PMID- 36494293 OWN - NLM STAT- MEDLINE DCOM- 20230214 LR - 20230215 IS - 1871-403X (Print) IS - 1871-403X (Linking) VI - 17 IP - 1 DP - 2023 Jan-Feb TI - Naringin reduces fat deposition by promoting the expression of lipolysis and beta-oxidation related genes. PG - 74-81 LID - S1871-403X(22)00129-6 [pii] LID - 10.1016/j.orcp.2022.11.004 [doi] AB - AIMS: Naringin, a flavonoid present in citrus fruits, has been known for the capacity to reduce lipid synthesis and anti-inflammatory. In this study, we investigated whether naringin increases lipolysis and fatty acid beta-oxidation to change fat deposition. METHODS: In in vivo experiment, obese adult mice (20-weeks-old, n = 18) were divided into control group fed with normal diet and naringin-treated group fed with naringin-supplemented diet (5 g/kg) for 60 days, respectively. In in vitro experiment, differentiated 3T3-L1 adipocytes were treated for four days with or without naringin (100 microg/mL). RESULTS: Supplementing naringin significantly reduced the body weight, abdominal fat weight, blood total cholesterol content of mice, but did not affect food intake. In addition, naringin decreased levels of pro-inflammatory factors in adipose tissue including interleukin-1beta (IL-1beta), interleukin-6 (IL-6), and monocyte chemotactic protein 1 (MCP-1). Naringin increased the expression of AMP-activated protein kinase (AMPK), a key factor in cellular energy metabolism, and raised the ratio of p-AMPK/AMPK in mouse liver tissue. The protein expression of hormone-sensitive lipase (HSL), phospho-HSL563 (p-HSL563), p-HSL563/HSL, and adipocyte triglyceride lipase (ATGL) was significantly increased in the adipose tissue of naringin-treated mice. Furthermore, naringin enhanced the expression of fatty acid beta-oxidation genes, including carnitine palmitoyl transferase 1 (CPT1), uncoupling protein 2 (UCP2), and acyl-coenzyme A oxidase 1 (AOX1) in mouse adipose tissue. In in vitro experiment, similar findings were observed in differentiated 3T3-L1 adipocytes with naringin treatment. The treatment remarkably reduced intracellular lipid content, increased the number of mitochondria and promoted the gene expression of HSL, ATGL, CPT1, AOX1, and UCP2 and the phosphorylation of HSL protein. CONCLUSION: Naringin reduced body fat in obese mice and lipid content in differentiated 3T3-L1 adipocytes, which was associated with enhanced AMPK activation and upregulation of the expression of the lipolytic genes HSL, ATGL, and beta-oxidation genes CPT1, AOX1, and UCP2. CI - Copyright (c) 2022 Asia Oceania Association for the Study of Obesity. Published by Elsevier Ltd. All rights reserved. FAU - Wang, Jing AU - Wang J AD - Chongqing Academy of Animal Science, Chongqing, PR China. FAU - Wang, Qi AU - Wang Q AD - Chongqing Academy of Animal Science, Chongqing, PR China. FAU - Zhu, Siyuan AU - Zhu S AD - Southwest University of Science and Technology, Sichuan, PR China. FAU - Huang, Jinxiu AU - Huang J AD - Chongqing Academy of Animal Science, Chongqing, PR China. FAU - Liu, Zuohua AU - Liu Z AD - Chongqing Academy of Animal Science, Chongqing, PR China. Electronic address: liuzuohua66@163.com. FAU - Qi, Renli AU - Qi R AD - Chongqing Academy of Animal Science, Chongqing, PR China. Electronic address: qirenli1982@163.com. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20221207 PL - Netherlands TA - Obes Res Clin Pract JT - Obesity research & clinical practice JID - 101303911 RN - N7TD9J649B (naringin) RN - EC 2.7.11.31 (AMP-Activated Protein Kinases) RN - EC 3.1.1.13 (Sterol Esterase) RN - EC 3.1.1.3 (Lipase) RN - 0 (Fatty Acids) RN - 0 (Lipids) SB - IM MH - Mice MH - Animals MH - *Lipolysis MH - *AMP-Activated Protein Kinases/metabolism MH - Sterol Esterase/metabolism MH - Lipase MH - Fatty Acids MH - Lipids MH - 3T3-L1 Cells OTO - NOTNLM OT - Differentiated 3T3-L1 adipocytes OT - Fatty acid beta-oxidation OT - Lipolysis OT - Naringin OT - Obese mice COIS- Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. EDAT- 2022/12/10 06:00 MHDA- 2023/02/15 06:00 CRDT- 2022/12/09 22:08 PHST- 2021/03/13 00:00 [received] PHST- 2022/11/17 00:00 [revised] PHST- 2022/11/21 00:00 [accepted] PHST- 2022/12/10 06:00 [pubmed] PHST- 2023/02/15 06:00 [medline] PHST- 2022/12/09 22:08 [entrez] AID - S1871-403X(22)00129-6 [pii] AID - 10.1016/j.orcp.2022.11.004 [doi] PST - ppublish SO - Obes Res Clin Pract. 2023 Jan-Feb;17(1):74-81. doi: 10.1016/j.orcp.2022.11.004. Epub 2022 Dec 7.