiments performed in Caco-2 cells.ResultsL. reuteri alleviated high-fat diet-associated metabolic dysfunction, reducing body-weight gain, dyslipidemia, and hepatic steatosis. Formal interaction analyses further supported metabolic-context-dependent effects for several metabolic and endocrine endpoints. L. reuteri supplementation altered gut microbial composition and was associated with increased abundances of colonic fatty-acid features putatively annotated as FA(22:5), FA(24:5), and FA(24:6). These colonic lipid-profile changes occurred alongside increased jejunal GPR120 expression, reduced PPARγ abundance, and lower CD36/FABP2 expression. AH-7614 co-treatment attenuated several metabolic, reproductive, and intestinal effects associated with L. reuteri supplementation. In Caco-2 cells, pharmacological modulation or overexpression of GPR120 reduced FFA-induced CD36 and FABP2 expression and intracellular lipid accumulation, whereas AH-7614 or Barbadin treatment attenuated these responses.ConclusionL. reuteri improves diet-associated metabolic dysfunction in PCOS-like rats, accompanied by gut microbiota remodeling, altered intestinal lipid profiles, reduced intestinal lipid accumulation, and GPR120-associated regulation of CD36 and FABP2. These findings support a potential role for altered intestinal lipid handling in the metabolic effects of L. reuteri, although the identities, origins, and direct receptor activities of the relevant lipid mediators require further investigation.
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BibTeX
@article{wang2026limosilactobacillus,
title = {{Limosilactobacillus reuteri ameliorates diet-associated metabolic dysfunction in PCOS-like rats: associations with intestinal lipid remodeling and GPR120-related regulation}},
author = {Cong Wang and Cong Wang and Shang Li and Shang Li and Junyu Zhai and Junyu Zhai and Juanjuan Yu and Juanjuan Yu and Xiying Zhou and Xiying Zhou and Kewei Wu and Kewei Wu and Yuliu Xu and Yuliu Xu and Meiyi He and Meiyi He and Lexin Yang and Lexin Yang and Min Hou and Min Hou and Zi-Jiang Chen and Zi-Jiang Chen and Zi-Jiang Chen and Zi-Jiang Chen and Yanzhi Du and Yanzhi Du},
journal = {Frontiers in Nutrition},
year = {2026},
month = nov,
doi = {10.3389/fnut.2026.1952526},
url = {https://doi.org/10.3389/fnut.2026.1952526},
note = {CC BY},
}
RIS
TY - JOUR
TI - Limosilactobacillus reuteri ameliorates diet-associated metabolic dysfunction in PCOS-like rats: associations with intestinal lipid remodeling and GPR120-related regulation
AU - Cong Wang
AU - Cong Wang
AU - Shang Li
AU - Shang Li
AU - Junyu Zhai
AU - Junyu Zhai
AU - Juanjuan Yu
AU - Juanjuan Yu
AU - Xiying Zhou
AU - Xiying Zhou
AU - Kewei Wu
AU - Kewei Wu
AU - Yuliu Xu
AU - Yuliu Xu
AU - Meiyi He
AU - Meiyi He
AU - Lexin Yang
AU - Lexin Yang
AU - Min Hou
AU - Min Hou
AU - Zi-Jiang Chen
AU - Zi-Jiang Chen
AU - Zi-Jiang Chen
AU - Zi-Jiang Chen
AU - Yanzhi Du
AU - Yanzhi Du
PY - 2026
DA - 2026/11/03
JO - Frontiers in Nutrition
DO - 10.3389/fnut.2026.1952526
UR - https://doi.org/10.3389/fnut.2026.1952526
AB - BackgroundPolycystic ovary syndrome (PCOS) is a common endocrine-metabolic disorder frequently accompanied by dyslipidemia. However, the relationships among Limosilactobacillus reuteri (L. reuteri) supplementation, gut microbiota-associated lipid remodeling, and PCOS-related metabolic dysfunction remain unclear.MethodsA high-fat diet combined with dehydroepiandrosterone-induced PCOS-like rat model (HFHA) was established to evaluate the effects of L. reuteri supplementation. Gut microbiota composition, lipidomic profiles, jejunal GPR120/PPARγ-related molecular markers, and fatty-acid transporter expression were assessed. Potential GPR120-associated involvement was pharmacologically evaluated using AH-7614, with complementary experiments performed in Caco-2 cells.ResultsL. reuteri alleviated high-fat diet-associated metabolic dysfunction, reducing body-weight gain, dyslipidemia, and hepatic steatosis. Formal interaction analyses further supported metabolic-context-dependent effects for several metabolic and endocrine endpoints. L. reuteri supplementation altered gut microbial composition and was associated with increased abundances of colonic fatty-acid features putatively annotated as FA(22:5), FA(24:5), and FA(24:6). These colonic lipid-profile changes occurred alongside increased jejunal GPR120 expression, reduced PPARγ abundance, and lower CD36/FABP2 expression. AH-7614 co-treatment attenuated several metabolic, reproductive, and intestinal effects associated with L. reuteri supplementation. In Caco-2 cells, pharmacological modulation or overexpression of GPR120 reduced FFA-induced CD36 and FABP2 expression and intracellular lipid accumulation, whereas AH-7614 or Barbadin treatment attenuated these responses.ConclusionL. reuteri improves diet-associated metabolic dysfunction in PCOS-like rats, accompanied by gut microbiota remodeling, altered intestinal lipid profiles, reduced intestinal lipid accumulation, and GPR120-associated regulation of CD36 and FABP2. These findings support a potential role for altered intestinal lipid handling in the metabolic effects of L. reuteri, although the identities, origins, and direct receptor activities of the relevant lipid mediators require further investigation.
SN - 2296-861X
ER -