GI 8 Flashcards

1
Q

Aside from social and cultural factors what does short term regulation of feeding behaviour depend on

A

How long it has been since the last meal and how much we consumed at that time

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2
Q

After meal

A

Decreased orexigenic (food seeking behaviour)
Increased satiety after meal

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3
Q

In hours following meal

A

Decreased satiety
Increase orexigenic

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4
Q

What acts on long term regulation of feeding behaviour

A

Ghrelin, gastric distension, CCK, insulin/glucose

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5
Q

When and where ghrelin released

A

By cells in stomach in response to emptying (less distension)

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6
Q

What does ghrelin stimulate

A

NPY/AGRP containing neurons in arcuate to increase feeding behaviour

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7
Q

What will ghrelin injection stimulate

A

Food intake

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8
Q

Mice lacking NPY/AgRP neurons

A

Will not respond to ghrelin

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9
Q

What is gastric distension sensed by

A

Mechanosensory neurons

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10
Q

Where is gastric distension info sent to

A

NTS which has connections to PVN and ARC

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11
Q

What is CCK released by

A

I cells

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12
Q

What is CCK released in response to

A

Fat and amino acids entering small int

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13
Q

CCK does what

A

Inhibits meal frequency and size

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14
Q

What do both gastric distension and CCK act on

A

NTS to stimulate the feeling of satiety

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15
Q

During cephalic and gastric phase increased insulin

A

Causes a drop in blood glucose driving hunger through activation of NPY/AgRP neurons

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16
Q

During intestinal phase the increased blood glucose and increased insulin acts as

A

Satiety signal through activation of aMSH/CART neurons in arcuate nucleus

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17
Q

Why did marijuana cause munchies in mice

A

Enhanced sense of smell

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18
Q

Why marijuana causes munchies in humans

A

Indirect activation of NPY/AgRP neurons in ARC
- CB1 receptors in LH

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19
Q

Energy output

A

Heat 50%
Work 50%.

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20
Q

How is energy input measured

A

Bomb calorimeter

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21
Q

How is bomb calorimeter used

A

Heat released from burned food is measured

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22
Q

Heat needed to raise temp of 1L of water by 1C

A

One kilocalorie

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23
Q

Why is bomb calorimeter a slight over estimation

A

Do not completely digest and absorb most foods

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24
Q

Energy output=

A

Work+heat

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25
Q

Two ways of measuring energy output

A

Direct calorimetry (most accurate)
Indirect calorimetry

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26
Q

What does direct calorimetry measure

A

Amount of heat person produces

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27
Q

What does indirect calorimetry measure

A

O2 consumption or CO2 production

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28
Q

An individuals lowest metabolic rate

A

Measured as resting metabolic rate (RMR)

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29
Q

Basal metabolic rate

A

Amount of energy just to be alive

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30
Q

6 factors affecting overall metabolic rate

A
  1. Age and sex
  2. Amount of lean muscle mass
  3. Activity level- metabolic activity above BMR
  4. Diet, diet induced thermogenesis
  5. Hormones
  6. Genetics
31
Q

Age and sex

A

Male 1kcal/hour per Kg of body mass, females 0.9 kcal/hour/kg

32
Q

Diet induced thermogenesis

A

Energetic cost of food digestion and storage differs between food components (ie. diet high in protein)

33
Q

Hormones

A

Thyroid hormones considered biggest determinant of BMR, influence O2 consumption and heat production of most tissues in body

34
Q

Metabolism

A

Sum of all chemical reactions in body

35
Q

3 categories of metabolism

A
  1. Extract energy from nutrients
  2. Use energy for work (transport, mechanical, synthesis)
  3. Store excess energy for later use
36
Q

Energy metabolism during fed state

A

Mainly anabolic
Taking small molecules and converting to larger storage molecules

37
Q

Where is glucose stored

A

As glycogen in liver and muscle
Converted to triglycerides for liver and adipose

38
Q

Where is fattty acids stored

A

Liver and adipose tissue as triglycerides

39
Q

Where are amino acids stored

A

Liver as fatty acids
Muscle ad other cells as protein

40
Q

How many carbs, proteins and fats can be stored

A

Finite amount carbs and proteins
Unlimited to store fats so all excess converted to fatty acids

41
Q

Skeletal muscle storage fed state

A

Glucose for energy usage and stores glucose as glycogen (70%)
AA’s taken up for natural protein turnover

42
Q

Liver fed state

A

Converts glucose to glycogen (24%)
Convert glucose to fatty acids (to adiposcytes)
AAs used for synthesis and converted to keto acids

43
Q

Adipocytes fed state

A

Dietary triglycerides from chylomicrons
Excess glucose taken and converted to triglycerides
Store triglycerides synthesized in liver

44
Q

Glycogen stores can sustain activity for

A

Quiet activity for only a few hours

45
Q

Proteins can sustain activity for

A

Potentially long periods but decreased protein levels eventually compromise cellular function

46
Q

Fats can sustain activity for

A

Approximately 2 months

47
Q

During fasted state between meals what occurs

A

Catabolism to utilize stored energy

48
Q

What is maintaining glucose levels important for

A

Nervous system functioning
- most cells utilizes FAs to spare glucose for CNS

49
Q

Skeletal muscle fasted state

A
  • can convert glycogen to glucose-6-P (glycogenolysis) for own use
  • forms pyruvate and lactate to make more glucose
50
Q

liver in fasted state

A
  • glycogen converted to glucose (glycogenolysis) and transported throughout body
  • produced new glucose from pyruvate, lactate, glycerol and certain AA’s
  • converts FA to ketone bodies for energy
51
Q

Adipocytes during fasted state

A

Lipolysis occurs
Fatty acids and glycerol enter bloodstream to be used as energy in most cells

52
Q

Hormones are primarily dependent on

A

Blood glucose concentration

53
Q

Review of fed state

A
  • glucose primarily used by cells
  • glycogenesis (liver and muscle)
  • lipogenesis
  • AA uptake and protein synthesis (muscle)
54
Q

Fasted state review

A
  • FAs used by most cells for energy
  • glycogenolysis (liver and muscle)
  • lipolysis
  • gluconeogenesis
  • ketogenesis
  • protein degradation
55
Q

Hormone during fed state

A

Insulin

56
Q

Hormone during fasted state

A

Glucagon

57
Q

What drive anabolism (fed state)

A

Insulin

58
Q

What increases insulin secretion

A

Increased plasma glucose, plasma AAs, plasma GLP-1, parasympathetic activity

59
Q

What secretes insulin

A

Beta cells

60
Q

During increase insulin what happens in most tissues

A

Increased glucose uptake
Increased AA uptake
Increased protein synthesis
Decreased protein breakdown

61
Q

What does increased insulin cause in adipose tissue

A

Increase fatty acid and triglyceride synthesis
Decreased lipolysis

62
Q

Increased insulin affects on liver and muscle

A

Increase glycogen synthesis
Decreased glycogenolysis

63
Q

Increased insulin affect on liver

A

Increased fatty acid and triglyceride synthesis
Decreased gluconeogenesis

64
Q

How do beta cells get activated by increased in glucose to drive insulin secretion

A

Increase ATP production in response to elevated glucose results in blockage of some ATP-K leak channels
K leakage drops and cell retains K and cell depolarizes causing Ca to enter cell and trigger exocytosis of insulin

65
Q

How does glucose enter beta cells

A

Facilitated diffusion

66
Q

What is the insulin receptor

A

Tyrosine kinase receptor

67
Q

The tyrosine kinase receptor causes

A

Insertion of glucose transporter (glut 4 usually internalized)
Increase or decrease metabolic enzyme activity

68
Q

What regulates fasted state

A

Glucagon

69
Q

What does glucagon promote

A

Catabolism

70
Q

What is fasted state stimulated by

A

Decreased plasma glucose
Sympathetic activity

71
Q

What cells have G protein coupled receptors for glucagon

A

Alpha cells in pancreas

72
Q

What does catabolism cause

A

Adenylate cyclase pathways
Changes in enzymatic activity

73
Q

What does increased glucagon do to liver

A

Increase glycogenolysis, gluconeogenesis, ketone sysnthesis, protein breakdown
Decrease glycogen synthesis, protein sysnthesis

74
Q

What does increased glucagon cause in adipose tissue

A

Increase lipolysis
Decrease triglyceride synthesis