Faculty Opinions recommendation of Time-Restricted Feeding Prevents Obesity and Metabolic Syndrome in Mice Lacking a Circadian Clock.

Author(s):  
Qingchun Tong ◽  
Kristin Eckel-Mahan
2019 ◽  
Vol 29 (2) ◽  
pp. 303-319.e4 ◽  
Author(s):  
Amandine Chaix ◽  
Terry Lin ◽  
Hiep D. Le ◽  
Max W. Chang ◽  
Satchidananda Panda

Nutrients ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 1234 ◽  
Author(s):  
Humaira Jamshed ◽  
Robbie Beyl ◽  
Deborah Della Manna ◽  
Eddy Yang ◽  
Eric Ravussin ◽  
...  

Time-restricted feeding (TRF) is a form of intermittent fasting that involves having a longer daily fasting period. Preliminary studies report that TRF improves cardiometabolic health in rodents and humans. Here, we performed the first study to determine how TRF affects gene expression, circulating hormones, and diurnal patterns in cardiometabolic risk factors in humans. Eleven overweight adults participated in a 4-day randomized crossover study where they ate between 8 am and 2 pm (early TRF (eTRF)) and between 8 am and 8 pm (control schedule). Participants underwent continuous glucose monitoring, and blood was drawn to assess cardiometabolic risk factors, hormones, and gene expression in whole blood cells. Relative to the control schedule, eTRF decreased mean 24-hour glucose levels by 4 ± 1 mg/dl (p = 0.0003) and glycemic excursions by 12 ± 3 mg/dl (p = 0.001). In the morning before breakfast, eTRF increased ketones, cholesterol, and the expression of the stress response and aging gene SIRT1 and the autophagy gene LC3A (all p < 0.04), while in the evening, it tended to increase brain-derived neurotropic factor (BNDF; p = 0.10) and also increased the expression of MTOR (p = 0.007), a major nutrient-sensing protein that regulates cell growth. eTRF also altered the diurnal patterns in cortisol and the expression of several circadian clock genes (p < 0.05). eTRF improves 24-hour glucose levels, alters lipid metabolism and circadian clock gene expression, and may also increase autophagy and have anti-aging effects in humans.


Cell Reports ◽  
2017 ◽  
Vol 20 (5) ◽  
pp. 1061-1072 ◽  
Author(s):  
Hong Wang ◽  
Elyse van Spyk ◽  
Qiang Liu ◽  
Mikhail Geyfman ◽  
Michael L. Salmans ◽  
...  

2012 ◽  
Vol 302 (9) ◽  
pp. E1027-E1035 ◽  
Author(s):  
Tao Wu ◽  
Fen ZhuGe ◽  
Lu Sun ◽  
Yinhua Ni ◽  
Ou Fu ◽  
...  

There is increasing awareness of the link between impaired circadian clocks and multiple metabolic diseases. However, the impairment of the circadian clock by type 2 diabetes has not been fully elucidated. To understand whether and how the function of circadian clock is impaired under the diabetic condition, we examined not only the expression of circadian genes in the heart and pineal gland but also the behavioral rhythm of type 2 diabetic and control rats in both the nighttime restricted feeding (NRF) and daytime restricted feeding (DRF) conditions. In the NRF condition, the circadian expression of clock genes in the heart and pineal gland was conserved in the diabetic rats, being similar to that in the control rats. DRF shifted the circadian phases of peripheral clock genes more efficiently in the diabetic rats than those in the control rats. Moreover, the activity rhythm of rats in the diabetic group was completely shifted from the dark phase to the light phase after 5 days of DRF treatment, whereas the activity rhythm of rats in the control group was still under the control of the suprachiasmatic nucleus (SCN) after the same DRF treatment. Furthermore, the serum glucose rhythm of type 2 diabetic rats was also shifted and controlled by the external feeding schedule, ignoring the SCN rhythm. Therefore, DRF shows stronger effect on the reentrainment of circadian rhythm in the type 2 diabetic rats, suggesting that the circadian system in diabetes is unstable and more easily shifted by feeding stimuli.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ana Cristina García-Gaytán ◽  
Manuel Miranda-Anaya ◽  
Isaías Turrubiate ◽  
Leonardo López-De Portugal ◽  
Guadalupe Nayeli Bocanegra-Botello ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document