Eating 1. Flashcards
Essay Plan:
- Introduction: Define the primary purpose of eating
- Define Hunger, Degestion & Satiety
- 3 phases of metabolism: Lipids, protein and glucose
- Food absorption and conversion to fuel: cephalic, absorbative and post absorbative/fasting=feedback loop
- Glucoprivation and dual centre model
- Neurocircitury model of energy compsumtion
Introduction
The primary purpose of hunger is to increase the probability of eating and the primary purpose of eating is to supply the body with monocular building blocks and the energy needed to survive. Satiety is the condition of being full and is only achieved by digestion, the gastrointestinal process of breaking down food and absorbing its constituents into the body. This easy shall outline the chemical messengers that lead to the neural control of hunger and satiety.
Food absorption and conversion to fuel:
As a consequence of digestion, energy is delivered to the body in three forms (1) lipids (fats) (2) amino acids (broken down from proteins) (3) glucose (simple sugar by-products of carbohydrates). Energy can be stored as fat, glycogen, and protein. There are three phases of energy metabolism, the chemical changes by which the energy is made available for an organisms use. The first is the cephalic phase which often begins with the sight/smell of food and this often leads into the absorptive stage. This is when the gastrointestinal tract is full and the anabolic processes (building up of energy) exceeds catabolism (breaking down). In this phase nutrients are broken down and absorbed into capillaries that line the wall of the intestine and travel in the hepatic portal vein to the liver. At the liver they are dispatched immediately for use by tissue or chemically converted and stored. After absorption of a meal is complete, the post-absorptive fasting state occurs. This is the period in which all of the unstored energy from the meal has been used and the body is withdrawing energy from its reserves to meet energy requirements. These three phases act as a feedback loop contributing to feelings of hunger and satiety.
Chemical messengers & hunger: Appetite triggers and Appetite suppressants:
Glucoprivation is the lack of glucose by access insulin of excess deoxgylucose which is detected by the liver and the brain. Often detected when the stomach is empty, the hunger peptide ghrelin is secreted from the stomach and directly picked up by circumventricular organs in the brain in which motivate food intake.
The first theory of hunger and satiety: Link between brain areas involved in eating: the Dual Center Hypothesis
The first theory of hunger and satiety to explain this was the dual centre model, which advocated eating behaviour was controlled by two distinct areas in the hypothalamus, satiety by the ventralmedial hypothalamus (VMH) and hunger by the lateral hypothalamus (LH). As a continuous loop, hunger signals arising from factors such as glucoprivation stimulate the lateral hypothalamus (LH) which motives one to eat and inhibits activity in the ventralmedial hypothalamus (VMH). As the stomach enters the absorptive phase and nutrients enter the capillaries, satiety signals such as CCK (cholecystokinin) and PPY (pancreatic peptide YY) eventually overcome the inhibition of the ventralmedial hypothalamus (VMH) and feeding ceases.
Hetherington and Ranson (1940): Induced large bilateral lesions in the ventralmedial hypothalamus (VMH) of rats
Hetherington and Ranson (1940): Induced large bilateral lesions in the ventralmedial hypothalamus (VMH) of rats which resulted in over eating and obesity which confirms the dual centre model. However after weeks of excessive eating and weight gain the food consumption gradually declined resulting in the rats returning to previous body weight homeostasis. If the ventralmedial hypothalamus (VMH) soely functioned independently as a satiety centre as the dual centre model posits, lesioning this area should induce continuous hunger and eating. Similarly rats stimulated in the lateral hypothalamus (LH) hunger centre were not just motivated to eat but were motivated to do other things besides eating, e.g. running or other activities. Therefore the lesion/stimulation to this area cannot be explained by the simplicity of the dual centre model.
What controls eating: theories Set-point theory (Nisbett, 1972)
Therefore Nibett (1972) explained these centres that controll hunger and satiety through a set-point mechanism in which individuals engage in eating behaviour to maintain internal homeostasis (a stable, constant internal state). The system aims for a set-point or target in terms of glucos eand fat level (glucostatic set-point theory and lipostatic set-point theory) maintainece so if energy levels are below that target then eating is commenced and once set-point is reached then we will stop eating.
According to the set-point theory, there is a control system built into every person dictating how much fat he or she should carry, a kind of thermostat for body fat. Some individuals have a high setting, others have a low one. According to this theory, body fat percentage and body weight are matters of internal controls that are set differently in different people.
THE NEUROCIRUITARY MODEL OF ENERGY
The idea that the ventralmedial hypothalamus (VMH) is exclusively a satiety centre and the lateral hypothalamus (LH) a hunger centre no longer warrants serious consideration, instead a more complex theory of hunger and satiety has been put forward, the neurocircuitary of energy homeostasis. This theory advocates that hunger and satiety are regulated by a number of peptides released in the gastrointestinal tract. In terms of glucoprivation, ghrelin is released from the stomach and neuro peptide Y (NPY) from the ventrolateral medulla, these travel via the arcuate nucleus to the LH. The peptides released hert, orexin and melanin concentrating hormone (MCH) are the two that ultimately motivate eating behaviour.
Conclusion
THE NEUROCIRUITARY OF MODELOF ENERGY consumption is the main scientific theory that explains short term hunger and satiety suffciently. It acknowledges there is a comlex network involved along with a number of peptides. The discovery of these peptides has major effects on the search for neural mechanisms of hunger and satiety. The number of peptides discovered so far indicate the neuroal system reacts to many different signals, not just glucose and fat. Although the hypothalamous has been largely impliacted in short term hunger and satiety,
