Ingestive Behaviour units - Sheet1 Flashcards
(29 cards)
What is the process responsibile for regulating food and water?
The homeostatic process: a process that keeps body varibales, such as water and nutrient contents, within a certain range.
How does this mechanisam operate?
These mechanisms operate via negative feedback: The effect of a correctional mechanism causes that corectional mechanism to stop
What is the satiety mechanism?
A mechanism that controls the behaviour of injesting food and warter for replenishment. It monitors eating and drinking behaviours and stop them in anticipation of the replenishment whtat will occur later.
Two-thirds of the body’swarer is… and the rest is…?
Intracellular fluid: the fluid portion of the cytoplasm in cells. Extracellular fluid: Includes intravascular fluid, cerebrospinal fluid (blood plasma), and interstitial fluid (fluid surroundingcells). They are kept at a certain level.
Keeping intracellular fluid and extracellular (intravascular) fluid at a level prevents what?
Too much of intracellular fluid causes cells to burst and too little stops cells from functioning. Too little intravascular fluid stops the heart being able to pump blood around the body: this is hypovolemia.
What monitors intrecellular and intravasular volumes; and what are the mechanisms that cause us to be thirsty?
Two different receptors one of them is osmoreceptor. Volumetric thirst is caused by low intraVASCULAR water volumes ; Osmometric thirst is cause by low intraCELLULAR water values.
How does osmometric thirst happen?
Osmorecptors detect a high concentration of solutes in the interstial fluid. High salt conc. of blood plasma causes water to move via osmosis from interstitial fluid to blood plasma increasing the solute concetration of interstitial fluid. Water in the intracel. fluid moves from cells to the interstitial fluid, via osmosis. Osmoreceptors are a type of mechanoreceptor.
Where are Osmoreceptors located?
They are located in the lamina termialis. Nect to the third ventricle. The lamina terminalis doesn’t produce a feeling of satiety after drinking, this feeling is caused by the anterior cingulate cortex. (ACC)
When water is reabsorved into the osmoreceptors…?
they will stop firing.
What is volumetric thirst the result of?
Low intravascular (blood plasma) volume, these decreases are caused by evaporation of water (as is the case in osmometric thirst), as well as blood loss, vomiting, and diarrhoea. Loss of intravascular fluid produces a loss of water and the sodium that the cluid contains. This thurst produces a salt appetitie, as the sodium must also be replenished.
Cells in the kidneys detect low blood flow (as a results of low intravascular vol.) and induce the secretion of what hormone?
Angiotensin, it initiates drinking and produces a salt appetite, causes the kindeys to conserve water and salt and increases blood pressure. Stretch-receptor cells in the heart detect when blood vol. in the heart decreases, initiating drinking.
Where is the hormone for volumetric thirst detected?
It is processes in the lamina terminalis, outside the blood-brain barrier, meaning that angiotensin can interact with the lamina terminalis to prooduce the sensation of thirst.
Damage to the lamina terminalis can produce what disorder?
Adipsia. An abnormal lack of drinking due to inability to detect low water levels. Patients must deliberatly drink water at regular intervals.
There are two main types of hunger signals, what are they?
They are sent by the digestive system and the other is produced by the liver and the medulla. The short-term satiety signals are CCK (p by the intestines) and insulin (p by the pancreas), messages sent from the liver to the brain via the vagus nerve. Long-term satiety singal are produced by fact cells in the body.
What is the main hunger singlas produced by the digestive systems involves the release of what hormone?
Ghrelin hormone is released from the stomach and duodenum (inital part of small intestine). Gh. ibinds to receptors in the hypothalamus (results in hunger). More gh facilitates eating, and blocking gh inhibits eating. PRADER-WILLI SYNDROME: charactersied by obsity due to almost continuous eating and is partly caused by high blood levels of ghrelin.
What are the key metabolic and intestinal signals involved in hunger and satiety regulation?
Metabolic signals of hunger arise when brain and liver cells detect low glucose and fatty acid levels.
The brain relies only on glucose, while the rest of the body uses both glucose and fatty acids.
Liver cells signal hunger via the vagus nerve, and medulla cells also detect low glucose.
Satiety signals include short-term signals from the intestines that stop eating at the end of a meal, even before nutrients are absorbed.
When food enters the duodenum, the release of ghrelin is suppressed, signaling fullness.
What are the key sources and mechanisms of satiety signals in the body?
Intestinal and liver signals:
Food entering the duodenum triggers cholecystokinin (CCK) release, aiding digestion and sending satiety signals via the vagus nerve.
Once nutrients are absorbed, the liver detects them and reinforces satiety by signaling the brain.
Insulin signals:
Eating stimulates insulin release from the pancreas, allowing glucose metabolism and fat storage.
Insulin crosses the blood-brain barrier and activates hypothalamic neurons, enhancing the feeling of fullness.
What are other satiety signals?
Memory (STS): a patient with short term memory deficit because of damage to the hippocampus and amygdala would eat up to 3 meals after short breaks due to memory loss. Environmnetal factors: larger portions and eating in company causes people to eat more. Sensory factors: contribute to satiety
What role does leptin play in long-term satiety regulation?
Leptin is a hormone secreted by fat cells that signals long-term satiety.
It reduces eating, increases metabolism, and boosts activity levels.
Mice without the OB gene (ob mice) lack leptin, leading to overeating and obesity.
Injecting leptin into ob mice normalizes their weight.
In humans, leptin-based treatments for obesity have shown little or no success.
How does the brain stem contribute to hunger and satiety control?
The caudal medulla, including the nucleus of the solitary tract (NST), receives signals from:
Taste receptors,
The stomach, duodenum, and liver,
And detects blood glucose levels.
These signals are relayed to higher brain areas like the hypothalamus, which control eating and metabolism.
What roles do different parts of the hypothalamus play in regulating eating?
The arcuate nucleus regulates appetite, and detects ghrelin, insulin, leptin, nicotine, and CCK.
The lateral hypothalamus acts as an accelerator: it promotes eating and food reward.
The ventromedial hypothalamus acts as a brake: it suppresses eating; damage leads to overeating.
What are the hypothalamic connections involved in eating, and what are the health risks of obesity?
The lateral hypothalamus connects to:
The NST (enhancing taste perception when hungry),
The nucleus accumbens (facilitating ingestion),
The spinal cord (controlling digestive secretions).
Obesity increases risk for heart disease, diabetes, stroke, arthritis, and some cancers.
Its causes are complex and include environmental, physical activity, and genetic factors.
How does the modern environment contribute to obesity?
High-calorie, inexpensive, and convenient foods with large portions promote weight gain.
Many processed foods contain fructose, which doesn’t trigger insulin secretion, weakening satiety signals.
These environmental factors increase the risk of overeating and obesity.
What is the role of physical activity in obesity?
Modern jobs involve less vigorous activity, so less food is needed than in the past.
Non-exercise activity thermogenesis (NEAT)—like fidgeting, posture shifts—is higher in lean people.
Workplaces promoting standing or treadmill use can reduce obesity risk.
