Evidence map›Paper›PMID 38937659›Full record

ArticleNature metabolism2024

Ketogenic diet-induced bile acids protect against obesity through reduced calorie absorption.

Xiao Li, Jie Yang, Xiaofeng Zhou, Chen Dai, Mengmeng Kong, Linshan Xie, Chenglin Liu, Yilian Liu, Dandan Li, Xiaonan Ma and 12 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  8. Article
  9. Risk factor obesity: treatment standard.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026
    Review
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  17. Article
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  19. Article
  20. Ketogenic diet and Parkinson's disease.Frontiers in molecular neuroscience · 2026
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

22 authors.

Xiao Li *State Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai, P.R. China.ORCID http://orcid.org/0000-0002-8733-813X
Jie Yang *State Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai, P.R. China.ORCID http://orcid.org/0009-0002-4258-1627
Xiaofeng Zhou *State Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai, P.R. China.
Chen DaiState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai, P.R. China.
Mengmeng KongState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai, P.R. China.
Linshan XieState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai, P.R. China.
Chenglin LiuState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai, P.R. China.ORCID http://orcid.org/0000-0001-5626-4097
Yilian LiuState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai, P.R. China.ORCID http://orcid.org/0000-0002-7642-7727
Dandan LiState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai, P.R. China.
Xiaonan MaState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai, P.R. China.ORCID http://orcid.org/0000-0001-6485-0184
Yuxiang DaiDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Disease, Shanghai, P.R. China.
Yan SunMasonic Medical Research Institute, Utica, NY, USA.ORCID http://orcid.org/0000-0002-8776-0832
Zhijie JianDepartment of Radiology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, P.R. China.
Xiaohuan GuoInstitute for Immunology, Tsinghua University, Beijing, P.R. China.ORCID http://orcid.org/0000-0001-5152-3010
Xu LinShanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, P.R. China.
Yixue LiBio-Med Big Data Center, Key Laboratory of Computational Biology, CAS-MPG Partner Institute for Computational Biology, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, P.R. China.ORCID http://orcid.org/0000-0002-1198-7176
Liang SunDepartment of Nutrition and Food Hygiene, School of Public Health, Institute of Nutrition, Fudan University, Shanghai, P.R. China.
Xin LiuDepartment of Epidemiology and Biostatistics, School of Public Health, Global Health Institute, Xi'an Jiaotong University Health Science Center, Xi'an, P.R. China.ORCID http://orcid.org/0000-0001-5105-0532
Li JinState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai, P.R. China.ORCID http://orcid.org/0000-0001-9201-2321
Huiru TangState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai, P.R. China.ORCID http://orcid.org/0000-0002-7139-2756
Yan ZhengState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai, P.R. China. yan_zheng@fudan.edu.cn.ORCID http://orcid.org/0000-0003-1129-3147
Shangyu HongState Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai, P.R. China. shangyu_hong@fudan.edu.cn.ORCID http://orcid.org/0000-0001-6144-5618

Funding

Ministry of Science and Technology of the People's Republic of China (Chinese Ministry of Science and Technology) 2018YFA0800600Ministry of Science and Technology of the People's Republic of China (Chinese Ministry of Science and Technology) 2019YFA0802302Ministry of Science and Technology of the People's Republic of China (Chinese Ministry of Science and Technology) 2021YFA0804801Ministry of Science and Technology of the People's Republic of China (Chinese Ministry of Science and Technology) 2021YFA1301000National Natural Science Foundation of China (National Science Foundation of China) 31971082National Natural Science Foundation of China (National Science Foundation of China) 32271217National Natural Science Foundation of China (National Science Foundation of China) 81970684National Natural Science Foundation of China (National Science Foundation of China) 91957117Natural Science Foundation of Shanghai (Natural Science Foundation of Shanghai Municipality) 23ZR1403700Science and Technology Commission of Shanghai Municipality (Shanghai Municipal Science and Technology Commission) 2017SHZDZX01Science and Technology Commission of Shanghai Municipality (Shanghai Municipal Science and Technology Commission) 2023SHZDZX02State Key Laboratory of Genetic Engineering (SKLGE) SKLGE-2315University of Chinese Academy of Sciences (Graduate University of Chinese Academy of Sciences) XDB38010300
6 · The paper itself

Abstract

The low-carbohydrate ketogenic diet (KD) has long been practiced for weight loss, but the underlying mechanisms remain elusive. Gut microbiota and metabolites have been suggested to mediate the metabolic changes caused by KD consumption, although the particular gut microbes or metabolites involved are unclear. Here, we show that KD consumption enhances serum levels of taurodeoxycholic acid (TDCA) and tauroursodeoxycholic acid (TUDCA) in mice to decrease body weight and fasting glucose levels. Mechanistically, KD feeding decreases the abundance of a bile salt hydrolase (BSH)-coding gut bacterium, Lactobacillus murinus ASF361. The reduction of L. murinus ASF361 or inhibition of BSH activity increases the circulating levels of TDCA and TUDCA, thereby reducing energy absorption by inhibiting intestinal carbonic anhydrase 1 expression, which leads to weight loss. TDCA and TUDCA treatments have been found to protect against obesity and its complications in multiple mouse models. Additionally, the associations among the abovementioned bile acids, microbial BSH and metabolic traits were consistently observed both in an observational study of healthy human participants (n = 416) and in a low-carbohydrate KD interventional study of participants who were either overweight or with obesity (n = 25). In summary, we uncover a unique host-gut microbiota metabolic interaction mechanism for KD consumption to decrease body weight and fasting glucose levels. Our findings support TDCA and TUDCA as two promising drug candidates for obesity and its complications in addition to a KD.

Indexed as

Bile Acids and SaltsDiet, KetogenicGastrointestinal MicrobiomeObesityAnimalsEnergy IntakeHumansMaleMiceMice, Inbred C57BLTaurochenodeoxycholic AcidTaurodeoxycholic AcidBile Acids and SaltsTaurochenodeoxycholic AcidTaurodeoxycholic Acidursodoxicoltaurine

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Registered trials

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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 OpenQuestion graph.