A central-acting connexin inhibitor, INI-0602, prevents high-fat diet-induced feeding pattern disturbances and obesity in mice View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-12

AUTHORS

Tsutomu Sasaki, Rika Numano, Hiromi Yokota-Hashimoto, Sho Matsui, Naobumi Kimura, Hideyuki Takeuchi, Tadahiro Kitamura

ABSTRACT

A high-fat diet (HFD) causes obesity by promoting excessive energy intake, and simultaneously, by disturbing the timing of energy intake. Restoring the feeding pattern is sufficient to prevent HFD-induced obesity in mice. However, the molecular mechanism(s) underlying HFD-induced feeding pattern disturbances remain elusive. Saturated fatty acids activate microglia and cause hypothalamic inflammation. Activated microglia cause neuroinflammation, which spreads via inflammatory cytokines and gap-junction hemichannels. However, the role of gap-junction hemichannels in HFD-induced obesity remains unaddressed. We used a novel, central-acting connexin inhibitor, INI-0602, which has high affinity for gap junction hemichannels and does not affect the induction of inflammatory cytokines. We analyzed ad libitum feeding behavior and locomotor activity in mice that were fed normal chow (NC), a HFD with elevated saturated fatty acids (SFAs), or a HFD with very high SFAs. We found that HFD feeding induced acute hyperphagia, mainly during the light cycle. Feeding pattern disturbances were more pronounced in mice that consumed the HFD with very high SFAs than in mice that consumed the HFD with elevated SFAs. When INI-0602 was administered before the HFD was introduced, it blocked the feeding pattern disturbance, but not locomotor activity disturbances; moreover, it prevented subsequent diet-induced obesity. However, when INI-0602 was administered after the HFD had disturbed the feeding pattern, it failed to restore the normal feeding pattern. Therefore, we propose that SFAs in HFDs played a major role in disrupting feeding patterns in mice. Moreover, the feeding pattern disturbance required the function of central, gap junction hemichannels at the initiation of a HFD. However, altering hemichannel function after the feeding pattern disturbance was established had no effect. Thus, preventing the occurrence of a feeding pattern disturbance by blocking the hemichannel pathway was associated with the prevention of the HFD-induced obesity in mice. More... »

PAGES

28

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s13041-018-0372-9

DOI

http://dx.doi.org/10.1186/s13041-018-0372-9

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1104168569

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29793524


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RDF/XML is a standard XML format for linked data.

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303 https://www.grid.ac/institutes/grid.412804.b schema:alternateName Toyohashi University of Technology
304 schema:name Department of Environmental and Life Sciences, Toyohashi University of Technology, 1-1 Hibarigaoka Tempaku-cho, 441-8580, Toyohashi, Japan
305 Electronics-Interdisciplinary Research Institute (EIIRIS), Toyohashi University of Technology, 1-1 Hibarigaoka Tempaku-cho, 441-8580, Toyohashi, Japan
306 rdf:type schema:Organization
 




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