Learning of food preferences: mechanisms and implications for obesity & metabolic diseases

Abstract

Omnivores, including rodents and humans, compose their diets from a wide variety of potential foods. Beyond the guidance of a few basic orosensory biases such as attraction to sweet and avoidance of bitter, they have limited innate dietary knowledge and must learn to prefer foods based on their flavors and postoral effects. This review focuses on postoral nutrient sensing and signaling as an essential part of the reward system that shapes preferences for the associated flavors of foods. We discuss the extensive array of sensors in the gastrointestinal system and the vagal pathways conveying information about ingested nutrients to the brain. Earlier studies of vagal contributions were limited by nonselective methods that could not easily distinguish the contributions of subsets of vagal afferents. Recent advances in technique have generated substantial new details on sugar- and fat-responsive signaling pathways. We explain methods for conditioning flavor preferences and their use in evaluating gut–brain communication. The SGLT1 intestinal sugar sensor is important in sugar conditioning; the critical sensors for fat are less certain, though GPR40 and 120 fatty acid sensors have been implicated. Ongoing work points to particular vagal pathways to brain reward areas. An implication for obesity treatment is that bariatric surgery may alter vagal function.

Validation of the Dutch Eating Behavior Questionnaire in a Romanian Adult Population

“…There are many pathways to obesity-some arising from lifestyle [5] but also from metabolic risk factors [6] with complex interactions between genetic, physiological, psychological and social factors [7]. The description of a single defective control mechanism for food consumption in people with obesity is not an achievable goal [8,9]. Physiological mechanisms such as hunger and satiety [10] are dependent on homeostatic feedback, but also environmental, hedonic feedback, in relation to biological and psychological learning mechanisms (retention/disinhibition) [11][12][13].…”

Brain Signaling of Indispensable Amino Acid Deficiency

“…The mechanisms for this rapid recognition of IAAD involve an enzyme important in the initiation of new protein synthesis: General Control Nonderepressible 2 (GCN2) and its target, phosphorylated eIF2α can be seen in Figure 6 of [ 40 , 41 ] and has been the subject of many reviews. For example, in 2021 alone, see [ 42 , 43 , 44 , 45 ]. The mechanisms involve an accumulation of uncharged tRNA because the limiting IAA that is deficient in the plasma and brain cannot adequately charge its cognate tRNA.…”

Brain Signaling of Indispensable Amino Acid Deficiency

“…The mechanisms for this rapid recognition of the IAAD involve an enzyme important in initiation of new of protein synthesis: the General Control Nonderepressible 2 (GCN2) [37,38] and have been the subject of many reviews. For example, in 2021 alone, see [39][40][41][42]. The mechanisms involve an accumulation of uncharged tRNA because the limiting IAA that is deficient in the plasma and brain cannot adequately charge its cognate tRNA.…”