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Behavioural Neuroscience > Feeding Behaviour > Flashcards

Feeding Behaviour Flashcards

1
Q

BMI

A
  • BMI=weight (kg)/height (m)
  • 600million clinically obese
  • 1.9 billion overweight adults globally (26%)
  • 62% of Canadians overweight or obese
  • continuing BMI increase is being observed in many countries and all age groups
  • BMI not perfect indication
    • abdominal fat thickness better indicator
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2
Q

Obesity causes and consequences

A
  • lifestyle
    • reduced physical activity
    • choice of high fat foods
    • quitting tobacco smoking
    • use of drugs (cannabis)
  • diseases
    • Cushings
    • growth hormone deficiency
    • hypothyroidism
    • psychiatric disorders
    • cohens
  • genes
    • polymorphism and mutations of genes involved in energy homeostasis
  • consequences
    • increase BP, high cholesterol
    • diabetes
    • non-alcoholic fatty liver
    • CV disease
    • strokes/cancers etc
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3
Q

Energy on request

A
  • brain constitutes 2% of body mass but uses 50% of body glucose
  • brain burns average of 100g of glucose per day
  • discrepancy between brain energy needs and rest body energy needs require precise balancing mechanisms
    • these can be disrupted by disorders or stress
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4
Q

Central control of feeding

A
  • AArcuate nucleus (ARC) in hypothalamus controls feeding
  • ARC contains neuropeptide Y (NPY/AgRP) which activate feeding
  • ARC also contains POMC neurons which reduce feeding
  • inhibitory hormones are leptin and insulin, which stimulate POMC and inhibit NPY/AgRP signalling
  • activation of neurons in PVH reduce food intake
  • activation of lateral hypothalamic area/perfornical area stimulate food intake
  • neurons from all structure project to nucleus tractus solitary (NTS in hindbrain

-obesity is a disruption of neuronal and neuro-hormonal regulation of energy balance and accumulation of adipose tissue

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5
Q

Hunger-satiety signalling molecules

A

Inhibitory

  • POMC/MSH
  • serotonin
  • histamine
  • leptin
  • insulin
  • CCK
  • Stimulatory
    • NPY
    • orexins
    • endocannabinoids
    • ghrelin
    • GIP
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6
Q

Central factors in feeding

A
  • POMC/melanocortin neurons are inhibitory

- AgRP and NPY stimulate feeding

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7
Q

Peripheral factors in feeding

A
  • inhibitory
    • CCK and PYY are acute peripheral signals (released on demand)
    • leptin and insulin are chronic inhibitory peripheral factors (reflect long term nutrition state)
  • stimulatory
    • ghrelin is an acute peripheral factor

-PYY and ghrelin also synthesized by some neurons in brain

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8
Q

Melanocortin

A

Agonists increase energy expenditure as measured by indirect calorimeters

-antagonists induce opposite effects

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9
Q

Adipose tissue

A
  • build up supports inflammation
  • high fat diet and obesity induces activation of pro-inflammatory mediators
    • counteracts satiety signalling in hypothalamus
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10
Q

Maintaining energy balance

A
  • thermogenesis
    • shivering
    • non shivering (brown fat)
  • heat is mostly produced in mitochondria by uncoupling proteins
  • mitochondrial ATP metabolism and thermogenesis
    • fatty acids and glucose oxidized to generate NADH and FADH2 which donate to ETC
    • energy from electrochemical gradient of protons can be involved in ATP synthesis or leaks as heat by action of UCP

-mice lacking UCP1 are not hyperphagic and obese byt are extremely sensitive to cold

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11
Q

Brown adipocytes

A
  • white adipose tissue is responsible for energy storage
  • brown adipose tissue involved in energy spending
  • BAT contain small lipid granules
    • high conc of mitochondria (give brown colour)
    • high density of UCPs
    • non shivering thermogenesis
    • innervated by adrenergic sympathetic neurons (B3 neurons)
  • WAT contain single fat droplets that constitute that majority of cell volume
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12
Q

B3 knockout mice

A
  • survive prolonged cold by compensation mechanisms
    • increased shivering
    • increase B1 adrenergic signalling
  • B3 adrenergic agonist inhibits weight gain in rodents kept on high fat diet
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13
Q

WAT can become BAT

A
  • transdifferentiation of WAT into BAT was shown in rodents exposed to prolonged cold (6 degrees for 10 days)
  • not observed in B3 knockout mice
  • B3 agonist induced white adipose differentiation
    • indicated that differentiation process depends on B3 adrenoreceptor activation
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14
Q

Corticosteroids and obesity

A

-HPA axis and regulation of feeding controlled within hypothalamus

  • cortisol availability is dependent on activity of 11B-hydroxysteroid dehydrogenase (11B-HSD)
    • 11BHSD1 isoform converts inactive cortisone to cortisol
    • 11BHSD2 isoform converts cortisol to cortisone
  • cortisone induces adipose cell differentiation
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15
Q

Cushing’s syndrome

A
  • pathological hypercortisolemia
  • associated with obesity, glucose intolerance, hypertension
  • adrenalectomy in cushings patients reverses glucose intolerance and obesity
  • genetically obese mice demonstrate hypercorticosteronemia
    • adrenalectomy in rodents reduces food intake and can be reverse by glucocorticoids
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16
Q

Addison’s disease

A
  • hypoactivity of adrenal cortex

- associated with low body weight and hypotension

17
Q

Low birth weight and obesity - HPA axis

A
  • blood cortisol levels are reversely proportional to birth weight
  • antenatal betamethasone (steroid) increases insulin resistance
  • in rodents, administration of dexamethasone or inhibition of 11BHSD2 increases fetal glucocorticoid load
    • results in diabetes in offspring
  • blood cortisol levels increase naturally in late pregnancy and glucocorticoids are require to induce lung maturation
  • low birth weight can be associated with increased risk of type 2 diabetes and dyslipidemia and hypertension
18
Q

Link between anxiety and feeding

A
  • anorectic peptides (inhibit feeding) —> anxiogenic factors (increase anxiety)
  • orexigenic peptides (stimulate feeding) —> anxiolytics factors (decrease anxiety
19
Q

Central inhibitory melanocortins

A
  • melanocortins
    • a POMC derived agonist of MC1-5 receptors
  • mice lacking POMC or MC4-R are hyperpagic (excessive hunger), obese, hyperglycemic, hyperinsulinemia
  • 6 week treatment with intranasal a-MSH4-10 in healthy volunteers reduced body fat by 1.68kg
  • MC3-R knockouts have increased adipocity but normal body weight
  • AgRP is an antagonist of melanocortin receptors
20
Q

Stimulatory NPY

A
  • discovered as a peptide inducing vasoconstriction
  • highest density of NPY neurons in PVN in hypothalamus
  • high levels found in post mortem in CSF of anorexic patients
  • repeated stress and high-fat/carb diet stimulate release of NPY in rat hypothalamus
  • NPY receptor subtypes Y1 and Y5 stimulate feeding
    • Y2 and Y4 inhibit appetite
  • PYY and PP act on same Y receptors
21
Q

Inhibitory leptin

A
  • primarily produced in WAT but some in other tissues
  • possible mutation in mouse LEP gene
  • ob/ob obese moulds shows nonsense mutation in codon 105 resulting in a sense of leptin production
    • mutation causes obesity, hyperphagia, hypothermia, extreme insulin resistance, infertility
  • administration of leptin resorts wild-type phenotype
  • db/db mouse (lacks leptin receptor) also obese
  • Some human mutations within LEP gene also associated with hyperphagia and obesity
22
Q

Cytokines

A
  • some act as anorectic mediators
  • adipose produces adipocytokines that may influence energy balance
  • adiponectin-deficient mice develope insulin resistance, glucose intolerance, dylipidemia etc
  • central injection of adiponectin in rats increases energy loss and decreases fat mass without affecting food intake
  • adiponectin associated with energy expenditure and to protect against insulin resistance
23
Q

Cytokines continued

A
  • resistin
    • peptide produced by adipocytes that increase insulin resistance
    • serum levels of resistin are increased in obesity
  • Tumor necrosis factor-a serum conc is correlated with amount of body fat
    • TFNa inhibits feeding, increases metabolic rate, and induces cachexia (los of body mass that cannot be revered nutritionally)
    • possible that TNFa helps trigger weight loss
  • IL-6 administered intracerebrally increases energy expenditure
    • CSF IL6 negatively correlated with fat mass
    • IL6 knock out mice develop obesity in adulthood
24
Q

Stimulatory ghrelin

A
  • gastrointestinal hormone
  • stimulates growth hormone release
    • called growth hormone secretagogue receptor (GHS-R)
  • arcuate nucleus in hypothalamus has highest density of GHS-R
  • gremlin stimulated food intake but also dopamine release
    • induces locomotor activity
25
Q

Ghrelin knockouts

A
  • ghrelin injected significantly increases food intake in wild type mice
  • ghrelin doesnt increase food intake in mice with knockout of growth hormone secretagogue receptor (Ghsr-/-)

-ghrelin doesnt increase food intake in mice lacking AgRP and NPY

26
Q

Nesfatin-1

A
  • elevated in some neurological and psychiatric disorders
  • patients with newly diagnosed epilepsy have hundreds-fold higher nesfatin1
    • normalized after epilepsy treatment
  • patients with major depressive disorder have elevated plasma nesfatin1
  • plasma nefatin1 also correlated positively with Hamilton depression rating scale in depressed patients and healthy controls
27
Q

Sleep deprivation augments obesity

A
  • sleep deprivation
    • decreases leptin
    • increases ghrelin
    • increases hunger
  • chronic HPA axis dysregulation can cause changes in feeding behaviour
  • possible increase of sugar to sustain brain during active state
28
Q

Inhibitory PYY

A
  • synthesized by L cells of gastrointestinal tract
  • blood PYY dependent on volume and kind of food
    • dietary fat is most potent releases of PYY
  • 2 endogenous PYYs:
    • PYY1-36 (long)
    • PYY3-36 (short)
  • in fasting, PYY1-36 predominated
  • after meal PYY3-36 is height
  • both bind to same Y receptor
  • PYY3-36 binds to Y2R receptors which are most dense in hypothalamic arcuate nucleus
    • knockout is insensitive to exogenous PYY anorexic effect
29
Q

PYY effects

A
  • rats injects with PYY3-36 or agonist of Y2A in PVN or ARC

- PYY3-36 injected mice significantly reduced caloric intake\

30
Q

Serotonin

A
  • inhibits food intake
  • serotonin transporter over-expressing mice are lighter and shorter than wild type
  • serotonin transporter knockout mice develop obesity (no hyperphagia)
  • mice lacking serotonin receptors exhibit hyperphagia and obesity
31
Q

Histamine

A
  • reduces food intake
  • H1 knockout mice develop age related obesity/hyperphagia
    • disruption of sleep/wake cycle (especially orexin)
  • administration of H3 antagonist surprises food intake
    • H1 receptor agonist decrease food intake
  • histamine increases expression of UCP mRNA in adipose (increase energy expenditure)
32
Q

Orexins and obesity

A
  • orexin A and B
  • orexinergic neurons act as sensor for nutritional status of body
  • glucose, ghrelin, AgRP most important mediators for orexin neurons
  • adminitration of anti-orexin antibody or OX1R selective antagonist reduced food intake
    • mice lacking orexin neurons ate less than control wild type
  • OX2R selective agonists suppresses food intake in mice on high-fat diet
  • orexin knockouts show cataplexy, fragmented sleep-wake cycles
33
Q

Obesity treatment

A
  • most effective treatment is bariatric surgery
  • Orlistat is most common medication (inhibit pancreatic lipase)
  • liraglutide
34
Q

Muscles

A

-skeletal muscles produce and secrete myokines (involved in adipose tissue build up)

35
Q

Beneficial effects of runnning

A
  • runners has 30% lower risk of death from CVD and artery disease
    • 45% lower risk of death from heart disease or stroke
  • lived bag 3 years longer
  • people who ran for less that an hour a week benefited as much as those running more than three hours a week
36
Q

HSP70 and obesity

A
  • hot tub bath (6 days/week for 21 day reduces blood glucose levels and induces weight loss in diabetes patients
  • possibly due to increased HSP7
37
Q

Water preloading

A

-decreases caloric intake

38
Q

Bacteria and obesity

A
  • mice receiving the obese twin microbiota showed increase in adiposity
    • those receiving lean twin microbiota remained lean
  • mice inoculated with obese microbiota were co-housed with mice with lean microbiota
    • lean bacteria invaded obese infected animals preventing weight gain

Behavioural Neuroscience (6 decks)

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