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Cardiovascular, Pulmonary, and Hepatic Physiology > Dietary Balances > Flashcards

Dietary Balances Flashcards

1
Q

how much energy is liberated from 1 gram of carbohydrates? from fat? from protein?

A

carbohydrates: 4.1 calories
fat: 9.3 calories
protein: 4.35 calories

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2
Q

what percent of carbohydrates are absorbed in the GI tract? fats? protein?

A

carbohydrates: 98%
fat: 95%
protein: 92%

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3
Q

what is the average physiologically available energy from carbohydrates? from fat? from protein?

A

carbohydrates: 4 calories/gram
fat: 9 calories/gram
protein: 4 calories/gram

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4
Q

what is complete protein?

A

contains all essential amino acids in correct balance

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5
Q

what is partial protein?

A

has an inaddequate concentration of one or more essential amimo acids

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6
Q

what percent nitrogen is protein?

A

16%

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7
Q

how can protein metabolism be determined?

A

by measuring nitrogen in urine and feces (which can be esitamed by adding 10% to urine value) and multiplying by 6.25

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8
Q

how can protein balance be determined?

A

by subtracting protein metabolized from protein intake

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9
Q

what is respiratory quotient?

A

the ratio of carbon dioxide output to oxygen usage (CO2/O2)

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10
Q

what can respiratory quotient be used to estimate? (2)

A
  1. fat utilization
    carbohydrate utilization
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11
Q

what is the respiratory quotient for carbohydrates? for fat? for protein?

A

carbohydrates: 1
fat: 0.7
protein: 0.8

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12
Q

if measured for one hour or more, what will respiratory quotient equal?

A

will be exactly equal to repiratory exchange ratio

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13
Q

what is one method to end up determining fat and carbohydrate metabolism?

A

determine protein metabolism by nitrogen excretion, then fat and carbohydrate metabolism can be calculated using respiratory exchange ratio

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14
Q

what 2 centers in the brain are responsiblle for appetite regulation?

A
  1. hunger (feeding) center
  2. satiety center
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15
Q

describe the hunger (feeding) center of the brain; where located and how operates

A

located in the lateral nuclei of the hypothalamus and operate by exciting motor that drives the animal to search for food

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16
Q

what does stimulation of the hunger (feeding) center of the brain result in? what does this mean?

A

hyperphagia; eating and eating

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17
Q

describe the satiety center of the brain; where located and what it provides

A

located in the ventromedial nuclei of the hypothalamus and gives a sense of nutritional satisfaction that inhibits the feeding center

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18
Q

what does stimulation of the satiety center of the brain result in? what does this mean?

A

apagia; stop eating

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19
Q

what type of signals does the hypothalamus receive and from where? (4)

A
  1. nervous signals from the GI tract
  2. hormonal signals from the GI tract
  3. hormonal signals from adipose tissue
  4. signals from the cerebral cortex
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20
Q

what are the 6 signalsand hormones for control of feed intake?

A
  1. stretch receptors in stomach
  2. peptide YY
  3. cholecystokinin
  4. insulin
  5. ghrelin
  6. leptin
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21
Q

how do stretch receptors in the stomach control feed intake?

A

stretch receptors in the stomach activate sensory pathways in the vagus nerve that inhibit food intake

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22
Q

what is peptide YY, cholecystokinin, and insulin? what do they do?

A

GI homrones that are released by ingestion of food that suppress further feeding

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23
Q

what is ghrelin? what does it do?

A

a hormone released by the stomach, especially during fasting that stimulates appetite

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24
Q

what is leptin? what does it do?

A

a hormone produced in increasing amounts by fat cells as they increase in size that inhibits food intake

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25
Q

what do anorexigenic mechanisms do?

A

decrease feeding

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26
Q

what do orexigenic mechanisms do?

A

increase feeding

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27
Q

what are the 2 types of neurons in the arcuate nuclei of the hypothalamus and what are they important for?

A

they are important as controllers of appetite/energy expenditure
1. POMC neurons
2. neurons that produce orexigenic substances (NPY-AGRP neurons)

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28
Q

what do the POMC neurons produce (2)

A
  1. alpha-melanocyte stimulating hormone (a-MSH)
  2. cocaine and amphetamine-related transcript (CART)
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29
Q

what orexigenic substances are produced by neurons in the arcuate nuclei? (2)

A
  1. neuropeptide Y (NPY)
  2. agouti-related protein (AGRP)
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30
Q

what does activation of POMC neurons do? (2)

A
  1. decrease food intake
  2. increase energy expenditure
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31
Q

what does activation of NPY-AGRPY neurons do? (2)

A
  1. increase food intake
  2. decrease energy expenditure
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32
Q

what does alpha-melanocyte stimulate hormone released by POMC neurons do?

A

acts on melanocortin receptors found in neurons of the paraventricular nuclei (PVN)

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32
Q

what does alpha-melanocyte stimulate hormone released by POMC neurons do?

A

acts on melanocortin receptors found in neurons of the paraventricular nuclei (PVN)

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33
Q

what 3 melanpcortin receptors in the PVN does alpha-melanocyte stimulating hormone released by POMC neurons act on?

A
  1. MCR
  2. MCR-3
  3. MCR-4
34
Q

what does activation of MCR, MCR-3, and MCR-4 by alpha-MSH released by POMC neurons do?

A

decreases food intake while increasing energy expenditure

35
Q

what does inhibition of MCR-3 and MCR-4 so that can’t bind alpha-MSH do?

A

greatly increases food intake and decreases energy expenditure

36
Q

what is the hypothalamic melanocortin system important for?

A

important in regulating energy stores of the body

37
Q

what does defective signaling of melanocortin pathways lead to?

A

extreme obesity

38
Q

what is the result of mutations of MCR-4? (2)

A
  1. the most common known single gene cause of human obesity
  2. may account for approx 5% of early onset severe obesity in children
39
Q

what does excessive activation of the melanocortin system do?

A

reduces appetite

40
Q

what is the natural agonist of MCR-3 and MCR-4? what does it do?

A

AGRP released from orexigenic neurons of the hypothalamus; probably increases feeding by inhibiting the effects of alpha-MSH to stimulate melanocortin receptors

41
Q

what are gene mutations that lead to excessive formation of AGRP in mice and humans associated with? (2)

A
  1. increased food intake
  2. obesity
42
Q

what happens in the arcuate nucleuswhen energy stores are low? (2)

A
  1. orexigenic neurons are activated to release NPY which stimulates appetite
  2. at the same time, firing of POMC neurons is reduced, decreasing activity of the melanocortin pathway, further stimulating appetite
43
Q

describe nervous control of the mechanical processes of feeding and what this means

A

salivation, licking lips, chewing, and swallowing are controlled by centers in the brain stem, so if the brain is sectioned (cut/damaged) below the hypothalamus but above the mesencephalon (midbrain) the animal can still perform mechanical feeding processes

44
Q

how do higher brain centers influence feed intake?

A

areas of the amygdala (olfactory, emotions) and prefrontal cortex (decisions: get food or digest?) stimulate and inhibit feeding

45
Q

what are the 2 main components of short-term regulation of feed intake?

A
  1. gastrointestinal filling
  2. gastrointestinal hormones
46
Q

describe how gastrointestinal filling contributes to short-term regulation of feed intake

A

stretch inhibitory signals transmitted by the vagus nerve inhibit intake

47
Q

what 4 gastrointestinal hormones contribute to short-term regulation of feed intake?

A
  1. cholecystokinin
  2. peptide YY
  3. glucagon-like peptide (and insulin)
  4. ghrelin
48
Q

what does cholecystokinin do? when is it released?

A

released in response to fat entering the duodenum and decreases feeding by activating the melanocortin pathway

49
Q

how is peptide YY secreted and what does it do?

A

secreted by the gastrointestinal tract and decreases feed intake

50
Q

describe glucagon-like peptide’s role in short term regulation of feed intake (3)

A
  1. stimulated by food in the intestines
  2. enhances insulin production
  3. both glucagon-like peptide and insulin suppress appetite
51
Q

describe insulin’s role in short-term regulation of feed intake

A

stimulate by glucagon-like peptide, is released from the pancreas in response to high blood glucose and suppresses appetite

52
Q

what releases ghrelin and what does it do?

A

ghrelin is releases from the stomach, increases with fasting, and stimulates feed intake

53
Q

what 3 thing contribute to intermediate and long-term regulation of food intake?

A
  1. glucostatic theory of hunger and feeding regulation
  2. aminostatic and lipostatic theories of regulation
  3. temperature
54
Q

what does a decrease in blood glucose cause?

55
Q

what does increased blood glucose cause? (2)

A
  1. increased rate of firing of glucoreceptors in the satiety center of the ventromedial and paraventricular nuclei of the hypothalamus
  2. decreases firing of glucosensitive neurons in the hunger center of lateral hypothalamus
56
Q

what does exposure to cold do to food intake? why (2)

A

increases food intake
1. to increase metabolic rate since heat is a byproduct of metabolism and will warm you up
2. increases fat for insulation

57
Q

what does exposure to heat do to food intake?

A

decreases food intake

58
Q

what is leptin?

A

a protein hormone produced by adipocytes

59
Q

as adipose tissue increases, what happens to the amount of leptin and its levels in the blood?

A

as adipose tissue increases, the amount of leptin produced by adipocytes and released into the blood increases

60
Q

what nifty thing can leptin do?

A

cross the blood brain barrier to reach receptors in the hypothalamus

61
Q

what does stimulation of leptin receptors in the hypothalamus result in? (5)

A
  1. decreased production of NPY and AGRP
  2. activation of POMC neurons
  3. increased production in hypothalamus of substances (such as CRH) that decrease food intake
  4. increased sympathetic nerve activity
  5. decreased insulin secretion
62
Q

what is CRH? what does it do?

A

corticotropin releasing hormone; stimulates the sympathetic nervous system

63
Q

what could cause leptin resistance? (2)

A
  1. deficient or defective leptin receptors
  2. some issue in the post-receptor signaling cascade
64
Q

what is the result of leptin resistance?

A

animal will continue to be stimulated to eat and will put on weight

65
Q

what is obesity?

A

excess body fat

66
Q

how is obesity measured in humans? (2)

A
  1. body mass index, or weight in kg divided by height in m2
  2. percent total body fat
67
Q

what BMI range is overweight?

A

25-29.2kg/m2

68
Q

what BMI range is obese?

69
Q

how is percent total body fat measured? (3)

A
  1. skin-fold thickness
  2. bioelectrical impedance
  3. underwater weighing
70
Q

on the scale of percent total body fat, what is obese in men and women?

A

men: >25%
women: >35%

71
Q

what can happen to adipocytes in obesity?

A

can increase in size and number

72
Q

what are 5 causes of obesity?

A
  1. sedentary lifestyle
  2. abnormal feeding behavior
  3. childhood overnutrition
  4. neurogenic abnormalities
  5. genetic factors
73
Q

what are 4 treatments for obesity?

A
  1. decrease energy intake and increase activity
  2. various drugs such as amphetamines or orlistat
  3. gastric bypass surgery
  4. gastric banding surgery
74
Q

describe amphetamines as used to treat obesity (2)

A
  1. inhibit feeding centers but people adapt so theya re addictive
  2. overexcite CNS, resulting in nervousness and elevated blood pressure
75
Q

describe orlistat as a drug to treat obesity

A

lipase inhibitor that reduces digestion of fat

76
Q

what is gastric bypass surgery?

A

construction of a small pouch in the stomach

77
Q

what is gastric banding surgery?

A

an adjustable band is placed around the stomach

78
Q

what is inanition? (2)

A
  1. the opposite of obesity
  2. characterized by extreme weight loss
79
Q

what is anorexia?

A

reduced food intake caused by diminished appetite

80
Q

what is anorexia nervosa?

A

abnormal psychic state in which a person loses all desire for food and even becomes nauseated by food

81
Q

what is cachexia?

A

a metabolic disorder of increased energy expenditure resulting in weight loss greater than that caused by reduced food intake alone

82
Q

what can cause anorexia and cachexia? give 4 examples

A

inflammatory cytokines (TNF-a, IL-6, IL-1Beta, proteolysis-inducing factor)

83
Q

describe what energy sources are burned in what order and speed during starvation

A

carbohydrates burned quickly, then fat is burned at a slower rate, and finally if starvation increases the body breaks down muscle for energy

Cardiovascular, Pulmonary, and Hepatic Physiology (12 decks)

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