Hunger and Satiety Gauge Reward Sensitivity

Abstract

Many of the neurocircuits and hormones known to underlie the sensations of hunger and satiety also substantially alter the activity of the dopaminergic reward system. Much interest lies in the ways that hunger, satiety, and reward tie together, as the epidemic of obesity seems tied to the recent development and mass availability of highly palatable foods. In this review, we will first discuss the basic neurocircuitry of the midbrain and basal forebrain reward system. We will elaborate how several important mediators of hunger—the agouti-related protein neurons of the arcuate nucleus, the lateral hypothalamic nucleus, and ghrelin—enhance the sensitivity of the dopaminergic reward system. Then, we will elaborate how mediators of satiety—the nucleus tractus solitarius, pro-opiomelanocortin neurons of the arcuate nucleus, and its peripheral hormonal influences such as leptin—reduce the reward system sensitivity. We hope to provide a template by which future research may identify the ways in which highly rewarding foods bypass this balanced system to produce excessive food consumption.

Serum concentration of appetite‐regulating hormones of mother–infant dyad according to the type of feeding

“…In particular, the center of hunger in the hypothalamus is a nuclear region of the brain currently considered responsible for controlling appetite (Cassidy & Tong, 2017). In particular, the center of hunger in the hypothalamus is a nuclear region of the brain currently considered responsible for controlling appetite (Cassidy & Tong, 2017).…”

“…Appetite and body weight regulation are controlled by the central nervous system (CNS) in a rather complicated manner. In particular, the center of hunger in the hypothalamus is a nuclear region of the brain currently considered responsible for controlling appetite (Cassidy & Tong, 2017). However, most of the available evidence derives from experiments in rodents, and the role of this system in regulating appetite in states of hunger/starvation and in the pathogenesis of overeating/obesity remains to be fully elucidated in humans (Farr, Li, & Mantzoros, 2016).…”

Cross-disorder genetic analyses implicate dopaminergic signaling as a biological link between Attention-Deficit/Hyperactivity Disorder and obesity measures

“…Increasing evidence suggests that such metabolic hormones also affect food-related sensitivity of the dopaminergic reward system [34], pointing to an overlap between the homeostatic and reward/reinforcement systems related to obesity [23].…”

Encoding of an engram for food location by satiety-promoting Drd2 hippocampal neurons

“…D2R cells also regulate valence through a LS pathway in fasted, but not sated mice (Figure 5M). This suggests that internal states also contribute, at some level, to how cells in the D2R-LS circuit, or cells that are downstream of it, sense and process reward (Cassidy and Tong, 2017). This might contribute to satiety itself and memory encoding by linking food to an unpleasant sensation (Cassidy and Tong, 2017).…”

“…This suggests that internal states also contribute, at some level, to how cells in the D2R-LS circuit, or cells that are downstream of it, sense and process reward (Cassidy and Tong, 2017). This might contribute to satiety itself and memory encoding by linking food to an unpleasant sensation (Cassidy and Tong, 2017). This change in valence might also explain the memory deficts observed in our Food Location task after D2R activation.…”