Time-Restricted Feeding without Reducing Caloric Intake Prevents Metabolic Diseases in Mice Fed a High-Fat Diet

被引：1498

作者：

Hatori, Megumi ^{[1
]}

Vollmers, Christopher ^{[1
]}

Zarrinpar, Amir ^{[1
,2
]}

DiTacchio, Luciano ^{[1
]}

Bushong, Eric A. ^{[3
]}

Gill, Shubhroz ^{[1
]}

Leblanc, Mathias ^{[1
]}

Chaix, Amandine ^{[1
]}

Joens, Matthew ^{[1
]}

Fitzpatrick, James A. J. ^{[1
]}

Ellisman, Mark H. ^{[3
]}

Panda, Satchidananda ^{[1
]}

机构：

[1] Salk Inst Biol Studies, La Jolla, CA 92037 USA

[2] Univ Calif San Diego, Dept Gastroenterol, La Jolla, CA 92037 USA

[3] Univ Calif San Diego, Natl Ctr Microscopy & Imaging Res, La Jolla, CA 92093 USA

来源：

CELL METABOLISM | 2012年 / 15卷 / 06期

基金：

日本学术振兴会;

关键词：

REV-ERB-ALPHA; CIRCADIAN CLOCK; INSULIN-RESISTANCE; LIPID-METABOLISM; PROTEIN; OBESITY; LIVER; LEPTIN; CREB; TRANSCRIPTION;

D O I：

10.1016/j.cmet.2012.04.019

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

While diet-induced obesity has been exclusively attributed to increased caloric intake from fat, animals fed a high-fat diet (HFD) ad libitum (ad lib) eat frequently throughout day and night, disrupting the normal feeding cycle. To test whether obesity and metabolic diseases result from HFD or disruption of metabolic cycles, we subjected mice to either ad lib or time-restricted feeding (tRF) of a HFD for 8 hr per day. Mice under tRF consume equivalent calories from HFD as those with ad lib access yet are protected against obesity, hyperinsulinemia, hepatic steatosis, and inflammation and have improved motor coordination. The tRF regimen improved CREB, mTOR, and AMPK pathway function and oscillations of the circadian clock and their target genes' expression. These changes in catabolic and anabolic pathways altered liver metabolome and improved nutrient utilization and energy expenditure. We demonstrate in mice that tRF regimen is a non-pharmacological strategy against obesity and associated diseases.

引用

页码：848 / 860

页数：13

共 53 条

[1] CREB and the CRTC co-activators: sensors for hormonal and metabolic signals [J].