Fasting may be the reason why diets are good for you: mouse study

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Fasting daily - rather than just reducing your caloric intake - is likely responsible for the longer lifespan and metabolic benefits that are usually associated with a calorie-restricted diet, say US researchers in a study on mice. The team found mice that were forced to fast - as compared to those who were on a diet, or had three equal meals a day - had changes in their sensitivity to insulin and how they metabolised nutrients. The authors say their study gives insight into how the regulation of metabolic health and longevity might not just be about how much is eaten but also when.

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From: Springer Nature

Physiology: Fasting may mediate the beneficial effects of calorie restriction in mice

Daily prolonged fasting — not solely reducing calorie intake — is likely to be responsible for the lifespan-promoting and beneficial metabolic effects associated with a calorie-restricted diet in mice, according to a study published in Nature Metabolism. Further research, however, will be required to decipher the generalisability of these findings, for example in different strains and sexes of mice.

Calorie restriction is known to promote healthy ageing in many species. Recently, evidence for the lifespan-promoting and metabolic benefits of fasting in mice has emerged. However, the exact physiological and molecular mechanisms which underlie the effects of controlling when food is eaten have so far remained elusive.

Dudley Lamming, Heidi Pak and colleagues placed 3 groups of male mice on different diets, all of which reduced their daily calorie intake by 30% for 16 weeks. Every day, one group would have unlimited access to their food, another group would receive food in 3 equal meals spaced over a 12-hour period, and the other group was trained to rapidly consume their food, subsequently ‘fasting’ for the remainder of the day. Mice receiving a normal rodent diet without calorie restriction acted as controls. The authors found that fasting was important for mediating changes in insulin sensitivity and nutrient metabolism. Indeed, fasting alone — without restricting calorie intake — was able to replicate certain metabolic and transcriptional effects associated with calorie-restriction. In a specific strain of male mice, fasting was required for calorie-restriction-induced improvements in glucose metabolism, frailty and lifespan.

The authors conclude that these results could provide preliminary insights into how the regulation of metabolic health and longevity might not just be about how much is eaten but also when. They go on to state that caution is warranted in applying these results to humans, which will represent an important area of future research.

Journal/
conference:
Nature Metabolism
Research:Paper
Organisation/s: University of Wisconsin–Madison, Madison, WI, USA
Funder: The laboratory of D.W.L. is supported in part by the National Institutes of Health (NIH)/ NIA (AG050135, AG051974, AG056771, AG062328 and AG061635 to D.W.L.), NIH/ National Institute of Diabetes and Digestive and Kidney Diseases (DK125859 to D.W.L and J.M.D.) and start-up funds from the UW School of Medicine and Public Health and Department of Medicine (to D.W.L.). Metabolomic and histone proteomic analysis was supported in part by a grant from the NIH (R37GM059785 to J.M.D.) and a UAB Nathan Shock Center of Excellence in the Basic Biology of Aging (P30AG050886) Core Services Pilot Award (to D.W.L.). Bomb calorimetry was supported by S10OD028739 (to C.-L.E.Y.), and gut integrity analysis was supported in part by DK124696 (to C.-L.E.Y.). H.H.P. is supported in part by a NIA F31 pre-doctoral fellowship (AG066311). C.L.G. is supported by a Glenn Foundation for Medical Research Postdoctoral Fellowship and was supported in part by a generous gift from D. Philanthropies. N.E.R. was supported in part by a training grant from the UW Institute on Aging (NIA T32 AG000213). S.A.H. was supported in part by a training grant from the UW Metabolism and Nutrition Training Program (T32 DK007665). Support for this research was provided by the UW Office of the Vice Chancellor for Research and Graduate Education with funding from the Wisconsin Alumni Research Foundation. This work was supported in part by the US Department of Veterans Affairs (I01-BX004031), and this work was supported using facilities and resources from the William S. Middleton Memorial Veterans Hospital.
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