Time-Restricted Feeding without Reducing Caloric Intake Prevents Metabolic Diseases in Mice Fed a High-Fat Diet. Hatori, M., Vollmers, C., Zarrinpar, A., DiTacchio, L., Bushong, E., Gill, S., Leblanc, M., Chaix, A., Joens, M., Fitzpatrick, J. J., Ellisman, M., & Panda, S. Cell Metabolism, 15(6):848–860, June, 2012. ![Time-Restricted Feeding without Reducing Caloric Intake Prevents Metabolic Diseases in Mice Fed a High-Fat Diet [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex Summary 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 nonpharmacological strategy against obesity and associated diseases.
@article{hatori2012TimeRestricted,
title = {Time-{Restricted} {Feeding} without {Reducing} {Caloric} {Intake} {Prevents} {Metabolic} {Diseases} in {Mice} {Fed} a {High}-{Fat} {Diet}},
volume = {15},
issn = {1550-4131},
url = {http://www.sciencedirect.com/science/article/pii/S1550413112001891},
doi = {10.1016/j.cmet.2012.04.019},
abstract = {Summary
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 nonpharmacological strategy against obesity and associated diseases.},
number = {6},
urldate = {2019-01-14},
journal = {Cell Metabolism},
author = {Hatori, Megumi and Vollmers, Christopher and Zarrinpar, Amir and DiTacchio, Luciano and Bushong, Eric A. and Gill, Shubhroz and Leblanc, Mathias and Chaix, Amandine and Joens, Matthew and Fitzpatrick, James A. J. and Ellisman, Mark H. and Panda, Satchidananda},
month = jun,
year = {2012},
keywords = {health},
pages = {848--860}
}
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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 nonpharmacological strategy against obesity and associated diseases.","number":"6","urldate":"2019-01-14","journal":"Cell Metabolism","author":[{"propositions":[],"lastnames":["Hatori"],"firstnames":["Megumi"],"suffixes":[]},{"propositions":[],"lastnames":["Vollmers"],"firstnames":["Christopher"],"suffixes":[]},{"propositions":[],"lastnames":["Zarrinpar"],"firstnames":["Amir"],"suffixes":[]},{"propositions":[],"lastnames":["DiTacchio"],"firstnames":["Luciano"],"suffixes":[]},{"propositions":[],"lastnames":["Bushong"],"firstnames":["Eric A."],"suffixes":[]},{"propositions":[],"lastnames":["Gill"],"firstnames":["Shubhroz"],"suffixes":[]},{"propositions":[],"lastnames":["Leblanc"],"firstnames":["Mathias"],"suffixes":[]},{"propositions":[],"lastnames":["Chaix"],"firstnames":["Amandine"],"suffixes":[]},{"propositions":[],"lastnames":["Joens"],"firstnames":["Matthew"],"suffixes":[]},{"propositions":[],"lastnames":["Fitzpatrick"],"firstnames":["James A.","J."],"suffixes":[]},{"propositions":[],"lastnames":["Ellisman"],"firstnames":["Mark H."],"suffixes":[]},{"propositions":[],"lastnames":["Panda"],"firstnames":["Satchidananda"],"suffixes":[]}],"month":"June","year":"2012","keywords":"health","pages":"848–860","bibtex":"@article{hatori2012TimeRestricted,\n\ttitle = {Time-{Restricted} {Feeding} without {Reducing} {Caloric} {Intake} {Prevents} {Metabolic} {Diseases} in {Mice} {Fed} a {High}-{Fat} {Diet}},\n\tvolume = {15},\n\tissn = {1550-4131},\n\turl = {http://www.sciencedirect.com/science/article/pii/S1550413112001891},\n\tdoi = {10.1016/j.cmet.2012.04.019},\n\tabstract = {Summary\nWhile 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. 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