Ursodeoxycholic Acid Alters Bile Acid and Fatty Acid Profiles in a Mouse Model of Diet-Induced Obesity.

bile acid diet-induced obesity free fatty acid metabolic dysfunction traditional Chinese medicine ursodeoxycholic acid

Journal

Frontiers in pharmacology
ISSN: 1663-9812
Titre abrégé: Front Pharmacol
Pays: Switzerland
ID NLM: 101548923

Informations de publication

Date de publication:
2019
Historique:
received: 06 03 2019
accepted: 01 07 2019
entrez: 13 8 2019
pubmed: 14 8 2019
medline: 14 8 2019
Statut: epublish

Résumé

Ursodeoxycholic acid (UDCA) is a bile acid (BA) approved by the U.S. Food and Drug Administration for the treatment of primary biliary cholangitis. It is also the major active component of bear bile used in traditional Chinese medicine to reduce fever, remove toxins, and treat liver and eye ailments. In addition, UDCA and its conjugated form have been evaluated for their potential to improve symptoms of metabolic diseases, but the results have been inconclusive. To address this issue, in this study, we investigated the effects of orally administered UDCA on mice with diet-induced obesity, including the BA and free fatty acid (FFA) profiles of serum, liver, and epididymis and brown adipose tissues. We found that UDCA treatment significantly improved most metabolic indices; tauroursodeoxycholic acid (TUDCA) and taurolithocholic acid (TLCA) contents were increased in all examined tissues, whereas saturated FA levels were decreased, and n-3 polyunsaturated fatty acid (n-3 PUFA) levels were increased in most tissues. A correlation analysis showed that the concentrations of UDCA and its derivatives were positively correlated with that of n-3 PUFA. To clarify the mechanism by which UDCA alters FFA profiles, we analyzed the expression levels of genes involved in FFA biosynthesis, uptake, and oxidation and found that FFA biosynthesis and uptake were inhibited while FFA oxidation was stimulated by UDCA treatment. Additionally, amino acid-conjugated derivatives of UDCA, such as TUDCA and TLCA, altered FFA profiles by modulating FFA biosynthesis, uptake, and oxidation. These findings provide evidence that UDCA can alleviate metabolic dysfunction and could therefore be effective in the treatment of obesity.

Identifiants

pubmed: 31402868
doi: 10.3389/fphar.2019.00842
pmc: PMC6669341
doi:

Types de publication

Journal Article

Langues

eng

Pagination

842

Subventions

Organisme : NCI NIH HHS
ID : P30 CA071789
Pays : United States

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Auteurs

Yunjing Zhang (Y)

School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Shanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.

Xiaojiao Zheng (X)

Shanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.

Fengjie Huang (F)

Shanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.

Aihua Zhao (A)

Shanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.

Kun Ge (K)

Shanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.

Qing Zhao (Q)

Shanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.

Wei Jia (W)

School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Shanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Cancer Biology Program, The University of Hawaii Cancer Center, Honolulu, HI, United States.

Classifications MeSH