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Intermittent Fasting Reduces Neuroinflammation and Cognitive Impairment in High-Fat Diet-Fed Mice by Downregulating Lipocalin-2 and Galectin-3open access

Authors
Lee, JaewoongAn, Hyeong SeokShin, Hyun JooJang, Hye MinIm, Chae OhJeong, YeonjunEum, KibaekYoon, SejeongLee, So JeongJeong, Eun AeKim, Kyung EunRoh, Gu Seob
Issue Date
Jan-2024
Publisher
MDPI
Keywords
intermittent fasting; high-fat diet; lipocalin-2; galectin-3; cognitive impairment
Citation
NUTRIENTS, v.16, no.1
Indexed
SCOPUS
Journal Title
NUTRIENTS
Volume
16
Number
1
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/69349
DOI
10.3390/nu16010159
ISSN
2072-6643
2072-6643
Abstract
Intermittent fasting (IF), an alternating pattern of dietary restriction, reduces obesity-induced insulin resistance and inflammation. However, the crosstalk between adipose tissue and the hippocampus in diabetic encephalopathy is not fully understood. Here, we investigated the protective effects of IF against neuroinflammation and cognitive impairment in high-fat diet(HFD)-fed mice. Histological analysis revealed that IF reduced crown-like structures and adipocyte apoptosis in the adipose tissue of HFD mice. In addition to circulating lipocalin-2 (LCN2) and galectin-3 (GAL3) levels, IF reduced HFD-induced increases in LCN2- and GAL3-positive macrophages in adipose tissue. IF also improved HFD-induced memory deficits by inhibiting blood-brain barrier breakdown and neuroinflammation. Furthermore, immunofluorescence showed that IF reduced HFD-induced astrocytic LCN2 and microglial GAL3 protein expression in the hippocampus of HFD mice. These findings indicate that HFD-induced adipocyte apoptosis and macrophage infiltration may play a critical role in glial activation and that IF reduces neuroinflammation and cognitive impairment by protecting against blood-brain barrier leakage.
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