Time-Restricted Feeding Improves Body Weight Gain, Lipid Profiles, and Atherogenic Indices in Cafeteria-Diet-Fed Rats: Role of Browning of Inguinal White Adipose Tissue

Abstract

Time-restricted feeding (TRF) showed a potent effect in preventing obesity and improving metabolicoutcomes in several animal models of obesity. However, there is, as of yet, scarce evidence concerning its effectiveness against obesogenic challenges that more accurately mimic human Western diets, such as the cafeteria diet. Moreover, the mechanism for its efficacy is poorly understood. White adipose browning has been linked to body weight loss. Herein, we tested whether TRF has the potential to induce browning of inguinal white adipose tissue (iWAT) and to attenuate obesity and associated dyslipidemia in a cafeteria-diet-induced obesity model. Male Wistar rats were fed normal laboratory chow (NC) or cafeteria diet (CAF) for 16 weeks and were subdivided into two groups that were subjected to either ad libitum (ad lib, A) or TRF (R) for 8 h per day. Rats under the TRF regimen had a lower body weight gain and adiposity than the diet-matchedad lib rats, despite equivalent levels of food intake and locomotor activity. In addition, TRF improved the deranged lipid profile (total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL-c), low-density lipoprotein (LDL-c)) and atherogenic indices (atherogenic index of plasma (AIP), atherogenic coefficient (AC), coronary risk index (CRI) in CAF-fed rats. Remarkably, TRF resulted in decreased size of adipocytes and induced emergence of multilocular brown-like adipocytes in iWAT of NC- and CAF-fed rats. Protein expression of browning markers, such as uncoupling protein-1 (UCP1) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), were also up-regulated in the iWAToftime-restricted NC- or CAF-fed rats. These findings suggest that a TRF regimen is an effective strategy to improve CAF diet-induced obesity, probably via a mechanismthe involving WAT browning process.

Diurnal variations of brown fat thermogenesis and fat oxidation in humans

“…The metabolic effects of TRF are thought to be based on the realignment of feeding and the circadian clock, which improves nutrient utilization and EE. Indeed, TRF results in increased and rhythmic expression of UCP1 in parallel with increased EE [ 48 , 49 ]. Moreover, in nocturnal mice the effects of TRF are greater when feeding time is restricted during the active (dark) phase than during the inactive (light) phase [ 50 , 51 ].…”

Beneficial Effects of Early Time-Restricted Feeding on Metabolic Diseases: Importance of Aligning Food Habits with the Circadian Clock

“…The mice also experienced decreased levels of insulin and fasting glucose levels, suggesting an improved glucose metabolism and insulin sensitivity [ 122 , 123 , 124 , 125 , 126 ]. Time-restricted feeding revealed beneficial effects in rat models as well [ 127 , 128 ]. The authors observed that it induced weight loss due to a significant reduction of visceral and subcutaneous adipose tissues and a better activation of PGC1α, a transcriptional coactivator involved in mitochondrial biogenesis and fatty acid oxidation.…”

“…The authors observed that it induced weight loss due to a significant reduction of visceral and subcutaneous adipose tissues and a better activation of PGC1α, a transcriptional coactivator involved in mitochondrial biogenesis and fatty acid oxidation. Rats improved glucose tolerance and had lower LDL levels and higher HDL levels, showing an improvement in CVD risk markers [ 127 , 128 ].…”

Time-restricted feeding improves blood glucose and insulin sensitivity in overweight patients with type 2 diabetes: a randomised controlled trial

“…Their endurance, motor control and cardiac function improved significantly. For cafeteria diet-induced obesity in rats, the 8-h TRF regimen for 16 weeks is an effective strategy to enhance body weight gain, lipid profiles, and atherogenic indices [18]. In mutant mice, 10-h TRF for 12 weeks prevented obesity and metabolic syndrome [19].…”