Limiting feeding to the active phase reduces blood pressure without the necessity of caloric reduction or fat mass loss

Abstract

Reducing body weight has been shown to lower blood pressure in obesity-related hypertension. However, success of those lifestyle interventions is limited due to poor long-term compliance. Emerging evidence indicates that feeding schedule plays a role on the regulation of blood pressure. With two studies, we examined the role of feeding schedule on energy homeostasis and blood pressure. In study 1, rats were fed a high-fat diet (HFD) ad libitum for 24 h (Control) or for 12 h during the dark phase (time-restricted feeding, TRF). In study 2, rats fed a HFD were administered a long-acting α-MSH analog at either light onset [melanotan II (MTII) light] or dark onset (MTII dark) or saline (Control). MTII light animals ate most of their calories during the active phase, similar to the TRF group. In study 1, Control and TRF rats consumed the same amount of food and gained the same amount of weight and fat mass. Interestingly, systolic and mean arterial pressure (MAP) was lower in the TRF group. In study 2, food intake was significantly lower in both MTII groups relative to Control. Although timing of injection affected light versus dark phase food consumption, neither body weight nor fat mass differed between MTII groups. Consistent with study 1, rats consuming their calories during the active phase displayed lower MAP. These data indicate that limiting feeding to the active phase reduces blood pressure without the necessity of reducing calories or fat mass, which could be relevant to obesity-related hypertension.

Intermittent Fasting for Twelve Weeks Leads to Increases in Fat Mass and Hyperinsulinemia in Young Female Wistar Rats

“…Restricting food intake to the resting phase worsened fasting and postprandial glucose concentrations, blood pressure, and lipid concentrations in humans [32,136], and induced leptin resistance that contributes to the development of obesity and metabolic disorders in mice [137]. However, restricting food intake to the active phase improved insulin sensitivity, blood pressure, glucose tolerance, and oxidative stress [8,138,139].…”

Early Time-Restricted Feeding Improves 24-Hour Glucose Levels and Affects Markers of the Circadian Clock, Aging, and Autophagy in Humans

“…While the benefits of some types of IF may stem mostly or entirely from energy restriction [8,9], one form of IF, called time-restricted feeding (TRF), has demonstrated benefits independent of energy restriction in both animals [10,11,12,13,14,15,16,17] and humans [18,19]. Since the median American eats over a 12-hour period [20], we define TRF as eating within a ≤10-hour period and fasting for at least 14 hours per day.…”

“…(Although TRF can include Ramadan fasting, we consider Ramadan fasting to be a separate type of IF.) Studies in rodents report that TRF reduces body weight, improves glycemic control, lowers insulin levels, reduces blood pressure, prevents hyperlipidemia, decreases hepatic fat, improves inflammatory markers, slows tumor growth, and increases lifespan, even when food intake is matched to the control group [10,11,12,13,14,15,16,17,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40]. To date, there have been nine pilot-sized trials of TRF in humans [18,19,41,42,43,44,45,46,47].…”

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

“…Interestingly, another study by the same group showed thata TRF of 8–12 h without reducing caloric intake in mice prevented and even reversed obesity and related metabolic disorders arising from a variety of obesogenic challenges, including high-fructose and high-fat, high-sucrose diets [ 9 ]. To date, there have been extensive studies in both rodents and humans reporting that TRF reduces body weight, improves glycemic control and insulin resistance, prevents atherogenic dyslipidemia, reduces blood pressure, prevents hepatic steatosis, and improves inflammatory markers in diet-inducedobesity models (DIO) [ 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 ]. It should be noted that most rodent studies have attempted to mimic the unhealthy human Western diet through the use of numerous obesogenic diets, which generally focused on a single or a combined macronutrient (s), in particular, fat and/or sugar.…”