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Block 3; Week 8 > Integration of Metabolism > Flashcards

Integration of Metabolism Flashcards

1
Q

What are the functions of the liver?

A

processes fats, carbs & proteins from the diet
synthesizes & distributes lipids, ketones bodies, & glucose
converts excess nitrogen to urea

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2
Q

How is the metabolism of the body integrated?

A

nervous & hormonal signals

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3
Q

Which part of the body is considered the savings account? Explain this.

A

Adipose Tissue
stores 100X more energy than glycogen
Note: when you are fasting–>you see more free fatty acids in your plasma.

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4
Q

Which part of the body is considered the checking account?

A

the liver

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5
Q

How much energy does the brain normally consume per day? How much energy does it consume when you are fasting?

A

Normally: 90g/day (20% of the resting energy)
Fasting: 30g/day

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6
Q

When are insulin levels the highest?

A

after a high carb meal

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7
Q

What stimulates the synthesis of insulin?

A

glucose & amino acids potentiate it.

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8
Q

What are the 3 main targets of insulin?

A

muscle, adipose, liver

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9
Q

Insulin is the hormone of the well-fed state. What does this mean?

A

It stimulates the storage of excess nutrients as glycogen or fat. Note: we don’t store protein.

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10
Q

What types of enzymes are stimulated by insulin?

A

glucose metabolizing enzymes

via phosphorylation or synthesis of these enzymes

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11
Q

What types of glucose transporters does the liver use?

A

GLUT 2

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12
Q

What is the main important enzyme of the glucose phosphorylation pathway?

A

Glucokinase

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13
Q

What process does PFK1 & pyruvate kinase promote?

A

glycolysis

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14
Q

What are 3 important enzymes that promote gluconeogenesis?

A

PEPCK
F16BPase
G6Pase

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15
Q

What process does glycogen synthase regulate?

A

glycogen synthesis

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16
Q

What is the main enzyme involved in glycogenolysis?

A

glycogen phosphorylase

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17
Q

What pathway are the following enzymes involved in: Acetyl CoA Carboxylase, ATP-Citrate Lyase, Malic Enzyme?

A

Fatty Acid synthesis

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18
Q

What is the main important enzyme in the pentose phosphate pathway?

A

G6P dehydrogenase

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19
Q 
Insulin in the liver causes an increase/decrease in the following pathways:
Glucose Phosphorylation
Glycolysis
Gluconeogenesis
Glycogen Synthesis
Glycogenolysis
Fatty Acid Synthesis
Pentose Phosphate Pathway
A 
Glucose Phosphorylation: increases
Glycolysis: increases
Gluconeogenesis: decreases
Glycogen Synthesis: increases
Glycogenolysis: decreases
Fatty Acid Synthesis: increases
Pentose Phosphate Pathway: increases
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20
Q

What are the general effects of insulin on adipose tissue?

A

stimulates glycolysis
stimulates FA synthesis & storage
prevents fat breakdown

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21
Q

What is the rate limiting step in adipose tissue & skeletal muscle of glucose metabolism?

A

Glut 4 receptors. Km =1 mM

most important enzyme for glucose uptake

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22
Q

What is the most important enzyme for glycolysis?

A

PFK1

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23
Q

G6P dehydrogenase is super important in which pathway?

A

pentose phosphate pathway

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24
Q

What is the most important enzyme in pyruvate oxidation?

A

pyruvate dehydrogenase

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25
Q

What is LPL really important for?

A

triglyceride (FFA) uptake

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26
Q

What is the most important enzyme in lipolysis?

A

HSL

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27
Q 
Insulin in adipose tissue increases/decreases the following pathways:
glucose uptake
glycolysis
pentose phosphate pathway
pyruvate oxidation
triglyceride uptake
TAG synthesis
lipolysis
A 
glucose uptake: increases
glycolysis: increases
pentose phosphate pathway: increases
pyruvate oxidation: increases
triglyceride uptake: increases
TAG synthesis: increases
lipolysis: decreases
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28
Q

What is the most important enzyme in glucose uptake in skeletal muscle?

A

GLUT 4 receptors

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29
Q

What is PFK1 super important in?

A

glycolysis

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30
Q

What is the most important enzyme in glycogen synthesis?

A

glycogen synthase

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31
Q

What is glycogen phosphorylase super important for?

A

glycogenolysis

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32
Q 
Insulin in skeletal muscle increases/decreases the following processes:
glucose uptake
glycolysis
glycogen synthesis
glycogenolysis
protein synthesis
A 
glucose uptake: increases
glycolysis: increases
glycogen synthesis: increases
glycogenolysis: decreases
protein synthesis: increases
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33
Q

What are 2 places in the body where glucose uptake is non-insulin dependent? Which glucose receptors do they use?

A

brain: Glut 3
RBCs: Glut 1

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34
Q

Pathways that remove excess fuels from the blood are active in the fed state. What are these pathways?

A

Glycogen Synthesis
Glycolysis
Fatty Acid Synthesis
Lipogenesis

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35
Q

We are talking about the effect of insulin on this process. Which parts of the body does this happen in? Which enzyme(s) are affected?
*Glucose Uptake

A

Increases

  • *adipose tissue, skeletal muscle, liver
  • *targets GLUT 4 transporters in adipose tissue & skeletal muscle
  • *targets glucokinase in the liver
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36
Q

We are talking about the effect of insulin on this process. Which parts of the body does this happen in? Which enzyme(s) are affected?
*glycogen synthesis

A

Increases

  • *liver, muscle
  • *targets glycogen synthase
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37
Q

We are talking about the effect of insulin on this process. Which parts of the body does this happen in? Which enzyme(s) are affected?
*Glycogenolysis

A

Decreases

  • *liver, muscle
  • *targets glycogen phosphorylase
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38
Q

We are talking about the effect of insulin on this process. Which parts of the body does this happen in? Which enzyme(s) are affected?
*Glycolysis & Acetyl-CoA Production

A

Increases

  • *liver, muscle
  • *targets PFK1 (targets PFK2 to stimulate PFK1)
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39
Q

We are talking about the effect of insulin on this process. Which parts of the body does this happen in? Which enzyme(s) are affected?
*Fatty Acid Synthesis

A

Increases

  • *liver
  • *targets Acetyl CoA Carboxylase
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40
Q

We are talking about the effect of insulin on this process. Which parts of the body does this happen in? Which enzyme(s) are affected?
*TAG synthesis

A

Increases

  • *adipose tissue
  • *targets lipoprotein lipase
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41
Q

What is the function of glucagon? Where is it secreted from?

A

secreted from pancreatic alpha cells

**function is to maintain blood glucose

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42
Q

What second messenger does glucagon use?

A

cAMP

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43
Q

What is the response of glucagon to hypoglycemia? What is the response of glucagon to hyperglycemia?

A

Hypoglycemia: glucagon increases 2-3 fold
Hyperglycemia: glucagon decreases to 1/2 of original

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44
Q

If you are trying to affect gluconeogenesis, which 3 enzymes do you target?

A

PEPCK
F16BPase
G6Pase

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45
Q

What is the main enzyme targeted when affecting glycogen synthesis? What is the main enzyme targeted when affect glycogenolysis?

A

Glycogen Synthesis: glycogen synthase

Glycogenolysis: glycogen phosphorylase

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46
Q

If you are trying to change fatty acid oxidation–>which enzyme do you alter? If you are trying to change fatty acid synthesis–>which enzyme do you alter?

A

Fatty Acid Oxidation: CPT1

Fatty Acid Synthesis: Acetyl CoA Carboxylase

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47
Q

Where is the main place that glucagon acts in the body?

A

the liver

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48
Q 
What are the effects of glucagon in the liver on the following pathways:
glycolysis
gluconeogenesis
glycogen synthesis
glycogenolysis
FA synthesis
FA oxidation
A

glycolysis: decreases
gluconeogenesis: increases
glycogen synthesis: increases
glycogenolysis: decreases
FA synthesis: increases
FA oxidation: decreases?

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49
Q

What do catecholamines do?

A

involved in acute & chronic stress response

**main effect: mobilization of glycogen & fat for muscle use

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50
Q

What are the main types of catecholamines? Where are they secreted from?

A

Norepi & Epi from the adrenal medulla

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51
Q

Starting from tyrosine…how do you get Epi?

A

Tyrosine–>L-DOPA–>Dopamine–>Norepi–>Epi

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52
Q

What are some things that prompt catecholamine release?

A

hypoglycemia
pain
hypoxia
hemorrhage

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53
Q 
What does the presence of epinephrine in the liver do to the following processes? 
Glycolysis
Gluconeogenesis
Glycogen Synthesis
Glycogenolysis
FA synthesis
A 
Glycolysis: decreases
Gluconeogenesis: increases
Glycogen Synthesis: decreases
Glycogenolysis: increases
FA synthesis: decreases
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54
Q

How does the presence of Epi in the liver act to decreases glycolysis?

A

By turning the PFK2 into PFK1.

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55
Q

How does the presence of Epi in the liver act to increases gluconeogenesis?

A 
inhibiting pyruvate kinase (don't continue glycolysis)
increasing F26BPase (decreases activity of PFK1)
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56
Q

Why would you want to increase the activity of F26BPase if you are trying to increase gluconeogenesis?

A

if you increase F26BPase activity, you get less F26BP. With less F26BP you get less stimulation of PFK1. This tells the glycolysis to chill out & the gluconeogenesis to step up.

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57
Q

How does the presence of Epi in the liver act to decrease glycogen synthesis?

A

glycogen synthase is phosphorylated. This reduces its activity

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58
Q

How does the presence of Epi in the liver act to increase glycogenolysis?

A

glycogen phosphorylase is phosphorylated. This increases its activity.

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59
Q

How does the presence of Epi in the liver act to decrease fatty acid synthesis?

A

acetyl CoA carboxylase is phosphorylated. this reduces its activity

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60
Q

Aside from glycogen phosphorylase…what are other ways that glycogenolysis is stimulated?

A

Glycogenolysis can also be stimulated via vasopressin, oxytocin, Ang II thru Ca++ or phosphatidylinositol bisphosphatase.

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61
Q

What do alpha adrenergic receptors have to do with epi in the liver?

A

The epi acts on these alpha adrenergic receptors and prompts them to raise the Ca++ levels. This activates a phosphorylase kinase that is sensitive to Ca++ & Calmodulin.
Note: a lot of the effects of epi in the liver involved phosphorylation–>good to have a kinase on the team!

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62
Q

Which receptors are activated when epi comes in contact with adipose tissue?

A

beta adrenergic receptors–>increases cAMP

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63
Q

What is the effect of epinephrine on adipose tissue?

A 
increases lipolysis (via HSL)
decreases TAG uptake from lipoproteins (via LPL)
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64
Q

What is the effect of epinephrine on the pancreas?

A

it increases glucagon secretion

decreases insulin secretion

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65
Q

Which receptors are activated by epinephrine acting on the skeletal muscle?

A

beta adrenergic receptors

this raises cAMP levels

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66
Q 
What does epinephrine do in the skeletal muscle to the following processes:
glycolysis
glycogen synthesis 
glycogenolysis
TAG uptake from lipoproteins
A

glycolysis: increases!!!!
glycogen synthesis: decreases
glycogenolysis: increases
TAG uptake from lipoproteins: increases

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67
Q

Whoa! Crazy…epinephrine stimulates glycolysis in skeletal muscle. How?

A

the kinase activity that is kicked off by cAMP does something weird in skeletal muscle. Phosphorylation of PFK2-F26BPase here stimulates the kinase activity. therefore, you end up with more F26BP. This stimulates PFK1 & glycolysis

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68
Q

What are the highlights of the overall effect of epinephrine on metabolism? which substances does epinephrine act a lot like?

A

Acts a lot like glucagon.
Stimulates glycogen breakdown in muscle & liver
stimulates gluconeogenesis in the liver
Stimulates lipolysis in adipose tissue.
increases secretion of glucagon & decreases secretion of insulin from the pancreas.

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69
Q

How does the presence of Epi in the liver act to decrease glycogen synthesis?

A

glycogen synthase is phosphorylated. This reduces its activity

70
Q

How does the presence of Epi in the liver act to increase glycogenolysis?

A

glycogen phosphorylase is phosphorylated. This increases its activity.

71
Q

How does the presence of Epi in the liver act to decrease fatty acid synthesis?

A

acetyl CoA carboxylase is phosphorylated. this reduces its activity

72
Q

Aside from glycogen phosphorylase…what are other ways that glycogenolysis is stimulated?

A

Glycogenolysis can also be stimulated via vasopressin, oxytocin, Ang II thru Ca++ or phosphatidylinositol bisphosphatase.

73
Q

What do alpha adrenergic receptors have to do with epi in the liver?

A

The epi acts on these alpha adrenergic receptors and prompts them to raise the Ca++ levels. This activates a phosphorylase kinase that is sensitive to Ca++ & Calmodulin.
Note: a lot of the effects of epi in the liver involved phosphorylation–>good to have a kinase on the team!

74
Q

Which receptors are activated when epi comes in contact with adipose tissue?

A

beta adrenergic receptors–>increases cAMP

75
Q

What is the effect of epinephrine on adipose tissue?

A 
increases lipolysis (via HSL)
decreases TAG uptake from lipoproteins (via LPL)
76
Q

What is the effect of epinephrine on the pancreas?

A

it increases glucagon secretion

decreases insulin secretion

77
Q

Which receptors are activated by epinephrine acting on the skeletal muscle?

A

beta adrenergic receptors

this raises cAMP levels

78
Q 
What does epinephrine do in the skeletal muscle to the following processes:
glycolysis
glycogen synthesis 
glycogenolysis
TAG uptake from lipoproteins
A

glycolysis: increases!!!!
glycogen synthesis: decreases
glycogenolysis: increases
TAG uptake from lipoproteins: increases

79
Q

Whoa! Crazy…epinephrine stimulates glycolysis in skeletal muscle. How?

A

the kinase activity that is kicked off by cAMP does something weird in skeletal muscle. Phosphorylation of PFK2-F26BPase here stimulates the kinase activity. therefore, you end up with more F26BP. This stimulates PFK1 & glycolysis

80
Q

What are the highlights of the overall effect of epinephrine on metabolism? which substances does epinephrine act a lot like?

A

Acts a lot like glucagon.
Stimulates glycogen breakdown in muscle & liver
stimulates gluconeogenesis in the liver
Stimulates lipolysis in adipose tissue.
increases secretion of glucagon & decreases secretion of insulin from the pancreas.

81
Q

Why do people today have a lot of cortisol in their system?

A

b/c they have a lot of stress in their lives & it is a dangerous world. It is a chronic stress response.

82
Q

What is the main mechanism of action of cortisol? Which substance does it work synergistically with? What class of substances does it belong to?

A

Cortisol–>Glucocorticoids
works thru gene regulation (more of an effect on the hours-days scale)
works w/ epinephrine

83
Q

What are the main effects of cortisol in the body?

A

Increased TAG degradation in adipose tissue
Breakdown of muscle protein
Gluconeogenesis increase in the liver
Glycogen synthesis increase

84
Q

How does cortisol increase gluconeogenesis in the liver?

A

thru increasing the synthesis of PEPCK

85
Q

What building block does cortisol use to stimulate an increase in glycogen synthesis?

A

uses all the extra G6P from gluconeogenesis

86
Q

What is the net effect of cortisol in the body?

A

restores blood glucose

glycogen stores increase

87
Q

What are the negative side effects of cortisol in the body?

A

overtime it destroys muscle & bone

it also impairs the endocrine & immune system

88
Q

What type of hormone is growth hormone?

A

it is a peptide hormone, not a glucocorticoid.

89
Q

What is the basic effect of growth hormone on the body?

A

increases free fatty acid availability for energy generation

spares the oxidation of glucose & amino acids

90
Q

What is the half life of GH?

A

20-50 minutes

91
Q

What are the direct effects of growth hormone on adipose tissue?

A

increased epinephrine sensitivity
decreased insulin sensitivity
decreased fatty acid esterification

92
Q

What are the indirect effect of growth hormone on adipose tissue?

A

increased lipogenesis
increased plasma free fatty acids & glycerol
decreased TAG synthesis
decreased glucose uptake

93
Q

What are the direct effects of growth hormone in the liver?

A

increased protein synthesis
increased free fatty acid oxidation
increased gluconeogenesis
decreased glycolysis

94
Q

What are the indirect effects of growth hormone in the liver?

A

Increase in IGF-1
Increased ketogenesis
increased glycogen synthesis

95
Q

What are the direct effects of growth hormone in skeletal muscle?

A

increased free fatty acid oxidation

increased amino acid transport (pos nitrogen balance)

96
Q

What are the indirect effects of growth hormone in skeletal muscle?

A

decreased glucose use (glucose sparing)
decreased glucose uptake
decreased glycolysis
increased protein synthesis (protein sparing)

97
Q

What are the half lives of T3 & T4?

A

T3: 1-1.5 days
T4: 7 days

98
Q

What are the main effects of thyroid hormone on the body?

A

an increase in fuel consumption

an increase in sensitivity of receptors that have insulin counter-regulatory effects

99
Q

Growth hormone on which 2 tissues causes an impaired insulin post receptor signaling?

A

skeletal muscle

adipose tissue

100
Q

What is the effect of thyroid hormone on the pancreas?

A

it increases the sensitivity of beta cells & prompts insulin release

101
Q

What is the direct effect of thyroid hormone on adipose tissue?

A

an increase in epinephrine sensitivity

102
Q

What are the indirect effects of thyroid hormone on adipose tissue?

A

So…this one is a little more complicated.
Usu: an increase in lipolysis
Sometimes: if there is enough insulin & glucose available–>an increase in TAG synthesis

103
Q

What are the direct effects of thyroid hormone on muscle?

A

an increase in gene expression

an increase in epinephrine sensitivity

104
Q

What are the indirect effects of thyroid hormone on muscle?

A

an increase in glucose uptake (prompted by insulin)
increased protein synthesis
increased glycogenolysis
increased glycolysis

105
Q

What are the direct effects of thyroid hormone on the liver?

A

increased glycolysis
increased cholesterol synthesis
with more cholesterol available–>increased bile salts
an increased sensitivity to epinephrine

106
Q

What are the indirect effects of thyroid hormone on the liver?

A

increased free fatty acids–>formation of more TAGs

107
Q

What percentage of glucose is metabolized by the liver?

A

20-30% of dietary glucose

108
Q

What happens to most of the glucose that is processed by the liver?

A

most of it is processed into glycogen

109
Q

Can the liver get TAGs from chylomicrons?

A

No, b/c they don’t have lipoprotein lipase. Therefore, they can only take in TAGs from remnant particles.

110
Q

Describe the basics of the conversion of carbs to fats in the liver.

A

Glucose–>Acetyl CoA–>Fatty Acids

111
Q

When does the liver make VLDL?

A

At all times.

112
Q

What happens to fatty acids when they are in liver mitochondria?

A

they undergo beta oxidation & form acetyl CoA

113
Q

What are the 2 possible fates of Acetyl CoA?

A

can either go into TCA or ketogenesis

114
Q

Malonyl CoA inhibits which enzyme?

A

Carnitine Palmitoyl Transferase 1

115
Q

What are 2 things that stimulate Acetyl CoA carboxylase?

A

insulin

citrate

116
Q

When does the liver start becoming a net producer of glucose?

A

3-4 hours after a meal…

117
Q

After a 12 hour fast, what happens to Carnitine palmitoyl transferase 1? how?

A

its activity increases

it is simulated by glucagon, its activity is no longer inhibited by the presence of malonyl CoA

118
Q

What happens to acetyl CoA carboxylase after a 12 hour fast?

A

its activity decreases b/c there is increased acyl CoA to inhibit it & there is less citrate around to activate it
it is also phosphorylated via glucagon/epi signaling.

119
Q

After a meal…what are the activity levels of carnitine palmitoyl transferase 1 & acetyl CoA carboxylase?

A

CPT1 inhibited

Acetyl CoA Carboxylase activity higher

120
Q

After a 12 hours fast…what are the activity levels of CPT1 & Acetyl CoA carboxylase?

A

CPT1 stimulated

Acetyl CoA carboxylase inhibited

121
Q

After a 4 day fast, what are the main sources of blood glucose?

A

amino acids

lactate

122
Q

After a 4 day fast you get a higher rate of beta oxidation…what 2 things does this supply?

A

ATP

NADH

123
Q

What happens to TCA & ketone body formation after a 4 day fast?

A

TCA decreases

ketogenesis increases

124
Q

What converts HMG CoA to acetoacetate?

A

3-hydroxy-3-methyl-glutaryl-CoA lyase

this enzyme increases after a 4 day fast

125
Q

The liver converts carbs to what 2 things?

A

Carbs converted to glycogen & fat

126
Q

During fasting, what are the 2 things that the liver supplies to the body?

A

glucose

ketone bodies

127
Q

What is the function of the enzyme HSL?

A

hormones sensitive lipase is found on adipose tissue. its function is to mobilize fats. Breaks TAGs into free fatty acids.

128
Q

Which processes are especially active in the starved state?

A 
glycogenolysis
gluconeogenesis
lipolysis
proteolysis
ketogenesis
129
Q

What kind of an effect does insulin have on adipocytes after a mixed meal?

A 
inhibits HSL: TAG breakdown
Glut4 glucose uptake stimulated
stimulates LPL: uptake of fatty acids
fatty acid synthesis increases
TAG synthesis increases
130
Q

What are the ways by which fatty acids increase in adipocytes after a mixed meal?

A

LPL stimulation: just take up more FFA.

More GLUT4 glucose uptake–>acetyl CoA–>fatty acids.

131
Q

How is TAG synthesis increased in adipocytes after a mixed meal?

A

A bunch of glucose uptake & DHAP formed. This turns into glycerol phosphate.
FFA & glycerol phosphate form TAGs in adipocytes.

132
Q

What happens to adipocytes during fasting?

A

during fasting you have more epinephrine–>stimulates HSL. More TAG breakdown to FFA, which are released. Glycerol is also released during the breakdown.

133
Q

What happens to the glycerol that is released from adipocytes during fasting?

A

it goes to the liver for gluconeogenesis

134
Q

What happens to free fatty acids that are released from adipocytes during fasting?

A

some go to muscles & other tissues for oxidation

some go to the liver for ketogenesis

135
Q

When a person is well fed, what is the state of their muscle?

A

strong

well-supplied

136
Q

When a person is fasting…what is the state of their muscle?

A

glucose sparing

protein degradation

137
Q

What is a tissue where insulin does not stimulate LPL?

A

muscle

138
Q

What is the source of energy for the brain during starvation?

A

ketone bodies

139
Q

After a meal…what substances go to the liver right away?

A

glucose
fatty acids
amino acids

140
Q

What does the liver do with glucose in a well-fed state?

A

some stored as glycogen
others converted to acetyl CoA–fatty acid synthesis. This forms TAGs that take a ride in a VLDL to adipose & muscle tissue.
Requires NADPH

141
Q

Where does the liver get the NADPH that is required to turn glucose into TAGs?

A

from glucose oxidation via the pentose phosphate pathway.

142
Q

What does the liver do with extra AA lying around?

A

turns into pyruvate or acetyl CoA for fatty acid synthesis, lipid synthesis

143
Q

How can lactate be transformed into usable energy? Where were the main sources of lactate?

A

by converting it into glucose in the liver

**main sources: muscle, RBCs

144
Q

So when someone is fasting…their muscles still need ATP energy. They get this in a way that is glucose sparing. How can that be done?

A

the muscle gets it ATP thru glycogenolysis instead of blood glucose
“glucose sparing”

145
Q

Early on in fasting…the brain can still get glucose…but only from 1 source. What is that source?

A

breakdown of liver glycogen

146
Q

Explain how liver glycogen is broken down for usable energy early on in fasting.

A

liver glycogen broken down
get a bunch of glucose-1-phosphate
G1P is converted into G6P
converted into free glucose–>released into the bloodstream.

147
Q

What happens to the body during starvation?

A

proteins in the liver & muscle are broken down.
adipose tissue breaks down TAGs.
AA & glycerol liberated from this catabolism used for gluconeogenesis.

148
Q

What do most tissues use for fuel during starvation?

A

ketone bodies

149
Q

What does the liver use for fuel during starvation?

A

fatty acids

150
Q

What is the main source of blood glucose during starvation?

A

liver (80%)

kidneys (20%)

151
Q

Where do the ketone bodies that most tissues use for their energy during starvation come from?

A

they come from the liver.

liver uses FA as fuel. Takes excess acetyl CoA & turns it into ketone bodies. This is used by other tissues!

152
Q

In the starved state, what percentage of gluconeogenesis has to do with AA? How much glucose does this process produce per day?

A

1/2 done w/ AA

produces 80-160 grams glucose/day

153
Q

Of the glucose that is produced by gluconeogenesis in the starved state: how much will be used by the brain?
Of the ketone bodies that are produced in the starved state: how much will be used by the brain?

A

1/2 the glucose will be used by the brain

70% of the ketones will be used by the brain

154
Q

When a certain percentage of the body’s nitrogen has been catabolized…it is too late to recover. What is the percentage?

A

when 1/3 of the body’s nitrogen has been catabolized–>too late.

155
Q

Why do patients with type I diabetes tend to be so thin?

A

b/c there isn’t sufficient insulin to turn off lipolysis. keep eating away the fat.

156
Q 
In patients with Type I Diabetes...insulin is away, so glucagon will play. What does that mean for the following processes:
glycolysis
gluconeogenesis
glycogen synthesis
glycogenolysis
FA synthesis
FA oxidation
A

glycolysis: down
gluconeogenesis: up
glycogen synthesis: down
glycogenolysis: up
FA synthesis: down
FA oxidation: up

157
Q

Describe the effects of glucagon on a patient with Type I Diabetes. Focus: liver

A

Liver–makes a bunch of glucose, but can’t make glycogen
increased beta oxidation of free fatty acids
a bunch of extra acetyl CoA–>ketone bodies abound.
Possible ketoacidosis

158
Q

Describe the effects of glucagon on a patient with Type I Diabetes. Focus: Adipose tissue

A

can’t take up glucose b/c of the lack of GLUT 4 translocation
increased lipolysis–>increased plasma FFA

159
Q

Describe the effects of glucagon on a patient with Type I Diabetes. Focus: muscle tissue.

A

can’t take up glucose b/c of the lack of GLUT 4 translocation

160
Q

What is the main danger of Type I Diabetes?

A

increase in ketone body formation–>possible ketoacidosis.

161
Q

What is the main danger of Type II Diabetes?

A

not ketoacidosis

hyper-osmolarity of the blood can dehydrate the brain & lead to a coma.

162
Q

What are the main treatment options for Type II Diabetes?

A

diet & exercise

oral hyperglycemics

163
Q

In patients with Type II Diabetes, what’s the deal with their metabolism?

A

adipose & muscle tissue don’t take up glucose–no GLUT 4 receptors
Liver CAN make glycogen in this case.
Adipose tissue lipolysis does NOT increase substantially
LPL activity decreases
plasma lipoproteins increase

164
Q

What are xenobiotics? What in the body usu metabolizes them?

A

foreign chemicals that must be removed from the body (could be foreign but from a plant, or could be drug)
Cytochrome P450

165
Q

How are xenobiotics excreted from the body?

A

thru the urine or bile if they are hydrophilic

if they are hydrophobic–>made to be hydrophilic & then excreted…

166
Q

How are lipophilic xenobiotics made water soluble? Where does this happen?

A

liver, intestines, lungs

happens in a 2 phase rxn

167
Q

Describe Phase I of the reaction to turn a lipophilic xenobiotic water-soluble before excretion.

A

metabolite is oxidized
hydroxyl groups added
Cytochrome P450 involved
requires NADPH

168
Q

What is the exact reaction of Phase I?

A

Substrate-H + O2 + NADPH + H+–>Substrate-OH + H2O + NADP+

169
Q

Where is Cytochrome P450 usu found?

A

in the smooth ER of the liver & the lungs

170
Q

What happens in Phase II of the lipophilic xenobiotic reaction?

A

metabolite is conjugated with a hydrophilic molecule to inactivate it & carry it out.

171
Q

What are some of the hydrophilic molecules that lipophilic xenobiotics are often conjugated to?

A 
glucuronic acid
sulfate
glycine
glutamine
glutathione

Block 3; Week 8 (8 decks)

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