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BMSC 208 > Digestive III > Flashcards

Digestive III Flashcards

1
Q

The ___ ______ does not regulate intake so we therefore rely on _________ mechanisms

A

GI system, behavioural

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2
Q

________ is characterized by anabolism and storage, some is immediately used, some goes into storage

A

Feeding

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3
Q

________ is characterized by catabolism, breakdown of stored nutrients

A

Fasting

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4
Q

Ideally, Intake ? expenditure

A

=

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5
Q

Obesity, Intake ? expenditure

A

>

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6
Q

Starvation, Intake ? expenditure

A

<

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7
Q

Lateral hypothalamus is considered the ______ center

A

hunger

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8
Q

Ventromedial hypothalamus is considered the _______ center

A

satiety

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9
Q

ARC: ______ ______

A

Arcuate nucleus

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10
Q

PVN: __________ _______

A

Paraventricular nucleus

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11
Q

LH: _______ _________

A

Lateral hypothalamus

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12
Q

3 main areas of the brain that are involved in appetite and satiety: ?

A

ARC, PVN, LH

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13
Q

NTS: ?

A

Nucleus tractus solitarii

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14
Q

____ – in the medulla, but also plays a part in hunger and satiety

A

NTS

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15
Q

Appetite and satiety is broken down into two main mechanisms:
1. _____ term regulation of feeding behavior (weeks, months)
2. ______ term regulation (within a day)

A

Long, Short

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16
Q

Long term regulation of feeding behaviour has 2 proposed theories: ?

A
  1. Glucostatic theory
  2. Lipostatic theory
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17
Q

Which theory is this describing?
Glucose metabolism in the hypothalamus regulates food intake (very likely short-term, not long-term). Glucose sensing neurons that detect the amount of glucose coming into the brain, and sensing neurons that detect it leaving the brain. If there is large amounts of glucose being utilized by the brain, so the amount leaving is really low, that will drive hunger

A

Glucostatic theory

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18
Q

Which theory is this describing?

Signals from the body’s fat stores regulate food intake. This would be considered more long-term. There are signals being produced from our body’s fat stores that regulate food intake in the long-term. Seen in the graph to the left

A

Lipostatic theory

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19
Q

_______ is produced by the ob gene, and is considered as one of the main drivers of the lipostatic theory

A

Leptin

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20
Q

This gene must encode a protein that tells the brain fat reserves are normal : ?

A

ob gene

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21
Q

A hormone that is released from adipocytes in response to high amounts of fat storage and regulates body mass by acting directly on neurons of the hypothalamus that decrease appetite and increase energy expenditure = ?

A

Leptin

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22
Q

Higher amount of fat storage = ______ release of leptin

A

higher

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23
Q

Response to elevated leptin acts on arcuate nucleus in two ways: ?

A
  1. inhibition of lateral feeding center
  2. activation of PVN
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24
Q

Response to elevated leptin activates the PVN in two ways:
i. ________ response - ↑TSH, ACTH from pituitary (increased metabolic rate throughout the body)
ii. ____________ response - increased sympathetic output (increase metabolism by ↑ body temp)

A

humoral, Visceromotor

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25
Q

What is TSH?

A

thyroid stimulating hormone

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26
Q

What is ACTH?

A

Adrenocorticotropic hormone

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27
Q

Response to decreased leptin acts on arcuate nucleus in two ways: ?

A
  1. reduced activation of a-MSH and CART neurons
  2. activation of NPY and AgRP containing neurons
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28
Q

Response to decreased leptin reduces activation of a-MSH and CART neurons in two ways:
i. _______ activation of PVN (↓TSH and ACTH) ↓ metabolic rate
ii. activation of ____________ output

A

reduced, parasympathetic

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29
Q

Response to decreased leptin activates NPY and AgRP containing neurons in two ways:
i. stimulation of _______ center
ii. further _______ PVN

A

feeding, inhibition

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30
Q

Melanin concentrating hormone (MCH): prolongs __________

A

consumption

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31
Q

Leptin supplementation failed to treat _______ due to a likely a _______ sensitivity to leptin in these individuals

A

obesity, decreased

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32
Q

Fat: __ blood leptin level
Lean: __ blood leptin level

A

↑, ↓

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33
Q

Fat: __ αMSH/CART neuron activity
Lean: __ αMSH/CART neuron activity

A

↑, ↓

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34
Q

Fat: __ NPY/AgRP neuron activity
Lean: __ NPY/AgRP neuron activity

A

↓, ↑

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35
Q

Fat: __ TSH/ACTH release
Lean: __ TSH/ACTH release

A

↑, ↓

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36
Q

Fat: __ sympathetic NS activity
Lean: __ sympathetic NS activity

A

↑, ↓

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37
Q

Fat: __ parasympathetic NS activity
Lean: __ parasympathetic NS activity

A

↓, ↑

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38
Q

Fat: __ feeding behavior
Lean: __ feeding behavior

A

↓, ↑

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39
Q

Aside from social and cultural factors, short-term regulation of feeding behaviour depends on ? and ?

A

how long it has been since the last meal, how much we consumed at that time.

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40
Q

If you haven’t eaten for awhile, you will have an _______ in orexigenic signals, and when you take a meal in, cause a ______ in orexigenic but an increase in satiety, after food digests, cycle repeats

A

increase, reduction

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41
Q

What are the 4 signals included in short-term regulation?

A
  1. Ghrelin
  2. Gastric distension
  3. CCK
  4. Insulin
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42
Q

______: released by cells in the stomach in response to emptying

A

Ghrelin

43
Q

_______: stimulates NPY/AGRP containing neurons in the arcuate

A

Ghrelin

44
Q

Ghrelin injection will stimulate _____ intake experimentally

A

food

45
Q

Mice lacking NPY/AgRP neurons will not respond to ______

A

ghrelin

46
Q

Distention of the stomach with decrease ________ production

A

ghrelin

47
Q

Gastric distension is sensed by ___________ neurons and this information is sent to the _____ which has connections to the PVN and ARC

A

mechanosensory, NTS

48
Q

_____ is released by I cells in response to fats and amino acids entering the small intestine; administration inhibits meal frequency and size

A

CCK

49
Q

Both _____ and _____ ______ act on the NTS to stimulate the feeling of satiety

A

CCK, gastric distension

50
Q

Ghrelin is an example of an ________ signal that drives increased behavior to take food in

A

orexigenic

51
Q

During the cephalic and gastric phase increased insulin would cause a ? driving hunger through activation of NPY/AgRP neurons

A

drop in blood glucose

52
Q

During the intestinal phase the increased blood glucose and corresponding increase in _______ would act as a _______ signal through activation of aMSH/CART neurons in the arcuate nucleus

A

insulin, satiety

53
Q

_________: prescribed as a means to stimulate appetite in patients with chronic diseases associated with reduced appetite

A

Marijuana

54
Q

One ________ is the amount of heat needed to raise the temperature of 1 L of water by 1oC

A

kilocalorie

55
Q

What do we use to measure energy input? The ______ released from burned food is measured

A

Bomb Calorimeter, heat

56
Q

By using a bomb calorimeter, there is a slight _____ estimation because we do not completely digest and absorb most foods

A

over

57
Q

What do we use to measure energy output?

A

Direct or indirect calorimetry

58
Q

What kind of calorimetry is the most accurate?

A

Direct

59
Q

How do we calculate energy output for direct calorimetry?

A

Work + heat

60
Q

How do we calculate indirect calorimetry?

A

O2 consumption/CO2 production

61
Q

What is BMR?

A

Basal metabolic rate

62
Q

______: An individuals lowest metabolic rate, usually taken while sleeping

A

BMR

63
Q

BMR is usually measured as ? , since taken while sleeping can be tough

A

resting metabolic rate (RMR)

64
Q

6 factors affecting overall metabolic rate:
1. ____ and ____: male 1kcal/hour per Kg of body mass, females 0.9 kcal/hour/kg

A

Age, sex

65
Q

6 factors affecting overall metabolic rate:
2. Amount of _____ muscle mass

A

lean

66
Q

6 factors affecting overall metabolic rate:
3. Activity level-metabolic activity above ____

A

BMR

67
Q

6 factors affecting overall metabolic rate:
4. _____, diet induced __________: energetic cost of food digestion and storage differs between different food components

A

Diet, thermogenesis

68
Q

6 factors affecting overall metabolic rate:
5. __________: Thyroid hormones considered single most important determinant of BMR, influence oxygen consumption and heat production of most tissues in the body

A

Hormones

69
Q

6 factors affecting overall metabolic rate:
6. ________

A

Genetics

70
Q

Higher protein diet gives a higher ____

A

RMR

71
Q

Metabolism falls in to one of three categories:
1. Extract energy from ________
2. Use energy for _____
3. _____ excess energy for later use

A

nutrients, work, Store

72
Q

Fed state is mainly ________ metabolism

A

anabolic

73
Q

In the _____ state:
Glucose primarily used by most cells for energy

A

Fed

74
Q

In the _____ state:
Glycogenesis (liver and muscle)

A

Fed

75
Q

In the _____ state:
Lipogenesis

A

Fed

76
Q

In the _____ state:
AA uptake and protein synthesis (muscle)

A

Fed

77
Q

________ stores can sustain quiet activity for only a few hours

A

Glycogen

78
Q

______ potentially for long periods of time but decreased levels eventually compromise cellular function

A

Proteins

79
Q

_____ for approximately two months

A

Fats

80
Q

Overall total energy reserve of glycogen: ?

A

1%

81
Q

Overall total energy reserve of triglycerides: ?

A

75-80%

82
Q

Overall total energy reserve of proteins: ?

A

20-25%

83
Q

The Fasted state is in between meals and ________ takes place to utilize stored energy

A

catabolism

84
Q

Most cells utilize FA’s to spare _______ for the CNS

A

glucose

85
Q

In the _____ state:
FA’s used by most cells for energy

A

Fasted

86
Q

In the _____ state: Glycogenolysis (liver and muscle*)

A

Fasted

87
Q

In the _____ state:
Lipolysis

A

Fasted

88
Q

In the _____ state:
Gluconeogenesis

A

Fasted

89
Q

In the _____ state:
Ketogenesis

A

Fasted

90
Q

In the _____ state:
Protein degradation

A

Fasted

91
Q

When blood glucose is high, ______ is high, _______ is low

A

insulin, glucagon

92
Q

When blood glucose is low, ______ is low, _______ is high

A

insulin, glucagon

93
Q

Whether we are in the Fed or Fasted state depends primarily on ?

A

blood glucose concentration

94
Q

What is the primary hormone in the regulation of the Fed state?

A

Insulin

95
Q

An increase in plasma [glucose] causes an ______ in insulin secretion

A

increase

96
Q

What kind of cells sense changes in glucose?

A

Beta cells

97
Q

In beta cells, when glucose levels are low, the potassium channel would be _____ because there are low amounts of ATP being produced in the cell

A

open

98
Q

Insulin’s cellular mechanism of action is a ?

A

Tyrosine kinase receptor

99
Q

Order these statements according to “insulin’s cellular mechanism:”
1. Membrane transport is modified
2. Receptor phosphorylates insulin-receptor substrates (IRS)
3. Cell metabolism is changed
4. Second messenger pathways alter protein synthesis an existing proteins
5. Insulin binds tyrosine kinase receptor

A

5, 2, 4, 1, 3

100
Q

Tyrosine kinase receptor: directly linked to an ________
-insertion of ________ transporters
-increase or decrease ______ enzyme activity

A

enzyme, glucose, metabolic

101
Q

What is the primary hormone in the regulation of the fasted state?

A

glucagon

102
Q

What is the mechanism of glucagon?

A

G-protein coupled receptor
-adenylate cyclase pathway
-changes in enzymatic activity

103
Q

The Fasted state is stimulated by:
________ Plasma glucose
_________ Sympathetic activity
Presence of certain ____

A

Decreased, Increased, AA

BMSC 208 (11 decks)

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