Control of Food Intake Flashcards
What starts to expand when you eat?
→ The fundic area expands to accomodate food
What two hormones are used in accommodation?
→ VIP and NO
What is PYY and what does it do?
→ Is a satiety factor and increases gut motility
Peptide YY
What do you feel when emptying occurs?
→ A sense of hunger (ghrelin)
Where do contractions occur and what are they mediated by?
→ Occur in the antrum
→ Mediated by AcH
What relaxation occurs when food is swallowed?
→ Receptive relaxation
What is receptive relaxation done by?
→ Vagal innervation
What kind of relaxation occurs in the stomach to allow accommodation?
→ adaptive relaxation
What is CCK stimulated by?
→ Lipids
What is affected if you cut vagus nerves?
→ Accommodation
→ Gastric compliance
What is the difference between appetite and hunger?
→ Appetite is a psychological desire
→ Hunger is a physiological craving
What is hyperphagia/polyphagia?
→ Abnormal desire for food
What does the hypothalamus control?
→ Hunger + thirst
Functions of the prefrontal cortex
→ Food seeking
→ Integration of sensory information from inside and outside the body
→ Receives emotional + cognitive information from the limbic system
→ Makes choices by translating the homeostatic and environmental information into adaptive behavioral responses,
What is the limbic system?
→ Complex system of nerves and networks in the brain
associated with instinct and mood
What sites is feeding behavior modulated by?
→ Lateral hypothalamus
→ Ventromedial hypothalamus
What is the role of the lateral hypothalamus?
→Hunger + thirst center
What is the role of the ventromedial nucleus ?
→ Satiety center
What happens if there is a lesion to the VMN?
→ Increased appetite with weight gain
What does the dorsomedial nucleus do?
→ Modulates energy intake (hunger center)
release NPY into DMN= increased feeding
What acts on the dorsomedial nucleus to increase feeding?
→ NPY into the DMN increases feeding
What does the paraventricular nucleus do and how?
→ Modulates feeding behavior
→Paraventricular nucleus and perifornical hypothalamus
→NPY, opioids, and GABA =↑ feeding
→leptin =↓ food intake
What does the arcuate nucleus produce?
→ Orexigenic signals
What are the types of relaxation of the reservoir?
→receptive (mechanical stimulation of pharynx – mechanoreceptors, sight)
→adaptive (vagal innervation (NO/VIP), tension of stomach)
→feedback (nutrients, CCK).
How do the inhibitory vagal fibres relax the stomach?
→inhibitory vagal fibres release ACH
→ACH activate inhibitory enteric pathways that release NO, VIP and ATP in order to relax the muscle
What is vagotomy?
impairs accommodation and emptying: a cause for early satiety in some patients
Define satiety
state of being full after eating food (joyous moments – no longer need to continue eating)
Define aphagia
the inability or refusal to swallow
What is the role of satiety signals?
→to prolong the interval until hunger or the onset of the next meal
Summarise the factors that control food intake
→hypothalamic control
→BMI
What are some diurnal variations in food metabolism?
→Carbohydrates metabolised during the day
→Fats metabolised at night
→Hypothalamus responds to the switch between carbohydrate and fat metabolism
How does the hypothalamus control food intake?
→The base of the hypothalamus has several nuclei that regulate energy homeostasis- bout 12 of them
→ Control the appetite; size of helping, and our ingestive behaviour
The nuclei communicate with each other
What happens with stimulation of ventromedial nuclei and removal?
→aphagia (swallowing difficulty)
→ removal= hyperphagia
What happens with stimulation of lateral hypothalamus?
→increased feeding
What happens with lesion of the lateral hypothalamus?
aphagia
What is opioid’s effect?
(growth hormone releasing hormone)
→increased appetite
What is the effect of naltrexone?
(opioid antagonist) reduces the positive ‘hedonic valence’ of food
What is the hedonistic system?
pleasant sensation
What is the arcuate nucleus?
Neurons produce orexigenic signals (NPY, the opioids, dynorphin, β-endorphin, POMC, galanin, amino acids, glutamate, and GABA) =increased feeding
What is GABA effects on feeding behaviour?
→Injection of GABA into the VMH reliably increases food intake
→Injection of GABA into the origin of the nigrostriatal dopamine (DA) neurons in the substantia nigra (SN) suppressed food intake
What is the suprachiasmatic nucleus?
→Human body clock is located in the suprachiasmatic nuclei
→Perception of the light-dark cycle (circadian rhythms)? Appetite or the sensation of hunger =mood/drive to eat
→Also stomach nerves
What is the medial amygdaloid nucleus?
→It is a sub-region of the amygdaloid complex
→Participates in the regulation of food intake
What are the ligands involved in regulation of appetite and food uptake?
→5-HT (via 5-HT2C and 5-HT1A)-
Regulation of appetite in the hypothalamus by 5-HT2C agonist
→balance between an appetite stimulating pathway that releases agouti-related peptide (AgRP) and neuropeptide Y (NPY)
→an appetite suppressing pathway that releases alpha-melanocyte stimulating hormone (alpha-MSH).
→The appetite suppressing neurons make the precursor pro-opiomelanocortin (POMC)
→broken down into alpha-MSH
→binds to melanocortin 4 receptors (MC4R) to suppress appetite
How is food intake controlled centrally?
→5-HT (5-HT2C and 5-HT1A), dopamine, GABA =reduced appetite
→anorexigenic factors
What does zimelidine do?
→inhibits the reuptake of 5-HT from synaptic cleft, allowing 5-HT to
persist in the synaptic cleft
What is the role of 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
What is the role of the limbic system?
→areas concerned with instinct, learning, reproductive behaviour; emotions/mood, pleasure (fear, anger, etc.)
Under what control is the cortico-limbic mechanisms?
executive control
What do higher functions do?
modulate responses to both CNS and peripheral cues (e.g. gut; environment)
Factors that affect if food is sought or not and the type we ingest….
Food preferences
Emotions; psychological; physiological
Environment
Life style
What is the role of the circadian rhythm?
→limits food intake to certain times (in some people)
What does the brain do in high and low glucose levels?
↓[glucose]blood →induces hunger
↑[glucose]blood → induces satiety
Why do diabetic patients feel hungry despite ↑[glucose]blood?
The blood glucose is not being taken up
What do cold and hot environments do?
→stimulate feeding while hot environments inhibit appetite
What is calcitonin?
hormone that reduces appetite
What are insulin’s effects in the brain?
→Different parts of the brain that insulin reduces levels of orexigenic factors that inhibits feeding
→Inhibits NPY/AgRP(co-expressed with NPY and acts to increase appetite) = reduce food intake, reduce body fat
Insulin and leptin act agonistically in reducing food intake via action on receptors within the brain
What hormones are secreted by the endocrine pancreas?
→insulin, glucagon, and amylin
What does insulin do to the liver and the forebrain
→to reduce energy intake as well as to suppress hepatic glucose production.
What does glucagon do?
→acts mainly at the liver
→increases glucose production while generating a signal to reduce energy intake that is relayed to the hindbrain
What does amylin do?
→acts directly at the hindbrain to reduce energy intake
inhibits glucagon secretion, delays gastric emptying, and acts as a satiety agent.
o-released with Insulin
What is the area postrema?
a medullary structure in the brain that controls vomiting.
What type of cells release CCK?
I-cells from the intestine and nerve ending
What is CCK?
→Fat ingestion causes CCK release and the slowing of gastric emptying – state of sense of fullness
→inhibit further food intake
→Injection of CCK in the brain → reduction of appetite
What is somatostatin?
growth hormone inhibiting hormone
→satiety factor
What is leptin?
Fat cells (adipocytes) secrete leptin- gene expressed mainly in adipocytes →Controls fat stores by operating a feedback mechanism between adipose tissue and brain →increased adipose tissue size and increased leptin secretion
What can administration of leptin lead to?
decrease food intake, induce weight loss and increase energy expenditure
What does leptin increase the expression of?
anorexigenic factors (pro-opiomelanocortin (POMC), cocaine- and amphetamine-regulated transcript (CART), corticotrophin-releasing hormone (CRH), neurotensin
What other things can leptin do?
→Stimulates metabolic rate
→Inhibits neuropeptide Y, which stimulates feeding
Can one be resistant to the effects of leptin?
Yes; →binge eating, despite adequate or growing adipose tissue (obese)
What are the properties of Ghrelin?
→An appetite-inducing hormone (an orexin) – stimulates hunger
→Fast-acting and stimulates food intake
→Suppresses the ability of leptin to stimulate anorexigenic factors
Which organs release ghrelin?
Released by stomach, pancreas, adrenals
When does ghrelin levels increase?
↑ preprandially and ↓ after a meal
→Increases central orexins, e.g. NPY, and AgRP (generate hunger signal
What inhibits ghrelin?
by leptin
→Leptin and ghrelin act reciprocally on food intake
What is obestatin?
→Produced by epithelial cells of stomach
→Encoded by ghrelin gene, but it opposes the effects of ghrelin on food intake
How does obestatin mediate its effects?
via different receptors to ghrelin
