Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block 3 Week 8 > Integration of Metabolism > Flashcards

Integration of Metabolism Flashcards

1
Q

What do you get when you put storage fuels, O2, and ATP together?

A

you get CO2, H20, and urea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

To maintain homeostasis what do you need?

A

continuous input of energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does the liver do?

A

process fats, carbs, proteins from diet, syntehsizes and distributes lipids, ketone bodies, and glucose for other tissues, converts nitrogen to urea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

WHen the brain is well fed, how much glucose does it consume?
When it is fasting?

A

90g/day

30g/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is considered the checking account of the body?
What is considered the savings account of the body?
how is this coordinated?

A

liver
adipose tissue
nervous and hormonal signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When you fast what happens to your adipose tissue?

A

you increase your FFAs

adipose tissue has 100X more energy than glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When are insulin levels the highest and what does it do?

A

after a high carb meal

stores glucose via liver adipose and muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Besides glucose what else can potentiate insulin?

A

amino acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does the liver use to transport glucose and is this a high or low affinity glucose transporters?

A

GLUT 2 (Km=15 mM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does glucokinase do?

A

increase glucose phosphorylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does PFKI and pyruvate kinase stimulate?

A

glycolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does PEPCK, F1,6 BPtase, and G6Ptase do?

A

Increases gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does glycogen synthase do?

A

increase glycogen synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does glycogen phosphorylase do?

A

increases glycogenolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does acetyl CoA carboxylase do?

A

it increases fatty acid synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does ATP-citrate lyase do?

A

Converts citrate to OAA and acetyl coa for fatty acid synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does the malic enzyme do?

A

Produces NADPH which is necessary for fatty acid biosynthesis (coverts malate to pyruvate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does G6P dehydrogenase do?

A

The regulated step of the pentose phosphate pathway and the step that provides NADPH to allow for proper RBC development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are insulins affects on the liver?

A 
increases glucose phosphorylation
increases glycolysis
decreases gluconeogenesis
increase glycogen synthesis
decreases glycogenolysis
increase FA synthesis
increase pentose phosphate pathway
(i.e gets rid of glucose through storage or through breakdown and puts the breakdown products into other storage areas like FAs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are insulin’s affects on adipose tissue?

A 
increase glucose uptake
increased glycolysis
Increase PPP
increase pyruvate oxidation(to become acetyl CoA)
increase TAG (FFA) uptake
Increase TAG synthesis
decreased lipolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the main idea of insulins affects on adipose tissue?

A

to decrease the amount of glucose via glycolysis and place the breakdown products (pyruvate) into storage (fat)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does insulin decrease lipolysis?

A

by inhibited HSL (the rate limiting step of lipolysis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does insulin increase TAG (FFA) uptake?

A

Increases LPL which will turn release TAGS into capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How will insulin increase pyruvate oxidation?

A

by increasing pyruvate dehydogenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How will insulin increase activity of PPP?

A

via increase in G6PD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How will insulin increase glucose uptake?

A

via Glut4 receptors (low affinity receptors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does insulin affect the skeletal muscle and how?

A

increases glucose uptake via GLUT4
Increase glucose breakdown via PFK1
increases protein synthesis by nonselective translation
increase glycogen synthesis via glycogen synthase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What breaks down glycogen?

A

Glycogen phosphorylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What 2 things are insulin INDEPENDENT?

A

brain and RBCs cuz they need glucose NO MATTER WHAT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what kind of transporter does the brain use?

What kind of transport does the RBC use?

A

Glut 3 Km (high affinity)

Glut 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Where does fatty acid synthesis take place?

A

in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Where do you get increase glucose uptake via inuslin?

A

muscle, adipose tissue, liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Where do you get increase glycogen synthesis via insulin?

A

liver and muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Where do you get increased glycolysis via insulin?

A

liver and muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Where do you get TAG synthesis via insulin?

A

adipose tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What does glucagon do?

A

makes glucose via cAMP second messengers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is reduced to 50% of basal levels during hyperglycemia?

A

glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How does glucagon effect the liver?

A 
forms glucose (build up glucose and breaks down glycogen)
Breaks down fatty acids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

So why does glucagon break down FA’s and insulin build FAs?

A

because when you have glucagon you dont have enough glucose so you dont want to use glucose for energy so you want to build your glucose levels and break down your FAs for energy instead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How does glucagon decrease glycolysis?

A

by making down regulating PFK2 so that it cannot allosterically activate PFK1 and thus pyruvate kinase. Instead it will result in high levels of F6P and promote gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How does glucagon increase gluconeogenesis?

A

Increases the activity of PEPCK, F1,6BPtase, G6Ptase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How does glucagon decrease glycogen synthase?

A

downregulates glycogen synthase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How does glucagon increase glycogenolysis?

A

increases glycogen phosphorylase :)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How does glucagon decrease FA synthesis?

A

It inhibits acetyl- Coa carboxylase

remember acetyl Coa Carboxylase turns acetyla coa into malonyl coa into palmitic acid (FA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How does glucagon increase FA oxidation?

A

it up regulates CPT1 (carnitine palmitoyl transferase 1) which will allow for acyl carnitine to cross the the mito membrane for beta oxidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Where does glucagon exclusively act on?

A

the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the most important response of catecholamines?

A

mobilization of glycogen and fat for muscle use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Catecholamine release is potently stimulated by (blank). It is also stimulated by what 2 things?

A

hypoglycemia

pain, hypoxia, and hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Explain how you get epinephrine?

A

Tyrosine-> L-DOPA-> Dopamine-> Norepinephrine-> Epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How does epinephrine effect the liver?

A

Increases levels of glucose (by decreasing glycolysis and increasing gluconeogenesis, decreasing glycogenesis and increasing glycogenolysis)
Decrease levels of FA synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How does epinephrine decrease glycolysis in the liver?

A

inhibits PFK2 so you end up with a lot of PFK1 and thus gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How does epinephrine increase gluconeogenesis?

A

decreases pyruvate kinase levels and increase F26BPtase which will result in decreased levels of PFK1 and thus increased gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How does epinephrine decrease glycogen synthesis in the liver and increase glycogenolysis?

A

It phosphorylates glycogen synthase (which takes away its activity) and phosphorylates glycogen phosphorylase thus increasing its activity
(remember glycogen phosphorylase is the first step in glycogen breakdown)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

How does epinephrine decrease FA synthesis in the liver?

A

It decreases Acetyl-CoA Carboxylase activity (step that converts acetyl coa into malonyl coa to make fatty acids) by phosphorylating acetyl coa carboxylase which will deactivate it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What does epinephrine do to calcium levels?

A

raises calcium levels through alpha 1 adrenergic receptors via ca2+/calmodulin sensitive phosphorylase kinase which will make all the effects of epinephrine in the liver possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

(Blank) is activated via vasopressin, oxytocin, and angiotensin II via Ca2+ or phophpatidylinositol bisphosphatase.

A

Glycogenolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the effects of epinephrine on adipose tissue?

A

increased lipolysis and decreased TAG uptake from lipoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How does epinephrine increase lipolysis in the adipose tissue?

A

By increasing HSL (hormone sensitive lipase) which will convert DAGs to MAGs :) and increase breakdown of fats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

How does epinephrine decrease TAG uptake from lipoproteins in the adipose tissue?

A

by decreasing LPL levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the mechanism that epinephrine affects adipose tissue?

A

Raise cAMP through B-adrenergic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the effects of epinephrine on the pancreas?

A

increased glucagon secretion and decreased insulin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the effects of epinephrine on the skeletal muscle?

A

increased glycolysis
decreased glycogen synthesis
increase glycogenolysis
increased TAG uptake from lipoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

How come in the skeletal muscle you get both increased glucose levels as well as increased breakdown of glucose via epinephrine?

A

Because F2,6 BP will stimulate PFK1 activity (i.e increase glycolysis) However the Kinase activity of PFK2-F2,6BPtase is sitmulated by cAMP induced phosphorylation SO what does this mean?
This means that epinephrine (which phosphorylates things) will phosphorylate PFK2 and it will act as a kinase !!! This kinase activity will stimulate glycolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

So what will catecholamines do to glycolysis?

A

increases glycolysis via B-adrenergic receptors and cAMP (in muscle ONLY)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Explain the effects of epinephrine on the pancreas, liver, adipose, and muscle

A

glycogenolysis in muscle, liver
gluconeogenesis in liver
lipolysis in adipose tissue
glycolysis in liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What hormone does epinephrine increase the secretion of?

A

glucagon (inhibits insulin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

How is cortisol regulated?

A

gene regulation

68
Q

What is this:

in large synergistic to epinephrine, but work through gene regulation and are cumulative over many hours and days

A

cortisol

69
Q

What does cortisol stimulate in the liver, protein, and adipose tissue?

A

gluconeogenesis in the liver (increased PEPCK synthesis)
Breakdown of muscle protein
TAG degredation in adipose tissue (glucose sparing)
increased glycogenesis (excess G6P from gluconeogenesis)

70
Q

What is the net effect of cortisol?

A

blood glucose restored, glycogen stores increase and you use fats (cuz glucose sparing)

71
Q

What are the negative effects of long term cortisol secretion?

A

over time destroys muscle and bone and impairs endocrine and immune function

72
Q

Explain the overall effects of glucocorticoids (i.e cortisol)

A
  • stimulate fat breakdown in adipose tissue
  • release of AAs from muscle protein
  • in the liver stimulates gluconeogenesis and glycogen synthesis
73
Q

The breakdown of liver glycogen is stimulated by what?

A

epinephrine

74
Q

How do glucocorticoids increase lipolysis?

A

increased HSL activation

Increased ATGL

75
Q

How do you increase glucose levels in the liver with glucocorticoids?

A

via PEPCK synthesis and excess G6P

76
Q

What is involved in nitrogen balance and muscle wasting?

A

glucocorticoids

77
Q

What effects the uptake and oxidation of fuels in adipose tissue, muscle and liver?

A

Growth hormone

78
Q

What is the overall action in growth hormones and what does this result in?

A

increases FFA availability for energy generation

results: indirectly spares the oxidation of glucose and amino acids

79
Q

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

A

increases epinephrine sensitivity
decreased insulin sensitivity
decreased FA esterification (making TAGs)
impairs insulin post receptor signaling
(i.e increased sensitivity and esterification)

80
Q

Since growth hormone in adipose tissue increases epinephrine sensitivity, what will be the indirect effect of this?

A

increased lipolysis (i.e. fatty acid degredation)

81
Q

Since growth hormone in adipose tissue decreases insulin sensitivity, what will be the indirect effect of this?

A

increased plasma FFA and glycerol (i.e increased lipolysis)

82
Q

Since growth hormone in adipose tissue decreases FA esterification what will be the indirect effect of this?

A

decreased TAG synthesis (remember FA esterification makes TAGS)

83
Q

Since growth hormone in adipose tissue impairs insulin post receptor signaling what will the indirect effect be?

A

decreased glucose uptake

84
Q

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

A

increased protein synthesis
increase FFA oxidation
Increased gluconeogenesis (due to increased glycerol)
decreased glycolysis

85
Q

Since GH hormone makes the liver increase protein synthesis, what will the indirect effect of this be?

A

increase IGF1 (insulin like GF effects on cell growth)

86
Q

Since GH hormone makes the liver increase FFA oxidation, what will be the indirect effect of this?

A

increased ketogenesis

remember fatty acids make ketone bodies

87
Q

Since GH hormone makes the liver increase gluconeogenesis, what will be the indirect effect of this?

A

increased glycogenesis

88
Q

What are the direct effects of growth hormone on the muscle?

A

increase FFA oxidation
increased AA transport (+ nitrogen balance)
impairs insulin post receptor signaling

89
Q

Since GH hormone makes the muscle increase FFA oxidation, what will be the indirect effect of this?

A

decrease use of glucose (since you are using FFA you wont be needing to use glucose)

90
Q

Since GH hormone makes the muscle have impaired insulin post receptor signaling, what will be the indirect effect of this?

A

decreased glucose uptake and decreased glycolysis

91
Q

Since GH hormone makes the muscle increase AA transport, what will be the indirect effect of this?

A

increased protein synthesis

allows for nitrogen balance and protein sparing

92
Q

Does T4 or T3 have a longer half life?

A

T4 (remember less potent and lasts longer)

93
Q

What are the main effects of thyroid hormones?

A

increased fuel consumption

increased sensitivity of receptors that have insulin counter-regulatory effects (i.e. glucagon)

94
Q

T or F, pathological effects of thryoid hormones are not simple extensions of physiological effects

A

T

95
Q

How will Thyroid Hormone effect the pancreas?

A

it will increase the sensitivity of beta cells and thus increase insulin release

96
Q

What are the effects of TH on adipose tissue?

A

increased epinephrine sensitivity and thus increased lypolysis
ABD
increased insulin secretion via the pancrea, thus increased glucose uptake and TAG synthesis

97
Q

Isnt it weird that you have lipid breakdown and TAG synthesis in adipose tissue when TH is around?

A

yes it is therefore the amount of glucose and insulin available determines if TAG synthesis occurs

98
Q

What are the direct effects of TH on the muscle?

A

increased Gene expression

increased epi sensitivity

99
Q

If TH causes increased Gene expression in the muscle, then what will be the indirect effect of this?

A

increased glucose uptake (via insulin)

increased protein synthesis

100
Q

If TH causes increase epi sensitivity, then what will be the indirect effect of this?

A

Increased glycogenolysis and increased glycolysis

101
Q

What are the direct effects of TH on the liver?

A

increased glycolysis, cholesterol synthesis, increase cholesterole (and bile salts), increased sensitivity to epinephrine

102
Q

If Th causes increased glycolysis in the liver, then what will be the indirect effect of this?

A

FFA being converted to TAGS in adipose tissue

103
Q

If Th causes increased sensitivity to epinephrine in the liver, then what will be the indirect effect of this?

A

increased glucose (via gluconeogenesis, glycogenolysis)

104
Q

What organ is central to metabolism?

A

liver

105
Q

20-30% of dietary glucose is metabolized in the (blank). What happens to the majority of this glucose?

A

liver

it is made into glycogen

106
Q

Does the liver have LPL?

A

NO it doesnt, so it cant take in tags, can only take chylomicron remnants

107
Q

In the liver, what is the first step in the conversion of carbs to fats

A

glycolysis

108
Q

In the liver, what kind of lipoprotein will it make all the tiem?

A

VLDL

109
Q

What is the only major fate of FAs in the mitochondria?

A

beta oxidation

110
Q

In the liver, when fatty acids undergo breakdown/oxidation, what are the two places the breakdown products can go?

A

to make ketone bodies or go into TCA cycle

111
Q

What is FA utilization controlled by?

A

substrate availability

112
Q

After a meal in the liver, carnitine palmitoyl transferase-1 (for FA degredation) is inhibited by (blank) which will result in decreased FA degredation.

A

malonyl-CoA

113
Q

After a meal in the liver, Acetyl-CoA carboxylase (FA synthesis) is stimulated by (blank) and (blank) which will result in increased FA synthesis

A

insulin (indirectly)

citrate

114
Q

3-4 hours after the meal the liver becomes a net producer of (blank)

A

glucose

115
Q

After a 12 hour fast in the liver, carnitine palmitoyl transferase 1 is induced by (blank) and there is no malonyl CoA to inhibit it. What will this do?

A

glucagon

increased FA degredation

116
Q

After a 12 hour fast in the liver, acetyl- CoA carboxylase is inhibited by (blank), (blank) and (blank) via glucagon/epi signaling.

A 
Increased acyl coA (intermediate in FA breakdown)
decreased citrate ( means your not having glycolysi)
phosphorylation
117
Q

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

A

amino acids and lactate

118
Q

After a 4 day fast in the liver, what does a high rate of beta oxidation supply?

A

ATP and NADH

119
Q

Since after a 4 day fast you have high rates of beta oxidation and thus high amounts of ATP and NADH, what will be inhibited and what will be induced?

A

TCA cycle is inhibited and ketogenic enzymes are induced

120
Q

What does malonyl-Coa inhibit?

A

Fatty acid oxidation (degredation)

121
Q

What does this do:

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

A

conversation of HMGCoA to acetoacetate

122
Q

50g of FA converted to acetoacetate supplies a lot of energy. It makes as much as (blank) grams of glucose from lactate.

A

190g

123
Q

What happens to the liver after it is re-fed after a 4 day fast?

A

start using glucose primarily and start utilizing the TCA cycle and increasing FA synthesis and glycogen synthesis and TAG synthesis

124
Q

How come in the 4 day fast stage (i.e. starvation) TCA cycle is inihibited?

A

because of high levels of ATP and NADH

125
Q

The liver converts dietary carbohydrates to (blank) and (blank)

A

glycogen and fat

126
Q

The liver supplies glucose and ketone bodies during (blank)

A

fasting

127
Q

What do adipocytes do after a mixed meal?

A 
inhibit HSL (so that you wont have FA degredation)
stimulates glucose uptake (Glut 4)
stimulates LPL (takes FA from blood and puts it into TAGS in adipocytes)
128
Q

What are active in the starved state?

A 
glycogenolysis
gluconeogenesis
lipolysis
proteolysis
ketogenesis
129
Q

How come you can have increased FA synthesiss in the adipocyte after a mixed meal?

A

because glucose will be converted to DHAP which will be converted to glycerol phosphate

130
Q

How do adipocytes respond during fasting?

A

TAGs are mobilized via increased HSL (i.e converted to FA and glycerol)
Increased Beta oxidation

131
Q

How does HSL get stimulated in the adipocytes during fasting?

A

by epinephrine

132
Q

Explain how the muscle maintains energy levels during the following stages:
Well Fed?
Fast?

A

strong and well supplies

glucose sparing and protein degradation

133
Q

Does muscle LPL get stimulated by insulin?

A

no

134
Q

In the starved state how does the brain get energy?

A

uses ketones via beta hydroxybutyrate

135
Q

Immediately after a calorie-rich meal, glucose, fatty acids, and amino acids enter the (blank). Insulin released in response to the high blood glucose concentration stimulates glucose (blank) by the tissues. Some glucose is exported to the brain for its energy needs, and some to adipose and muscle tissue. In the liver, excess glucose is oxidized to acetyl-CoA, which is used to synthesize (blank) for export as triacylglycerols in VLDLs to adipose and muscle tissue. The NADPH necessary for lipid synthesis is obtained by oxidation of glucose in the (blank). Excess (blank) are converted to pyruvate and acetyl-CoA, which are also used for lipid synthesis. Dietary fats move via the (blank) system, as chylomicrons, from the intestine to muscle and adipose tissues.

A 
liver
uptake 
fatty acids
pentose phosphate pathway
amino acids
lymphatic
136
Q

Early in fasting, the muscle uses glycogenolysis to produce (blank) rather than using blood glucose (glucose sparing)

A

ATP

137
Q

Early in fasting, the lactate produced by RBC’s and muscle are converted to (blank) in the liver

A

glucose

138
Q

Later during fasting what happens?

A

AAs from protein degredation in liver and muscle and glycerol from breakdown of TAGs in adipose tissue are used for gluconeogenesisq

139
Q

Later during fasting, the (blank) uses fatty acids as its principal fuel, and excess acetyl-CoA is converted to ketone bodies for export to other tissues.

A

liver

140
Q

During late fasting what 2 organs supply the bloodstream with glucose.

A

the liver (80%) and kidneys (20%)

141
Q

During starvation, gluconeogenesis makes how much glucose/day?

A

80-160 g glucose/day (1/2 of this is made from AAs)

142
Q

During starvation, the brain will use up to 70% (blank) for energy

A

ketones

143
Q

Assuming you have 16kg Fat
and BMR 1500kcal/day,
you can survive ≈ (blank) days
on water and vitamins.

A

100

144
Q

You lose 70-150g protein/day. When ≈1/3rd of the bodies nitrogen has been (blank) , it is too late to recover.

A

catabolized

145
Q

What process are active in the starved state?

A

glycogenolysis, gluconeogenesis, lipolysis, proteolysis, and ketogenesis

146
Q

Tell me about the metabolism of Type 1 diabetic patints

A

childhood autoimmune disease due to destruction of pancreatic beta cells which makes them insulin dependent.
Pnts tend to be thin

147
Q

Why are type 1 diabetic patients typically thin?

A

lipolysis in adipose tissue is constantly stimulated cuz theres no insulin to shut it down.

148
Q 
Explain how all of these will be affected (i.e either increase or decrease) in type 1 diabetic patients:
glycolysis
gluconeogenesis
glycogen synthesis
glycogenolysis
FA synthesis
FA oxidation
A 
decreased glycolysis
increased gluconeogenesis
decreased glycogen synthesis
increased glycogenolysis
decreased FA synthesis
Increased FA oxidation
(it will work as if they have a lot of glucagon)
149
Q

Tell me about how the liver works in type 1 diabetics?

A

liver makes glucose (glucagon)

liver cant make glycogen

150
Q

What does this describe:
Adipose and muscle do not take up glucose (no Glut4 translocation.
↑Adipose tissue lipolysis (fasting response, epi and/or cortisol).
↑ plasma FFAs.
Liver →ß oxidation of FFAs
Ketones are produced and ketoacidosis can be fatal.
Liver makes glucose (glucagon).
**Liver CANT make glycogen (glucagon → GS-P and GP-P).

A

Type 1 diabetes

151
Q

How do type 1 diabetics prevent ketoacidosis?

A

insulin injections

152
Q

What is this:
Adipose and muscle do not take up glucose (Glut4).
***Liver still makes glycogen (insulin).
Adipose tissue lipolysis is not substantially increased.
↓ LPL activity.
↑ Plasma lipoproteins.

A

Type 2 diabetes

insulin resistance

153
Q

What is an effective cure for type 2 diabetes?

A

diet and exercise

154
Q

What is this:
Complex origins, ↓ insulin receptors and altered insulin signaling.
No Ketoacidosis, but hyper-osmolarity can dehydrate the brain leading to coma.

A

Type 2 diabetes

155
Q

What is the worry with type 1 diabetes?

what is the worry with type 2 diabetes?

A

ketoacidosis (can be fatal)

hyperosmolarity resulting in dehydration in the brain and thus coma

156
Q

Protein requirements are increased during what three things?

A

growth, trauma, and illness

157
Q

(blank) can present in several forms depending on the age of the patient and the precipitating conditions, but the common feature is compromised immune function leading to decreased resistance to infection.

A

Protein/energy malnutrition

158
Q

What are xenobiotics?

A

useless foreign chemicals that have to be removed from the body such as plant metabolites, synthetic products

159
Q

Xenobiotics that are water soluble products are excreted in (blank) but lipid soluble ones are (blank)

A

urine or bile

NOT

160
Q

Lipophilic xenobiotics must be metabolized to (blank).

A

water soluble products

161
Q

Where do lipophilic xenobiotics metabolize to water soluble products?

A

liver, intestines, lungs

162
Q

What are the two phases that lipophlic xenobiotics are metabolized to water-soluble products?

A

phase 1: oxidization via addition of hydroxyl groups (this can increase or decrease toxicity)
phase 2: metabolite is conjugated with hydrophilic molecule (glucuronic acid, sulfate, glycine, glutamine, or glutathione) and inactive products are excreted

163
Q

(blank) is a superfamily of heme-containing membrane bound proteins (14 families and at least 150 isoforms).
Generally found in the smooth ER of the liver and lungs.
Inducible enzyme (can effect metabolism of other drugs).
Broad substrate specificity.
Metabolizes xenobiotics :)

A

Cytochrome P-450

164
Q

What is this:
Monooxygnease reactions with Cytochrome P-450 (electron carrier)
Substrate-H + O2 + NADPH + H+ → Substrate-OH + H2O + NADP +

A

Phase 1 of Lipophilic xenobiotic metabolism

165
Q

The phase 2 of lipophilic xenobiotic metabolism typically takes place in the (Blank)

A

liver

Block 3 Week 8 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions