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Human Physiology > Metabolism/metabolism Quiz > Flashcards

Metabolism/metabolism Quiz Flashcards

1
Q

From GI tract, glucose enters the bloodstream and effects the muscle by: (absorptive)

A

Biggest atp producer from glucose and stored as glycogen (by glycogenesis)

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2
Q

From GI tract, glucose enters the bloodstream and effects the fat by: (absorptive)

A

Glucose is oxidized for atp or converted to triglycerides (lipogenesis)

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3
Q

From GI tract, glucose enters the bloodstream and effects the liver by: (absorptive)

A

Glucose stored as glycogen and converted into triglycerides

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4
Q

Triglycerides are not stored in the __ long term

A

Liver

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5
Q

Liver gets its ATP from ( absorptive state)

A

Amino acids

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6
Q

Primary site of triglycerides

A

Liver

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7
Q

From GI tract, glucose enters the bloodstream and effects the brain by: (absorptive)

A

Glucose oxidized for atp

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8
Q

From GI tract, amino acids enters the bloodstream and effects the muscle by: (absorptive)

A

Replace lost protein and build new protein in muscle to replenish what was lost in post absorptive state

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9
Q

From GI tract, amino acids enters the bloodstream and effects the liver by: (absorptive)

A

Amino acids are oxidized to atp or converted to triglycerides

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10
Q

From GI tract, amino acids enters the bloodstream and effects the fat and brain by: (absorptive)

A

AA Build new protein in the cell

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11
Q

Triglyceride is synthesized in the ___ and exported to ___ for long term storage

A

Liver, adipose tissue by VLDL

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12
Q

How does liver and adipose tissue make triglycerides from excess glucose?

A

In the liver and adipose tissue, Glucose is broken down into glycerol backBone (3 C) + fatty acids = triglyceride

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13
Q

How does liver and adipose tissue make triglycerides from excess amino acids?

A
  1. In liver cell, amino acids are deaminated
  2. NH3 (ammonia) which is toxic, converted to urea
  3. Amino acid converted to keto acid
  4. Keto acid is converted into atp for liver and to glucose to make triglyceride
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14
Q

Amino acids are converted into Keto acid before…

A

Oxidized for atp and converted to triglyceride

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15
Q

Once triglyceride enters GI tract and into bloodstream it….

A
  1. Liver produces VLDL (newly synthesized fats)
  2. VLDL is then stored in adipose tissue for long term
  3. Chylomicrons in blood come from fat absorption of dietary fats
  4. Fat of CM dissolves in blood
  5. CM is stored in adipose tissue for long term
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16
Q

Why do VLDLs and CM’s dissolve in the blood or are more soluble?

A

Their phospholipid is a mono layer (polar head faces water and hydrophobic faces fat)

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17
Q

In a regular cell, the inside and outside environment is mainly __ which is why it’s a bilayer

A

Water

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18
Q

Chylomicrons=
Come from:
Carry:
Taken up by/converted into:

A

Come from: SI
Carry: dietary fats
Converted into CM remnants that are taken up liver and remaining triglyceride is packaged into VLDL

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19
Q

Chylomicron remnants release…

A

Cholesterol and triglycerides

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20
Q

VLDLs:
Come from=
Contain/carry=
Transport=

A

Come from= synthesized by liver
Contain/ carry: triglycerides made from excess AA and glucose, triglyceride found in CM remnant
Transport= leave liver, into blood, and deposit triglyceride into adipose tissue for long term storage

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21
Q

VLDLs carry what two things

A

Newly synthesized triglyceride and dietary triglyceride

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22
Q

Explain how glycogenesis in liver prevents large spikes of plasma glucose after a meal:

A

Glucose is stored as Glycogen in liver and skeletal muscle
-removing excess glucose from plasma and storing it as glycogen helps lower plasma glucose in absorptive state

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23
Q

Very heavy to store

A

Glucose

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24
Q

Explain how lipogenesis in liver prevents large spikes of plasma glucose after a meal:

A

Triglyceride formed from glucose and excess amino acids; formation of triglycerides from excess glucose helps lower plasma glucose in absorptive state

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25
Q

Fat/triglycerides are what kind of energy storage? Heavy or lighter than glycogen? Easier or harder to access?

A

Large potential energy storage
Lightweight
Energy harder and slower to access

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26
Q

What stimulates insulin release (4 things)

A
  1. Increase in plasma glucose levels (insulin can then pull glucose out of blood plasma)
  2. Increased plasma AA
    3 . Feedforward effects of incretins
  3. Increased parasympathetics, decreased sympathetic activity
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27
Q

Explain the Feedforward effects of incretins (GI hormone) in releasing insulin…

A

Anticipatory (main stimulus not there yet), says that glucose plasma will rise
1. Incretins get released in blood and circulate to pancreas even if glucose in plasma looks normal
2. Senses what you’ve eaten and what levels are high

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28
Q

Prepare for elevated glucose levels in plasma

A

Intecrins

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29
Q

Functions of insulin

A

Increases glucose transport into muscle, liver, fat
Suppresses gluconeogenesis (production of glucose)
Inhibits lipolysis (fat release from adipocytes)

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30
Q

Why don’t we want lipolysis when glucose is high?

A

We don’t want the body to use fats to make energy (want body to use glucose and pull glucose out of plasma)

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31
Q

How does insulin increase glucose transport into muscle, liver, and fat?

A

Insulin binds receptor on cell surface—> inserts glucose transporters in membrane —> glucose exits blood

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32
Q

Glucose can’t pass into cells of muscle, and fat unless…

A

Insulin is present (besides the brain)

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33
Q

What are the problems with the absorptive state?

A
  1. Increase plasma glucose levels after meal
  2. Increase plasma fatty acids and amino acids
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34
Q

Why is too much glucose in plasma bad

A

Glucose is acidic and too mushy can acidify blood and damage Blood vessels

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35
Q

Why is increasing plasma fatty acids and AA bad

A

Can lead to atherosclerosis, proper fat storage required for healthy body, muscle needs amino acids to replace proteins lost in absorptive state, amino acids need for cell growth and repair

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36
Q

What is insulin’s effect on the liver tissue?

A
  1. Stimulates activation of hexokinase
  2. Changes shape or glucose and maintains high influx of glucose
  3. Phosphorylates glucose before entry into cell
  4. Activates Intracellular pathways to keep moving glucose into cell
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37
Q

Helps maintain the concentration gradient for glucose movement

A

Hexokinase

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38
Q

What are insulin’s effects on muscle and fat?

A

Binding of insulin on receptors on cell membrane inserts glucose transporters into plasma membrane
- allowing for glucose movement, down gradient into cell

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39
Q

Insulin is what kind of hormone

A

Protein

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40
Q

In muscle and fat, glucose transporters are stored….
In liver, glucose transporter are…

How are they different?

A

In muscle and fat, glucose transporters are stored Intracellularly and are only present when insulin is present

In liver, glucose transporters are in membrane all the time (no translocation)

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41
Q

Due to insulin deficiency, autoimmune disease that destroys B cells

A

Type 1

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42
Q

Due to development of insulin resistance, leads to long term effects of kidneys, BV, and nervous system

A

Type 2

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43
Q

Diabetes results in what level of glucose

A

Too high

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44
Q

Insulin comes from…

A

Pancreas, islet or langerhan (beta cells)

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45
Q

Beta cells secrete….

A

Insulin which lowers plasma glucose back to normal

46
Q

Pancreas plays a role in…

A

Blood glucose regulation and releasing HCO3 and digestive enzymes

47
Q

Glycogen is what kind of energy source

A

Rapid

48
Q

Signal transduction pathway is NOT initiated and glucose transporters remain in intracellular vesicles–increase plasma glucose: in which form of diabetes

A

Both

49
Q

What tests are used to diagnose diabetes?

A

Hemoglobin A1C and Glucose Tolerance Test

50
Q

Blood test that measures the total amount of glucose bound to hemoglobin in bloodstream

A

Hemoglobin A1C

51
Q

Marker of hemoglobin modification by glucose

A

Glycation in Hemoglobin A1C test

52
Q

What indiciates diabetes in Hemoglobin A1C test?

A

increase glucose in blood, increase hemoglobin glycation

53
Q

Insulin resistance is the greatest predictor of

A

type 2 diabetes

54
Q

Fast overnight, ingest a large amount of glucose (75 g), watch how quickly your body is able to remove glucose from the bloodstream over time

A

Glucose tolerance test

55
Q

In type 1 diabetes, if given ___ than their glucose levels can come back down

A

insulin injection

56
Q

In type 2 diabetes, if given insulin injection…

A

not much change in high glucose levels

57
Q

AGE formation how?

A

Glucose binds proteins

58
Q

What happens when AGE binds a receptor (RAGE) for activation?

A
  1. Increase oxidative stress
  2. Increase inflammation
  3. Endothelial damage and increased permeability
  4. Reduction of NO–> limits vasodilation
59
Q

When hyperglycemia occurs, what forms as a result?

A

AGE and H2O2 (oxidative stress)—These activate PKC

60
Q

What is the role of PKC?

A

Activates vasoconstriction of blood vessels by communicating with smooth muscle

61
Q

Common symptoms seen in the clinic for a patient with type 2 diabetes

A

BV damage (Increase BP), nerve damage (capillary damage that cuts off nutrient supply, amputation), eye damage (damage BV of retina), and kidney damage (damage of filtering system)

62
Q

What is also increased when there is a low pH in the blood?

A

Ventilation

63
Q

Absence of functioning insulin releases….

A

inhibition of lipolysis (body thinks its in post-absorptive state)–release fatty acids into plasma

64
Q

When liver converts fatty acids into ___, which are acidic

A

Ketones

65
Q

What else is impaired in diabetes that results in lactic acid production through _____

A

Mitochondria; increased anaerobic respiration (rely on glycolysis)

66
Q

What from lactic acid moves into the blood to acidify blood in those with diabetes?

A

H+

67
Q

Increases a patients sensitivity to insulin, allowing plasma glucose levels to fall : who gets this drug

A

Insulin sensitizers, type 2

68
Q

Compounds capable of binding insulin receptors and mimicking the actions of insulin, causing plasma glucose levels to fall

A

insulin mimetics

69
Q

Compounds that stimulate beta cells to secrete insulin, plasma glucose levels will fall in response to increased insulin production/release

A

insulin secretagogues

70
Q

Prevents reabsorption of glucose which will then be excreted during urination, causing drop in plasma glucose levels

A

SGLT2 Inhibitors

71
Q

Glucagon functions?

A

Stimulates glycogenolysis, gluconeogenesis, muscle break down, and fatty acid release from fat tissue

72
Q

generates glucose from breaking down glycogen, released in the plasma and taken up by liver to brain: what pathway

A

Glycogenolysis

73
Q

Generates new glucose from non-carb substrates. What is this process and what are the substances?

A

Gluconeogenesis; pyruvate, lactate, glycerol, and AA

74
Q

Main source of energy for most tissues, besides brain, in post-absorptive state

A

Fatty acids

75
Q

Majority of glucose produced comes from

A

AA in liver

76
Q

What is glucose sparing

A

Instead of using glucose, liver uses AA & muscle/fat use fatty acids (brain uses glucose)

77
Q

Glucagon activates release of

A

fat

78
Q

When glucose arrives in the blood in post-absorptive state….

A
  1. Glucose goes straight to brain
  2. Fat tissues release fatty acids and glycerol into plasma (from triglyceride breakdown)
  3. Fatty acids travel to muscle and muscles glycogen storage are oxidized for ATP
  4. In muscle, lactate and pyruvate are made as a result of glucose oxidation, and muscle breakdown releases AA into plasma
  5. Lactate, pyruvate, and AA move into liver from blood
  6. Glycerol, fatty acids, AA, lactate, and pyruvate move into liver
  7. They are converted into glucose and ketone bodies
  8. Liver sends glucose to brain
79
Q

In liver metabolism, how is glucose produced?

A
  1. Liver glycogen broken down
  2. AA from muscle deaminated and converted to glucose
  3. Lactate, pyruvate, and glycerol are converted to glucose
80
Q

What are the gluconeogenic pathways in liver metabolism?

A

AA from muscle deaminated, lactate, pyruvate, and glycerol are converted

81
Q

In liver metabolism, how are ketones produced

A

from fatty acids by beta oxidation

82
Q

In liver metabolism, how is ATP produced

A

keto acids in the liver used to make ATP from AA

83
Q

Why does the liver make ketone bodies and not ATP from fatty oxidation?

A

Liver contains low levels of oxaloacetate (needed for atp production) so Acetyl-CoA is converted into ketone bodies

84
Q

Ketone bodies from liver enter the blood and go to the brain ONLY after

A

days of starvation/fasting

85
Q

Where does glucagon come from?

A

alpha cells (not exocrine cells)

86
Q

What stimulates glucagon release?

A
  1. decreased plasma glucose
  2. Increased plasma AA (same as insulin)
87
Q

If you eat a high protein meal and no sugar, insulin is released but there’s no glucose present so glucose falls more. As a result, what is released to help prevent a further fall in glucose if no sugar in diet?

A

Glucagon

88
Q

In a post-absorptive state in muscle and fat, in the absence of insulin—glucose transporters are….

A

removed from plasma membrane and sit in vesicles waiting for insulin stimulus

89
Q

Adipose tissue, in post-absorptive state in muscle and fat, doesn’t have access to glucose unless…

A

insulin is present

90
Q

In the liver in post-absorptive state, glucose transporters are….

A

always in plasma membrane

91
Q

In the liver, in a post-absorptive state, glucose is produced by ___ and moves ____

A

pyruvate, glycerol, lactate, and AA; down concentration gradient through GLUT2 transporter

92
Q

Glucose metabolism by hypothalamic centers regulate food intake

A

Glucostatic theory

93
Q

What is the glucostatic theory pathway

A

decreased glucose–> suppress satiety —-> activate feeding center

94
Q

Signal from body fat stores to the brain to modulate eating behavior so that the body maintains a particular weight

A

Lipostatic theory

95
Q

What is the lipostatic theory pathway

A

Increased fat stores–> activates satiety—-> inhibits feeding center

96
Q

Protein hormones produced by adipocytes that feeds back negatively on the brain, preventing increase in food intake

A

Leptin

97
Q

Leptin was thought to curen ___. Was this true?

A

obseity; obese humans and mice exhibit elevated leptin because they are leptin resistant

98
Q

Ketone bodies vs keto acids

A

Ketone bodies= from free fatty acids, doesn’t make glucose

Keto acids= from AA breakdown from muscle, used for glucose

99
Q

In diabetes, even though glucose is high, what is still released

A

Fatty acids, because no insulin

100
Q

Because insulin turns off lipolysis, what is released in diabetes

A

Fat

101
Q

Insulin sensitizers cannot be given to…

A

Type 1 (give to type 2 because they are resistant)

102
Q

Insulin secretagogues is given in what stage of diabetes

A

Early states while pancreas is still functioning

103
Q

Where is the SGLT 2 located and what does it promote

A

Renal epithelium, apical side: wants to reabsorb glucose

104
Q

If glucose concentrations are equal, and there is no gradient what is used to promote reabsorption

A

SLGT 2 (secondary transport), makes a gradient

105
Q

On the basolateral side, how can glucose get back into the blood if SGLT2 is making a gradient

A

Facilitated diffusion

106
Q

In diabetes, glucose is high in the plasma. This has what effect on filtration? What happens they to the glucose cotransporter?

A

Increases filtration (increases glucose in bowman’s capsule). Glucose cotransporter becomes too saturated and overwhelmed (excreted)

107
Q

Gluconeogenesis in the liver occurs in what stage

A

Post absorptive

108
Q

Which cannot be made into glucose by liver

Amino acids
Glycerol
Fatty acids

A

Fatty acids (only oxidized to make atp or converted into ketone bodies)

109
Q

Dominant pathway for glucose production during post absorptive state

A

Amino acids

110
Q

Lepton function

A

Acts on brain to decrease / inhibit food intake

111
Q

Fatty acids cannot become

A

Glucose

112
Q

Example of gluconeogenic pathway

A

Protein to amino acids to keto acids to glucose

Human Physiology (14 decks)

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