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Bmsc 208 > GI 8 > Flashcards

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
Two ways of measuring energy output
Direct calorimetry (most accurate) Indirect calorimetry
26
What does direct calorimetry measure
Amount of heat person produces
27
What does indirect calorimetry measure
O2 consumption or CO2 production
28
An individuals lowest metabolic rate
Measured as resting metabolic rate (RMR)
29
Basal metabolic rate
Amount of energy just to be alive
30
6 factors affecting overall metabolic rate
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
Age and sex
Male 1kcal/hour per Kg of body mass, females 0.9 kcal/hour/kg
32
Diet induced thermogenesis
Energetic cost of food digestion and storage differs between food components (ie. diet high in protein)
33
Hormones
Thyroid hormones considered biggest determinant of BMR, influence O2 consumption and heat production of most tissues in body
34
Metabolism
Sum of all chemical reactions in body
35
3 categories of metabolism
1. Extract energy from nutrients 2. Use energy for work (transport, mechanical, synthesis) 3. Store excess energy for later use
36
Energy metabolism during fed state
Mainly anabolic Taking small molecules and converting to larger storage molecules
37
Where is glucose stored
As glycogen in liver and muscle Converted to triglycerides for liver and adipose
38
Where is fattty acids stored
Liver and adipose tissue as triglycerides
39
Where are amino acids stored
Liver as fatty acids Muscle ad other cells as protein
40
How many carbs, proteins and fats can be stored
Finite amount carbs and proteins Unlimited to store fats so all excess converted to fatty acids
41
Skeletal muscle storage fed state
Glucose for energy usage and stores glucose as glycogen (70%) AA’s taken up for natural protein turnover
42
Liver fed state
Converts glucose to glycogen (24%) Convert glucose to fatty acids (to adiposcytes) AAs used for synthesis and converted to keto acids
43
Adipocytes fed state
Dietary triglycerides from chylomicrons Excess glucose taken and converted to triglycerides Store triglycerides synthesized in liver
44
Glycogen stores can sustain activity for
Quiet activity for only a few hours
45
Proteins can sustain activity for
Potentially long periods but decreased protein levels eventually compromise cellular function
46
Fats can sustain activity for
Approximately 2 months
47
During fasted state between meals what occurs
Catabolism to utilize stored energy
48
What is maintaining glucose levels important for
Nervous system functioning - most cells utilizes FAs to spare glucose for CNS
49
Skeletal muscle fasted state
- can convert glycogen to glucose-6-P (glycogenolysis) for own use - forms pyruvate and lactate to make more glucose
50
liver in fasted state
- 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
Adipocytes during fasted state
Lipolysis occurs Fatty acids and glycerol enter bloodstream to be used as energy in most cells
52
Hormones are primarily dependent on
Blood glucose concentration
53
Review of fed state
- glucose primarily used by cells - glycogenesis (liver and muscle) - lipogenesis - AA uptake and protein synthesis (muscle)
54
Fasted state review
- FAs used by most cells for energy - glycogenolysis (liver and muscle) - lipolysis - gluconeogenesis - ketogenesis - protein degradation
55
Hormone during fed state
Insulin
56
Hormone during fasted state
Glucagon
57
What drive anabolism (fed state)
Insulin
58
What increases insulin secretion
Increased plasma glucose, plasma AAs, plasma GLP-1, parasympathetic activity
59
What secretes insulin
Beta cells
60
During increase insulin what happens in most tissues
Increased glucose uptake Increased AA uptake Increased protein synthesis Decreased protein breakdown
61
What does increased insulin cause in adipose tissue
Increase fatty acid and triglyceride synthesis Decreased lipolysis
62
Increased insulin affects on liver and muscle
Increase glycogen synthesis Decreased glycogenolysis
63
Increased insulin affect on liver
Increased fatty acid and triglyceride synthesis Decreased gluconeogenesis
64
How do beta cells get activated by increased in glucose to drive insulin secretion
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
How does glucose enter beta cells
Facilitated diffusion
66
What is the insulin receptor
Tyrosine kinase receptor
67
The tyrosine kinase receptor causes
Insertion of glucose transporter (glut 4 usually internalized) Increase or decrease metabolic enzyme activity
68
What regulates fasted state
Glucagon
69
What does glucagon promote
Catabolism
70
What is fasted state stimulated by
Decreased plasma glucose Sympathetic activity
71
What cells have G protein coupled receptors for glucagon
Alpha cells in pancreas
72
What does catabolism cause
Adenylate cyclase pathways Changes in enzymatic activity
73
What does increased glucagon do to liver
Increase glycogenolysis, gluconeogenesis, ketone sysnthesis, protein breakdown Decrease glycogen synthesis, protein sysnthesis
74
What does increased glucagon cause in adipose tissue
Increase lipolysis Decrease triglyceride synthesis

Bmsc 208 (33 decks)

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