Gastrointestinal Satiety Signals

Abstract

The increasing prevalence of obesity worldwide has imparted renewed impetus to the study of the mechanisms of appetite regulation. Digestion and nutrient absorption take place in the gastrointestinal (GI) tract, whereas food intake is controlled by neuronal circuits in the central nervous system. The need for gut-brain cross talk is therefore clear. It is now recognized that hormones released into the circulation from the GI tract in response to nutritional stimuli form a key component of this gut-brain axis. Peptides such as glucagon-like peptide-1, oxyntomodulin, pancreatic polypeptide, and peptide YY3-36 reduce food intake in both animal models and in humans. Physiologically, such peptides are thought to act as satiety signals and meal terminators. Here, we review the current state of the field of the effects of gut hormone action on appetite control.

IMAGING IN ENDOCRINOLOGY: The use of functional MRI to study the endocrinology of appetite

“…It has long been understood that hormones have a part to play in controlling energy homoeostasis. They play an important role in transmitting information to the brain about peripheral nutrient availability and fat stores, and they therefore affect appetite and energy expenditure and influence body weight (3). However, humans can easily override hormonal satiety signals when confronted with appetising foods associated with a reward value.…”

Functional brain imaging and its application to uncover mechanisms driving food intake in humans

“…Neurohormonal signals from the gut and adipose tissue converge on the hypothalamus where they are integrated, and in turn regulate energy intake and energy expenditure [10][11][12] . Cortical inputs in terms of emotional, social, and learned behaviour, as well as inputs from reward circuits (see below), including the mesolimbic dopaminergic system, all impact upon energy balance and communicate with the hypothalamus [68,70] .…”

“…While the POMC/CART neurons appear to be activated by the presence of leptin, the NPY/AgRP are inhibited. Thus leptin, as an adiposity signal, acts by shifting the balance from the potent feeding system constituted by the NPY/AgRP neurons toward the POMC/CART satiety system [8,[10][11][12]66] . Neuroimaging of responses to food stimuli have confirmed such an action of leptin.…”

“…Thus all neuroimaging studies are consistent with a model in which leptin down-regulates hedonic activation in reward areas in response to food cues, and simultaneously up-regulates homeostatic control by enhancing the central response to peripheral satiety signals. Sensory terminals carrying this information terminate in the nucleus of the solitary tract, from where direct projections innervate several hypothalamic structures [10][11][12] .…”

“…Complex (and not completely known) brain mechanisms in the hypothalamic nuclei modulate the drive for feeding by receiving short-term gastrointestinal information (gut hormones) related to nutritional stimuli [10,11] and long-term adiposity signals (leptin) related to energy stores and body weight regulation [12] , and by integration of powerful inputs from higher cortical centres and nervous structures concerned with pleasure and reward [9] . Thus, eating results to be not a simple stereotyped task, but a complex set of processes carried out with the involvement of peripheral and central nervous system (CNS) to coordinate activities ranging from the obtainment of sensory information about food to the evaluation of desirability and selection of appropriate behaviour under the internal drive of appetite.…”