Satiety Associated with Calorie Restriction and Time-Restricted Feeding: Peripheral Hormones

Abstract

Calorie restriction (CR) is a common approach to inducing negative energy balance. Recently, time-restricted feeding (TRF), which involves consuming food within specific time windows during a 24h day, has become popular owing to its relative ease of practice and potential to aid in achieving and maintaining a negative energy balance. TRF can be implemented intentionally with CR, or TRF might induce CR simply due to the time restriction. This review focuses on summarizing our current knowledge on how time-restricted feeding (TRF) and continuous caloric restriction (CR) affect gut peptides that influence satiety. Based on peer-reviewed studies, in response to CR there is an increase in the orexigenic hormone ghrelin and reduction in fasting leptin and insulin. There is likely a reduction in glucagon-like-peptide-1 (GLP-1), peptide-YY (PYY), and cholecystokinin (CCK), albeit the evidence for this is weak. Following TRF, unlike CR, fasting ghrelin decreased in some TRF studies, while showing no change in several others. Further, a reduction in fasting leptin, insulin, and GLP-1 has been observed. In conclusion, when other determinants of food intake are held equal, the peripheral satiety systems appeared to be somewhat similarly affected by CR and TRF with regard to leptin, insulin and GLP-1. But unlike CR, TRF did not appear to robustly increase ghrelin suggesting different influences on appetite with a potential decrease of hunger following TRF when compared to CR. However, there are several established and novel gut peptides that have not been measured within the context of CR and TRF, and studies that have evaluated effects of TRF are often short-term, with non-uniform study designs, and highly varying temporal eating patterns. More evidence and studies addressing these aspects are needed to draw definitive conclusions.

Dietary regulation in health and disease

“…Nutritional complementarity is primary to an organism’s growth and development via regulation of multiple cytokines (leptin, adiponectin, asprosin, acyl-CoA-binding protein and so on) and growth factors and hormones (insulin/IGF-1, FGF21, thyroid-stimulating hormone, prolactin, corticosterone, etc.). 80 , 152 – 156 Insulin and IGF-1 were first discovered to be connected to diet and health. The orthologue of the mammalian insulin/IGF-1 receptor in C. elegans is encoded by the daf-2 gene, and its mutation has been found to dramatically prolong longevity.…”

Fasting: From Physiology to Pathology

“…[ 95 ] Additionally, TRF can regulate appetite by hormones and peptides, such as leptin, insulin, and ghrelin. [ 96 ] Leptin and insulin inhibit food intake by activating POMC/CART neurons and inhibiting NPY/AgRP neurons in the arcuate nucleus. [ 97,98 ] As opposed to insulin and leptin, ghrelin is an orexigenic hormone that can suppress POMC/CART neurons and stimulate NPY/AgRP neurons.…”

Diet containing stearic acid increased food intake in mice by reducing serum leptin compared with oleic acid

“…Other signals, such as insulin and leptin, are transported to the brain by blood through a saturation mechanism. 2 Therefore, ARC, as one of the most peripheral nuclei in the hypothalamus, is able to receive peripheral signals first. Therefore, it is known to play a key role in the signal integration of feeding.…”