Control of Food Intake Flashcards

1
Q

Define hunger

A

Discomfort caused by lack of food and desire to eat - Strong physiological craving/drive for food/ sensation of emptiness in stomach

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2
Q

Define appetite

A

Physiological desire/drive to satisfy body’s needs of food; a hunger stimulated response

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3
Q

Define satiety

A

State of being full after eating food

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4
Q

What is aphagia and hyperphagia?

A

Aphagia - Inability or refusal to swallow

Hyperphagia/polyphagia - Abnormal desire for food (unsatisfied extreme drive to eat)

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5
Q

How is satiety induced?

A
  • Mechanical distension of the stomach wall - Afferent fibres to brain to induce satiety
  • CCK potentiates/sensitises the vagal nerves to mechanical stimulation, and also reaches the brain where it inhibits feeding, has a catabolic effect. CCK is released by I cells in response to fatty chyme being within the intestines
  • CCK acts locally to stimulate bile release as causes gallbladder to contract, nutrient absorption and promote gastric emptying
  • The presence of nutrients in the intestine inhibits eating and gastric emptying
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6
Q

Describe the role of the vago-vagal reflex in accommodation of food

A

Food enters stomach, causes distension detected by stretch receptors, vagal afferents to dorsal medullary, vagal efferents secrete VIP/NO on fundus relaxing it, increasing area available for storage of food - Induces satiety

Distension of a full stomach inhibits appetite; contraction of an empty stomach stimulates appetite

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7
Q

What are the 3 types of relaxation of the fundus?

A
  • Receptive relaxation - Mechanical stimulation of pharynx - mechanoreceptors, sight)
  • Adaptive - Vagal innervation, NO/VIP
  • Feedback - Nutrients, CCK
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8
Q

How does the hypothalamus control food intake?

A

Hypothalmus = Control centre for appetite and food intake

  • Base of hypothalmus has several nuclei that regulate energy homeostasis
  • These nuclei control appeptite, size of meal, ingestive behaviour
  • Supraoptic nucleus (SON) contains neurosecretory ells that produce hormones (oxytocin, ADH)
  • Prefrontal cortex - Food seeking behaviours
  • Nucleus accumbens - Controls ingestion and swallowing
  • Somatosensory cortex - Taste and perception
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9
Q

Describe the location of the satiety centre and its role in food intake

A

Satiety centre = Hypothalamus, ventromedial (wall of paraventricular) nuclei

  • Stimulation of ventromedial nuclei → Aphagia (swallowing difficulty)
  • Lesions of ventromedial nuclei → Hyperphagia (increased appetite or excessive hunger; weight gain)
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10
Q

Describe the location of the feeding/hunger/thirst centre and its role in food intake

A

Feeding/hunger/thirst centre = lateral hypothalamus (nuclei)

  • Stimulation lateral hypothalmus - Increase feeding
  • Lesion of lateral hypothalamus - Aphagia
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11
Q

What do orexigenic and anorexigenic neurotransmitters do?

A

Both found in hypothalmus:

  • Orexigenic - Increase appetite
  • Anorexigenic - Decrease appetite

NTs modulate feeding behaviour by binding to hypothalmic nuclei

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12
Q

Describe the role of the dorsomedial nucleus (DMN)

A

Modulates energy intake (hunger centre) - Release of NPY into DMN - Increases feeding

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13
Q

Describe the role of the paraventricular nucleus (PVN)

A

Modulates feeding behaviour - Paraventricular nucleus and perifornical hypothalamus:

  • Control feeding behaviour
  • NPY, opioids → Increase feeding
  • Leptin → Decreases food intake
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14
Q

Describe the arcuate nucleus

A

Contains 2 neuronal populations with opposing effects:

  • 1 population stimulates food intake and co-express orexigenic signals (NPY, AgRP, opioids, dynorphin, B-endorphin, galanin, glutamate)
  • Another population suppresses feeding by co-expressing CART and POMC

Both types of neurons project to hypothalmic areas, which are involved in the control of appeptie including DMN, PVN and LHA

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15
Q

Describe the role of the suprachiasmatic nucleus

A

Location of human body clock

  • Perception of the light-darck cycle (circadian rhythms), directly above optic chiasm
  • Appetite or sensation of hunger → Mood/drive to eat
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16
Q

Describe the role of the medial amygadaloid complex

A

Sub-region of amygadaloid complex:

  • Participates in regulation of food intake
  • E.g 5-HT (serotonin) been shown to regulate appetite and food intake by binding to medial amygdaloid nucleus (Via 5-HT2C and 5-HT1A serotonin receptors)
17
Q

Describe the role of the prefrontal cortex

A

Influences food-seeking behaviour:

  • Integrates sensory information from inside and outside body
  • Receives emotional and cognitive information from limbic system
  • Helps one make choices by translating all of the homeostatic and environmental information into (adaptive) behavioural response
18
Q

Describe the role of the limbic system

A

Complex system of nerves and networks in brain; areas concerned with instinct, learning, reproducitve behaviours; emotions/mood, pleasure (fear,anger, etc)

  • Act of satiation of feeding behaviour associated with motor planning and execution
  • Overall, cortico-limbic mechanisms of reward under executive control
19
Q

Describe the role of higher functions in control of food intake

A

Signals from the periphery and CNS control nutrient intake

Modulate responses to both CNS and peripheral cues (e.g. gut; environment) → inhibition or stimulation of food intake

The activity of stomach nerves has a circadian rhythm, which may limit our food intake to certain times throughout the day

Higher functions can include:

  • Food preference
  • Emotions
  • Environment - Cold = Want to eat, Hot = Don’t want to eat
  • Lifestyle
  • Circadian rhythms
  • Executive function - Frontal cortex

These can all act directly on hypothalamus and change food intake

20
Q

Describe the role of glucose in control of food intake

A

Blood glucose - Stimulates gluco-receptors in hypothalamus

Brain has glucostat:

  • Low blood glucose - Induces hunger
  • High blood glucose - Induces satiety
21
Q

What are the central stimuli that increase food intake?

A
  • NPY
  • Orexin-A
  • Cannabinoids

Stimulated by ghrelin, cortisol

22
Q

What are the central stimuli that decrease food intake?

A
  • POMC
  • CART
  • CCK
  • NE/Noradrenaline (low dose) - Stimulation alpha-1 decreases eating, stimulation alpha 2 increases eating
  • CRH

Stimulated by glucose, amino acids, FAs, CCK, PYY, Insulin, Leptin

23
Q

Describe the role of ghrelin in control of food intake

A
  • Secreted by stomach fundus, pancreas, adrenals in response to nutritional status
  • Stimulates gastric emptying
  • Increases sense of hunger
  • Stimulates neuropeptide Y and AgRP neurones
  • Lvls also increase during periods of fasting, stimulates food intake. Decreases after feeding. Gastric bypass supresses lvls of ghrelin
  • Increases central orexins e.g. NYP and AgRP (hunger signals)
    • Circulating lvls of ghrelin increase pre-prandial and decreases post-prandial (after meal)
  • 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
24
Q

Describe the role of obestatin in control of food intake

A

Encoded by ghrelin gene, but opposes the effects of ghrelin on food intake

  • Produced by epithelial cells of stomach
  • Suppress appetite, decrease weight gain
  • Regulate GI motility
  • Antagonises ghrelin-induced food intake (and growth hormone secretion)
  • Regulate insulin secretion
  • Promoting proliferation
  • Reducing inflammation and apoptosis
25
Describe the role of amylin in control of food intake
Helps reduce food intake through medulla of brainstem by delaying gastric emptying
26
Describe the role of enterogastrones in control of food intake
Secretin, CCK, GIP: - Hormones secreted by ‘mucosa of duodenum’ in lower GI tract in rsponse to dietary lipids that inhibit aboral motion of chyme. - CCK and somatostain are satiety factors; inhibt further food intake - Injection of CCK in brain → reduces appetite
27
Describe the role of PYY in control of food intake
Signals satiety and inhibits gut motility
28
Describe the role of leptin in control of food intake
- Fat cells (white adipose tissue) secrete leptin - gene expressed mainly in apidocytes - Controls fat stores by operating a feedback mechanism b/w adipose tissue and brain - There is a high correlation of leptin lvls with body fat in humans and animals - Larger size of adipose tissue, greater leptin secreted by tissue - Administration of leptin can decrease food intake, induce weight loss (increase energy expenditure as well) - Leptin acts on hypothalamus (Ventromedial nuclei) → Changes food intake, alongside insulin, have agonistic effects via action on receptors within the brain - Increases expression of anorexigenic factors [pro-opiomelanocortin (POMC), cocaine- and amphetamine-regulated transcript (CART), corticotrophin-releasing hormone (CRH)] - Inhibits neuropeptide Y (NPY), which results in reduction in feeding - Leptin resistance may lead to binge eating, despite obesity - Hyperphagia and severe obesity occurs in humans with leptin deficiency or leptin receptor defects
29
Describe the physiological factors that cause early satiety
- Gastroparesis (reduced gastric emptying) - Cancer, reflux, peptic ulcer - Reduced capacity to eat/can only eat small meal → state of satiety Possible causations: - Disease, illness/infections, loneliness/social isolation (psychological), swallowing or dental problems, drugs, age, etc.
30
Describe the role of a vagotomy
Impairs accommodation and emptying - Can cause early satiety - Reduces accommodation and gastric compliance in 5% cases - Involves removing part of vagus nerve - denervation of intestine and stomach may/will have no effect on food intake, due to signals still coming from pancreas, apidocytes, GIT, environment, CNS