control of food intake Flashcards
how is the autonomic nervous system involved in the storage of food in the stomach ?
fasting:
* stomach is empty
* ghrelin is released to signal to the brain that food is needed
accommodation:
* occurs after food intake
* stomach expands to store ingested food
* VIP and NO allow for stomach relaxation and expansion
* PYY is released to promote feelings of fullness and reduce gut mobility
emptying:
* after digestion food is gradually emptied into small intestine
* ghrelin released again - hunger
* stomach contracts pushing food into intestines
describe accommodation of food in the gastric reservoir
- Receptive Relaxation:
* Triggered by mechanical stimuli in the pharynx (such as swallowing).
* The vagus nerve sends signals to the stomach, preparing it for food intake.
* This is a reflex that allows the stomach to expand without a significant increase in pressure. - Adaptive Relaxation:
* When food enters the stomach, nutrient distension activates tension receptors.
* These receptors signal the vagus nerve to release inhibitory neurotransmitters such as:
* Nitric Oxide (NO)
* Vasoactive Intestinal Peptide (VIP)
* PACAP (Pituitary Adenylate Cyclase-Activating Polypeptide)
* These neurotransmitters cause the smooth muscles of the stomach to relax, allowing for storage of food. - Feedback Relaxation:
* The stomach communicates with the duodenum (small intestine) and brain via the CCK (Cholecystokinin) hormone.
* This feedback mechanism helps regulate stomach emptying and satiety.
what is a vagotomy ?
- cutting of the vagus nerve
- impairs accommodation and emptying
- reduces accommodation and gastric compliance is 5 % of patients - early satiety
- denervation may have no effect on food intake due to other signals
define hunger appetite and satiety
hunger:
* discomfort caused by lack of food and the desire to eat – a strong physiological craving/drive for food/sensation of emptiness in the stomach
appetite:
* psychological desire/drive to satisfy the body’s needs of food; a hunger-stimulated response
satiety:
* state of being full after eating food (joyous moments – no longer need to continue eating)
what is aphagia and hyperphagia ?
aphagia:
* inability or refusal to swallow
hyperphagia:
* an abnormal desire for food
describe the role of the hypothalamus in the control of food intake
- is is the control center for appetite and food intake
- controls hunger and thirst
- has several nuclei that regulate energy homeostasis
- these nuclei control the appetite , size of helping and our ingestive behavior
- the satiety centre ( ventromedial nuclei) is in the hypothalamus
- stimulation of ventromedial nuclei - aphagia
- lesions of ventromedial nuclei - hyperphagia
- hunger centre - lateral hypothalamus
- stimulation of lateral hypothalamus - increased feeding
- legions of lateral hypothalamus - aphagia
what other inputs control feeding behaviour ?
- orexigenic and anorexigenic neurotransmitters have been found in the hypothalamus
- orexigenic - increase appetite
- anorexigenic - decrease appetite
describe some examples of hypothalamic nuclei in the control of food intake
- Dorsomedial nucleus (DMN) = modulates energy intake (hunger centre)
- Release of NPY into DMN → ↑ feeding
- Paraventricular nucleus (PVN) = modulates feeding behaviour
- Control feeding behaviour
- NPY, opioids →↑ feeding
- Leptin →↓ food intake
- Arcuate nucleus
- its neurons produce orexigenic signals (NPY, the opioids, dynorphin, β-endorphin, galanin, glutamate) * →↑ feeding
- Suprachiasmatic nucleus – location of human body clock
- Perception of the light-dark cycle (circadian rhythms)
- Appetite or the sensation of hunger → mood/drive to eat
- Medial amygdaloid nucleus
- It is a sub-region of the amygdaloid complex;
- A role for medial amygdaloid nucleus in feeding behaviour has been proposed
- Participates in the regulation of food intake
describe the roles of prefrontal cortex and limbic system in control of food intake
- The prefrontal cortex: influences food-seeking behaviour
- Integrates sensory information from inside and outside the body;
- Receives emotional and cognitive information from the limbic system
- Helps one make choices by translating all of the homeostatic and environmental information into (adaptive) behavioural response
- Limbic system: complex system of nerves and networks in the brain; areas concerned with instinct, learning, reproductive behaviour; emotions/mood, pleasure (fear, anger, etc.)
- The act of `satiation of feeding behaviour is associated with motor planning and execution
- Overall, the cortico-limbic mechanisms of reward are under executive control
describe the role of CCK
- hormone
- Fat ingestion causes CCK release and the slowing of gastric emptying – state of sense of fullness
- CCK (from I cells in the intestine or nerve endings) and somatostatin are satiety factors; inhibit further food intake
- Injection of CCK in the brain → suppresses appetite
- Therefore, CCK derivatives may have utility in obesity
describe the role of leptin
- Fat cells (adipocytes) secrete leptin (16kDa protein) - gene expressed mainly in adipocytes
- Controls fat stores by operating a feedback mechanism between adipose tissue and brain
- There is a high correlation of leptin levels with body fat in humans and animals
- The larger the size of the adipose tissue, the greater the leptin secreted by the adipose tissue
- Administration of leptin can decrease food intake, induce weight loss (and increase energy expenditure)
Leptin acts on the hypothalamus → changes in food intake - White adipose tissue → leptin (lipostat; signals fat stores in adipose tissue)
- Increases the expression of anorexigenic factors [pro-opiomelanocortin (POMC), cocaine- and amphetamine-regulated transcript (CART), corticotrophin-releasing hormone (CRH)]
- Inhibits neuropeptide Y (NPY); note, NPY stimulates feeding
- Leptin resistance may lead to binge eating, despite being obese
- Hyperphagia and severe obesity occurs in in humans with leptin deficiency or leptin receptor defects
describe the role of ghrelin
- An appetite-inducing hormone (an orexin) – stimulates hunger
- Fast-acting and stimulates food intake
Released by stomach, pancreas, adrenals in response to nutritional status - Increases central orexins, e.g. NPY, and AgRP (= hunger signals)
- Circulating levels of ghrelin ↑ pre-prandial and ↓ after a meal (post-prandial)
- Leptin can inhibit the secretion of ghrelin
- Ghrelin suppresses the ability of leptin to stimulate anorexigenic factors
- Leptin and ghrelin act reciprocally on food intake
Stimulation of their receptors in hypothalamus → changes in food intake
describe the role of obestatin
- Produced by epithelial cells of stomach
Encoded by ghrelin gene, but it opposes the effects of ghrelin on food intake - Suppresses food intake (suppresses appetite; ↓ body weight gain)
- Antagonises ghrelin-induced food intake (and growth hormone secretion)
- Obestatin mediates its effects via different receptors to ghrelin
What is the name of the well-known hormone that is synthesised by the gastric fundus during fasting, and induces the levels of NPY in the brain?
ghrelin
Which hormone is secreted by adipocytes which signals satiety?
leptin
Cholecystokinin (CCK) has a number of important functions in the body, including secretion of bile from the gallbladder, inhibition of gastric acid secretion, and control of food intake. what best describes the central and peripheral effects of CCK?
It slows down gastric emptying and inhibits appetitive if injected into the hypothalamus
A 54-year-old man was recently involved in a nasty road traffic accident which resulted in a lesion in the ventromedial wall of the paraventricular nucleus of his hypothalamus. Which condition best describes the effect of such an accident on the man?
He is likely to suffer with hyperphagia which will results in him gaining weight if he is less active
Some first-year undergraduate students went to Sam’s café for lunch. They each had a portion of regular meal and some fries. One of the students was heard asking the rest of the group to name one substance which is being released co-incident with their meal and involved in regulation of feeding. None of the students got it right; please identify the correct one
CCK
Which hormone pair act reciprocally to control food intake?
ghrelin / leptin
Provide a very brief answer to what the consequence will be of the denervation of the stomach and intestine on food intake
Denervation may/will have little or no effect on food intake; peripheral signals from adrenals, pancreas, adipose and GIT will continue to operate to control food intake and energy expenditure
Name 2 central and 2 peripheral substances that are important in the control of food intake
Central controls: NPY, AgRP
Peripheral controls: ghrelin, leptin, CCK
