Effects of caloric restriction on the expression of lipocalin-2 and its receptor in the brown adipose tissue of high-fat diet-fed mice
10.4196/kjpp.2019.23.5.335
- Author:
Kyung Ah PARK
1
;
Zhen JIN
;
Hyeong Seok AN
;
Jong Youl LEE
;
Eun Ae JEONG
;
Eun Bee CHOI
;
Kyung Eun KIM
;
Hyun Joo SHIN
;
Jung Eun LEE
;
Gu Seob ROH
Author Information
1. Department of Anatomy and Convergence Medical Science, Bio Anti-Aging Medical Research Center, Institute of Health Sciences, College of Medicine, Gyeongsang National University, Jinju 52727, Korea. anaroh@gnu.ac.kr
- Publication Type:Original Article
- Keywords:
Brown adipose tissue;
Caloric restriction;
Lipocalin 2;
Obesity
- MeSH:
Adipokines;
Adipose Tissue, Brown;
Animals;
Caloric Restriction;
Diet, High-Fat;
Inflammation;
Lipocalins;
Macrophages;
Mice;
Mice, Obese;
Mitochondrial Dynamics;
Neutrophils;
Obesity;
Oxidative Stress;
Phenotype
- From:The Korean Journal of Physiology and Pharmacology
2019;23(5):335-344
- CountryRepublic of Korea
- Language:English
-
Abstract:
Obesity causes inflammation and impairs thermogenic functions in brown adipose tissue (BAT). The adipokine lipocalin 2 (LCN2) has been implicated in inflammation and obesity. Herein, we investigated the protective effects of caloric restriction (CR) on LCN2-mediated inflammation and oxidative stress in the BAT of high-fat diet (HFD)-fed mice. Mice were fed a HFD for 20 weeks and then either continued on the HFD or subjected to CR for the next 12 weeks. CR led to the browning of the white fat-like phenotype in HFD-fed mice. Increased expressions of LCN2 and its receptor in the BAT of HFD-fed mice were significantly attenuated by CR. Additionally, HFD+CR-fed mice had fewer neutrophils and macrophages expressing LCN2 and iron-positive cells than HFD-fed mice. Further, oxidative stress and mitochondrial fission induced by a HFD were also significantly attenuated by CR. Our findings indicate that the protective effects of CR on inflammation and oxidative stress in the BAT of obese mice may be associated with regulation of LCN2.
