Title: Satiation and Satiety.
Key words: hypothalamus, neurotransmitters, peptides, GLP-1, paraventricular nucleus, leptin, vagus nerve, blood glucose
Date: April 1999
Category: 7. The Mind
Author: Dr van Rhijn
Satiation and Satiety.
The control mechanism for food intake is essential for the survival of the organism. It is a complex interplay between various signalling devices, ranging from sensory input, food composition and hypothalamic nuclei to neurotransmitters. A brief discussion will only examine the current understanding of physiological pre- and post-absorptive mechanisms.
Pre-absorptive signals arise from the presence of food in the gastrointestinal tract. These initiate synergistic mechanical, chemical and receptive elements in mediating eating behaviour. Stomach volume affects intake and the higher the rate of gastric emptying, the greater the appetite1. Peptide hormones [Somatostatin, Cholecystokinin (CCK), Glucogen like peptide 1(GLP-1) etc] are released as soon as food enters the small intestine, with glucagon and insulin from the pancreas contributing to the sensation of satiety2. Carbohydrate preloads reduce mealtime intake and the desire to eat, with dextrose and fructose being more effective than glucose in this respect3.
The best studied peptide, CCK 4, is released from the proximal small intestine following fat ingestion. It contributes to the process of satiation by contracting the pyloric sphincter, to slow gastric emptying, stimulating pancreatic and biliary secretion and through neuronal interaction with feeding centres in the hypothalamus.
The effect of GLP-1, released from the distal small intestine, is still unclear, but it may act by stimulating insulin secretion and inhibiting gastric emptying. It is more sensitive to carbohydrates. Protein-induced suppression of food intake is greater than that from a similar gastric load of fat or carbohydrate5. Macronutrients from digestion provide signals via the vagus nerve to the brain through chemoreceptors in the small intestine walls.
Post-absorptive signals reach the brain via the vagus nerve from peripheral metabolic signals (Glucose, fatty acids & amino acids) after absorption into the portal vein and plasma6. Although several nutrients have been studied, the specific metabolic signals remain unidentified. Despite a lot of controversy, blood glucose appears to play a central role in signalling satiety when plasma levels increase7.
Increased plasma amino acid concentrations inhibit feeding as noted in human and animal studies8, but not confirmed in others. The role of their precursor (tryptophan) on the synthesis of neurotransmitters with regards to the control of food intake also still remains unclear. The lipostatic effect is unclear and superceded by the discovery of leptin (OB protein)9. It has been proposed that reduced insulin levels following caloric deprivation10, and leptin secretion11, stimulate production of neuropeptide Y (NPY) in the paraventricular nucleus, followed by feeding behaviour. Intake of energy (CHO & fat) correlates negatively with leptin concentrations12. Centrally, the hypothalamus and the ventromedial wall of the paraventricular nucleus are thought to be the main satiety centres.
The mechanisms mediating appetite and satiety are a complex interaction involving numerous regulatory mechanisms and remain poorly understood. It is crucial for these mechanisms to function properly, to regulate nutritional intake and to prevent the dire consequences resulting from over or under feeding. Further research is required to obtain potential therapeutic avenues for eating disorders and the increasing incidence in obesity.