How Palatable Food Disrupts Appetite Regulation

Abstract

Appetite regulation is part of a feedback system that controls the energy balance, involving a complex interplay of hunger and satiety signals, produced in the hypothalamus as well as in peripheral organs. Hunger signals may be generated in peripheral organs (e.g. ghrelin) but most of them are expressed in the hypothalamus (neuropeptide Y, orexins, agouti-related peptide, melanin concentrating hormone, endogenous opiates and dopamine) and are expressed during situations of energy deficiency. Some satiety signals, such as cholecystokinin, glucagon-like peptide 1, peptide YY and enterostatin are released from the digestive tract in response to food intake. Others, such as leptin and insulin, are mobilized in response to perturbations in the nutritional state. Still others are generated in neurones of the hypothalamus (a-melanocyte-stimulating hormone and serotonin). Satiety signals act by inhibiting the expression of hunger signals and/ or by blunting their effect. Palatable food, i.e. food rich in fat and sugar, up-regulates the expression of hunger signals and satiety signals, at the same time blunting the response to satiety signals and activating the reward system. Hence, palatable food offsets normal appetite regulation, which may explain the increasing problem of obesity worldwide.

Brain neuropeptide Y and CCK and peripheral adipokine receptors: temporal response in obesity induced by palatable diet

“…33 Palatable food activates the reward system, to reinforce motives without homeostatic value. 20 Figure 5 …”

“…Overeating is stimulated by the ready availability of food rich in fat and sugar. 20 Thus, the aim of this study is to look at appetite regulation under palatable HFD and the contribution of central and peripheral metabolic mediators. The hypothesis is that animals will display marked overconsumption in the face of a palatable HFD, and this will be associated with a decrease in the putative satiety factors and an increase in the appetite stimulant NPY.…”

Intense sweeteners, energy intake and the control of body weight

“…Sweet-tasting foods with high-energy density are said to disrupt appetite regulation and overwhelm the body's regulatory mechanisms (Erlanson-Albertsson, 2005). Energydense diets cause insulin and leptin resistance in the central nervous system (CNS) (Schwartz, 2006) and blunt responses to physiological signals of satiety (Erlanson-Albertsson, 2005).…”

“…Energydense diets cause insulin and leptin resistance in the central nervous system (CNS) (Schwartz, 2006) and blunt responses to physiological signals of satiety (Erlanson-Albertsson, 2005). Diet-induced CNS insulin resistance is the suggested reason why pleasure response to energy-dense foods does not diminish even in the face of caloric repletion (Lustig, 2001;Isganaitis and Lustig, 2005).…”

Single nucleotide polymorphisms in the neuropeptide Y2 receptor (NPY2R) gene and association with severe obesity in French white subjects

“…Many neuropeptides affecting food intake and/or energy expenditure have been described to date [1][2][3][4]. The recent identification of hunger and satiety peptides, as well as their receptors, has increased the interest in appetite regulation, particularly for the treatment of eating disorders, from anorexia to overeating and obesity [2].…”