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β-aminoisobutyric acid attenuates LPS-induced inflammation and insulin resistance in adipocytes through AMPK-mediated pathway.
J Biomed Sci 2018; 25(1):27JB

Abstract

BACKGROUND

β-aminoisobutyric acid (BAIBA) is produced in skeletal muscle during exercise and has beneficial effects on obesity-related metabolic disorders such as diabetes and non-alcoholic fatty liver disease. Thus, it is supposed to prevent high fat diet (HFD)-induced inflammation and insulin resistance in adipose tissue though anti-inflammatory effects in obesity. Previous reports have also demonstrated strong anti-inflammatory effects of BAIBA.

METHODS

We used BAIBA treated fully differentiated 3T3T-L1 mouse adipocytes to investigate the effects of exogenous BAIBA on inflammation and insulin signaling in adipocytes. Insulin signaling-mediated proteins and inflammation markers were measured by Western blot analysis. Secretion of pro-inflammatory cytokines were measured by ELISA. Lipid accumulation in differentiated 3 T3-L1 cells was stained by Oil red-O. Statistical analysis was performed by ANOVA and student's t test.

RESULTS

BAIBA treatment suppressed adipogenesis assessed by adipogenic markers as well as lipid accumulation after full differentiation. We showed that BAIBA treatment stimulated AMP-activated protein kinase (AMPK) phosphorylation in a dose-dependent manner and lipopolysaccharide (LPS)-induced secretion of pro-inflammatory cytokines such as TNFα and MCP-1 was abrogated in BAIBA-treated 3 T3-L1 cells. Treatment of 3 T3-L1 cells with BAIBA reduced LPS-induced NFκB and IκB phosphorylation. Furthermore, BAIBA treatment ameliorated LPS-induced impairment of insulin signaling measured by IRS-1 and Akt phosphorylation and fatty acid oxidation. Suppression of AMPK by small interfering (si) RNA significantly restored these changes.

CONCLUSIONS

We demonstrated anti-inflammatory and anti-insulin resistance effects of BAIBA in differentiated 3 T3-L1 cells treated with LPS through AMPK-dependent signaling. These results provide evidence for the beneficial effects of BAIBA not only in liver and skeletal muscle cells but also in adipose tissue.

Authors+Show Affiliations

Research Administration Team, Seoul National University Bundang Hospital, 166 Gumi-ro, Bundang-gu, Seongnam, 463-707, Korea. Department of Surgery, Seoul National University Bundang Hospital, Seoul National University College of Medicine, 166 Gumi-ro, Bundang-gu, Seongnam, 463-707, Korea.Department of Surgery, Seoul National University Bundang Hospital, Seoul National University College of Medicine, 166 Gumi-ro, Bundang-gu, Seongnam, 463-707, Korea.Department of Surgery, Seoul National University Bundang Hospital, Seoul National University College of Medicine, 166 Gumi-ro, Bundang-gu, Seongnam, 463-707, Korea.Department of Surgery, Seoul National University Bundang Hospital, Seoul National University College of Medicine, 166 Gumi-ro, Bundang-gu, Seongnam, 463-707, Korea.Department of Surgery, Seoul National University Bundang Hospital, Seoul National University College of Medicine, 166 Gumi-ro, Bundang-gu, Seongnam, 463-707, Korea. tslee@snubh.org. Department of Surgery, Seoul National University College of Medicine, Seoul, Korea. tslee@snubh.org.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

29592806

Citation

Jung, Tae Woo, et al. "Β-aminoisobutyric Acid Attenuates LPS-induced Inflammation and Insulin Resistance in Adipocytes Through AMPK-mediated Pathway." Journal of Biomedical Science, vol. 25, no. 1, 2018, p. 27.
Jung TW, Park HS, Choi GH, et al. Β-aminoisobutyric acid attenuates LPS-induced inflammation and insulin resistance in adipocytes through AMPK-mediated pathway. J Biomed Sci. 2018;25(1):27.
Jung, T. W., Park, H. S., Choi, G. H., Kim, D., & Lee, T. (2018). Β-aminoisobutyric acid attenuates LPS-induced inflammation and insulin resistance in adipocytes through AMPK-mediated pathway. Journal of Biomedical Science, 25(1), p. 27. doi:10.1186/s12929-018-0431-7.
Jung TW, et al. Β-aminoisobutyric Acid Attenuates LPS-induced Inflammation and Insulin Resistance in Adipocytes Through AMPK-mediated Pathway. J Biomed Sci. 2018 Mar 28;25(1):27. PubMed PMID: 29592806.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - β-aminoisobutyric acid attenuates LPS-induced inflammation and insulin resistance in adipocytes through AMPK-mediated pathway. AU - Jung,Tae Woo, AU - Park,Hyung Sub, AU - Choi,Geum Hee, AU - Kim,Daehwan, AU - Lee,Taeseung, Y1 - 2018/03/28/ PY - 2017/12/26/received PY - 2018/03/22/accepted PY - 2018/3/30/entrez PY - 2018/3/30/pubmed PY - 2018/9/5/medline KW - AMPK KW - Adipocyte KW - BAIBA KW - Inflammation KW - Insulin resistance KW - NFκB SP - 27 EP - 27 JF - Journal of biomedical science JO - J. Biomed. Sci. VL - 25 IS - 1 N2 - BACKGROUND: β-aminoisobutyric acid (BAIBA) is produced in skeletal muscle during exercise and has beneficial effects on obesity-related metabolic disorders such as diabetes and non-alcoholic fatty liver disease. Thus, it is supposed to prevent high fat diet (HFD)-induced inflammation and insulin resistance in adipose tissue though anti-inflammatory effects in obesity. Previous reports have also demonstrated strong anti-inflammatory effects of BAIBA. METHODS: We used BAIBA treated fully differentiated 3T3T-L1 mouse adipocytes to investigate the effects of exogenous BAIBA on inflammation and insulin signaling in adipocytes. Insulin signaling-mediated proteins and inflammation markers were measured by Western blot analysis. Secretion of pro-inflammatory cytokines were measured by ELISA. Lipid accumulation in differentiated 3 T3-L1 cells was stained by Oil red-O. Statistical analysis was performed by ANOVA and student's t test. RESULTS: BAIBA treatment suppressed adipogenesis assessed by adipogenic markers as well as lipid accumulation after full differentiation. We showed that BAIBA treatment stimulated AMP-activated protein kinase (AMPK) phosphorylation in a dose-dependent manner and lipopolysaccharide (LPS)-induced secretion of pro-inflammatory cytokines such as TNFα and MCP-1 was abrogated in BAIBA-treated 3 T3-L1 cells. Treatment of 3 T3-L1 cells with BAIBA reduced LPS-induced NFκB and IκB phosphorylation. Furthermore, BAIBA treatment ameliorated LPS-induced impairment of insulin signaling measured by IRS-1 and Akt phosphorylation and fatty acid oxidation. Suppression of AMPK by small interfering (si) RNA significantly restored these changes. CONCLUSIONS: We demonstrated anti-inflammatory and anti-insulin resistance effects of BAIBA in differentiated 3 T3-L1 cells treated with LPS through AMPK-dependent signaling. These results provide evidence for the beneficial effects of BAIBA not only in liver and skeletal muscle cells but also in adipose tissue. SN - 1423-0127 UR - https://www.unboundmedicine.com/medline/citation/29592806/β_aminoisobutyric_acid_attenuates_LPS_induced_inflammation_and_insulin_resistance_in_adipocytes_through_AMPK_mediated_pathway_ L2 - https://jbiomedsci.biomedcentral.com/articles/10.1186/s12929-018-0431-7 DB - PRIME DP - Unbound Medicine ER -