4.5 Appetite Regulation and Nutritional Balance Flashcards

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1
Q

What are the three fundamental components of total daily energy expenditure, and their approx. proportions?

A
  • 70% resting energy expenditure
  • 20% Activity-induced
  • 10% Diet induced (energy of digestion)
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2
Q

What are Huberman’s two types of Activity-Induced energy expenditure?

A
  1. EAT: Exercise activity thermogenesis
  2. NEAT: non-exercise activity thermogenesis
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3
Q

Resting energy expenditure vs basal metabolic rate

A
  • REE: energy requried for vital organ function in resting state
  • Basal: REE as individual wakens in the morning (lowest)
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4
Q

Why does diet affect daily energy expenditure?

A

Because eating protein requires more energy than eating carbohydrates and fats.

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5
Q

List a whole bunch of factors that affect someone’s daily energy expenditure

A
  • Age
  • Gender
  • Disease
  • Weight
  • Genetics
  • Body composition
  • Sleep
  • Hormones
  • Diet
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6
Q

How does basal metabolic rate change with gender/age?

A

Gender: usually higher in men
Age: Declines w/ age; highest young, stable 20-40, declines in old age as body shuts down

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7
Q

How does the PALs plus scale tell you how to maintain your weight

A

It gives you a multiple of your BMR to consume each day based on activity level (e.g. “very active” men should consume 2.3x)

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8
Q

List the hypothalamic areas involved in appetite regulation

A
  • Arcuate nucleus
  • Ventro/dorsomedial nuclei
  • Paraventricular nucleus
  • Lateral hypothalamic nucleus
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9
Q

What are the two neuronal populations of the Arcuate nucleus that regulate hunger? Which reduces/increases food intake?

A

POMC/CART: Reduces (too much in the cart; too expensive)

NPY/AgRP: Increase (It’s entpy, get a grip)

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10
Q

Biochemically, how to POMC/CART neurons decrease hunger?

A
  • POMC is a precursor for many peptides, incl. alpha melanocyte stimulating hormone.
  • Alpha MSH bings to melanocortin receptor 3/4 (MCR3/MCR4)
  • This reduces hunger
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11
Q

Biochemically, how do NPY/AgRP neurons increase hunger

A

-NPY binds to Y1 receptors
- AgRP is an antagonist to MCR3 and MCR4 receptors (Agrip on the receptor market)

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12
Q

True or false: POMC/CART and NPY/AgRP neurons are only within the arcuate hypothalamic nucleus

A
  • False
  • Also affected by the other nuclei that regulate hunger
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13
Q

How do grehlin, leptin, and peptide tyrosine-tyrosine affect POMC/CART and NPY/AgRP neurons?

A
  • Grehlin is the “hunger hormone”, so increases NPY/AgRP and decreases POMC/CART
  • Leptin decreases hunger, so increases POMC/CART and decreases NPY/AgRP
  • PTT inhibits NPY/AgRP
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14
Q

What is the effect of glucose on the two opposing neuron systems of hunger in the hypothalamus?

A
  • Inhibits NPY/AgRP
  • Excites POMC/CART
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15
Q

List 5 areas from which afferent information can travel to the brain regarding hunger/appetite

A
  • Gallbladder
  • Pancreas
  • Adipose
  • Liver/GI Tract
  • Skeletal muscle
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16
Q

What is the link between white adipose levels and leptin? Why does this make sense?

A
  • The higher the white adipose, the higher the leptin
  • Leptin suppresses hunger, so this acts as a negative feedback to prevent too much fat
17
Q

Outline the adipostat theory for body weight control

A
  • The more/less fat, the more/less anorexigenic signals (e.g. leptin)
  • This means, when we have lots of fat, we are less hungry, and vice versa
  • In theory, this functions to keep weight within a certain range
18
Q

Describe two mechanisms of short-term hunger control in response to a meal

A
  1. (mechanical) stretch receptors are activated, sending vagal afferents to the solitary nucleus, and out to relevant brain centres
  2. (neuroendocrine) when nutrients bind to receptors in the GI tract, hormones such as GLP-1 are produced, either activating vagal afferents or travelling to the CNS via the bloodstream
19
Q

True or false: GI satiety signalling is constant throughout the day, leading to the classic 3-meal system

A
  • False
  • Varies w/ circadian rhythms