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Tim's Cards > Metabolism Part 3 > Flashcards

Metabolism Part 3 Flashcards

1
Q

What cleaves sucrose in the intestine?

A

Sucrase-isomaltase

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2
Q

What does loss of Sucrase-isomaltase cause?

A

Osmotic-fermentative diarrhea

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3
Q

What gets Fructose into the enterocyte?

A

GLUT5

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4
Q

Does GLUT5 saturate?

A

Yes, quickly

but fructose is inducible

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5
Q

What transporter does Fructose use to enter the blood from the enterocyte?

A

Mostly GLUT2 (some GLUT5)

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6
Q

What does Fructose get converted into in muscle?

A

Fructose-6-Phosphate

same as glucose

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7
Q

What enzyme phosphorylates fructose in the liver?

A

Fructokinase

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8
Q

What enzyme is skipped in the fructose pathway in the liver?

What enzyme is used instead?

A

PFK-1

Fructose-1-phosphate aldolase
aka ALDOLASE B

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9
Q

Does fructose need insulin to enter the cell?

A

no

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10
Q

What does the lack of PFK-1 cause in fructose metabolism?

A

Uncontrolled manufacture of Acetyl CoA and Citrate

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11
Q

T/F

Excessive dietary intake of fructose may lead to decrease in available Pi

A

True

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12
Q

The decrease of ATP in the cell due to fructose consumption caused by lack of available phosphate causes what?

A

Breakdown of residual ADP and AMP

results in hyperuricemia and gout

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13
Q

What is the slow step in fructose metabolism?

A

Fructose-1-phosphate aldolase

aka Aldolase B

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14
Q

Fructokinase pathologies tend to be ______, while Alsolase B (Fructose-1-phosphate aldolase) pathologies tend to be ________.

A

Benign

Severe

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15
Q

What is the first step metabolite of Fructose in the muscle?

The liver?

A

Frc-6-P

Frc-1-P

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16
Q

What does Mannose (after 2 steps) metabolize into?

A

Fructose-6-P

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17
Q

What rxn traps glucose in a cell without committing an ATP?

A

Glc - Sorbitol

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18
Q

What cells build up sorbitol during hyperglycemia?

A

Cells that store sorbitol (after conversion from glc) and can’t convert that into Fructose

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19
Q

What are the effects of too much sorbitol?

A

Osmotic effects and swelling

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20
Q

What happens to galactose when it enters the cell?

What is the main substrate here?

A

Galactose is broken down (first by Galactokinase) in 4 steps to G-6-P.

UDP-galactose-4-epimerase

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21
Q

Once galactose has a UDP power pack on, what are its options?

A

Can enter glycolytic pathway or GNG

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22
Q

What 3 (main) parts of the body are affected by fluctuations in Calcium concentration?

A

neurological
gastrointestinal
renal

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23
Q

What is necessary for the absorption of dietary Calcium in the intestine?

A

Vitamin D

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24
Q

What is the main source of stored Calcium in the body?

A

Hydroxyapatite

Ca10(PO4)5OH2

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25
Q

What does lack of Calcium (hypocalcenemia) cause?

A

Tetany (contractions)

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26
Q

What is the most concentrated protein in the blood?

Name two things it carries.

A

Serum Albumin

Fatty Acids (SCFA, MCFA)
Calcium
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27
Q

T/F

If Serum Albumin levels are abnormal, calcium can’t be calculated

A

False

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28
Q

What corrects the measurement of Calcium if Serum Albumin are off?

A

Corrected Calcium (equation)

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29
Q

What are the 3 main areas that maintain calcium homeostasis?

A

Gastrointestinal tract
Kidney
Bone

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30
Q

How much calcium goes into bone every day?

How much comes out?

A

500 mg

500 mg

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31
Q

What are the 2 types of ways calcium moves out of the lumen?

A

Transcellular transport (duodenum)

Paracellular (jejunum and ilium)

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32
Q

What type of transport out of the lumen is increased if calcium intake is low?

A

Transcellular (this can be controlled)

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33
Q

Why does Vitamin D deficiency often lead to Calcium deficiency?

A

poor absorption without Vita D

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34
Q

What are 3 foods that absorb calcium in the gut and prevent Vitamin D from doing its job?

A

rhubarb, spinach, and chard.

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35
Q

What are the main hormones that reciprocally regulate calcium?

A

PTH, Calcitonin, and Vitamin D

Vitamin D is a hormone

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36
Q

UV light hits cholesterol to make?

How is this activated?

A

Cholecalciferol
2 Hydroxylations to form Calcitriol

(aka 1,25 dihydroxycholecalciferol)

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37
Q

The key enzyme in Vitamin D activation controlled by PTH levels is?

A

1-Alpha-Hydroxylase

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38
Q

Where do the 2 hydroxylations that create activated Vitamin D occur?

A

Liver (1st hydroxylation)

Kidney (2nd hydroxylation forming Calcitriol)

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39
Q

What molecule, under the direct control of Vitamin D, mediates the transport of Calcium across the enterocyte (apical to basolateral)?

A

Calbindin-D9k

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40
Q

What is the rate limiting step of calcium transport?

A

Calbindin-D9k moving Calcium across the enterocyte

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41
Q

What 2 ways does Calcium enter the blood from the enterocyte?

A

via an ATP pump
(1 Ca++ out / 2 H+ in)

Na+/Ca++ exchanger
(3:1)

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42
Q

What often mediates intracellular calcium?

Are these under the control of Vitamin D?

A 
Troponin C (muscle)
Calmodulin (other cells)

*theses are calcium binding proteins

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43
Q

What has greater effects, PTH or Calcitonin?

A

PTH

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44
Q

Where is Calcitonin produced?

How long is the polypeptide?

A

Parafollicular (C) cells of Thyroid

32 AA and linear

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45
Q

T/F

Transcellular transport of Calcium is regulatable, while Paracellular is not.

A

True

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46
Q

Where does Paracellular transport take place?

A

Across tight junctions

and down the concentration gradient

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47
Q

What 3 things does Calcitriol (Vita D) control in the enterocyte?

A

Transporters on luminal (apical) side
Transporters on basolateral side
Calbindin (which takes it across the cell)

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48
Q

What are the epithelial Calcium channels called that go from lumen to enterocyte?

A

TRPV5 and TRPV6

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49
Q

What is the main cause of Hypocalcemia?

A

Vitamin D deficiency

rickets!

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50
Q

What are the 2 main counter regulatory hormones to insulin?

A

Glucagon

Epinepherine

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51
Q

Name 5 catabolic compounds that counter the action of insulin:

A 
Glucagon 
Epinepherine
Norepinepherine
Cortisol
Growth Hormone
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52
Q

What is the rate limiting step of Epinepherine synthesis and release?

What is the rxn?

A

Tyrosine Hydroxylase

Tyrosine > Dopa

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53
Q

Where does the rate limiting step of epinepherine synthesis occur?

A

Adrenal Medulla

chromaffin cells

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54
Q

What type of membrane transduction does epinepherine work through?

A

GPCR

G-Protein compound receptor

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55
Q

What are epinepherine’s effects in the:
pancreas?
adipose?

A

Pancreas - inhibits insulin release and stimulates glucagon release

Stimulates lipolysis

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56
Q

What are epinepherine’s metabolic effects in the liver and muscle?

A

Liver: increase GNG
Muscle: increase glycolysis

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57
Q

What is produced at the islets of Langerhans?

A

Glucagon - by the Alpha cells
Insulin - by the Beta cells

also, Somatostatin by the Delta cells

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58
Q

T/F

The pancreatic hormones have only endocrine effects.

A

False

also have local autocrine and paracrine effects

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59
Q

What is given to diabetics to counteract hypoglycemia?

A

Glucagon

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60
Q

What is Proglucagon broken down into in the pancreas and in the intestine?

A

pancreas: Glucagon
intestine: GLP-1 (and also GLP-2 and Oxyntomodulin)

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61
Q

What is the major target of Glucagon?

What is the mechanism to enter the cell?

A

Liver

G-protein second messengers

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62
Q

What are glucagon’s effects on:
glycogen phosphorylase
glycogen synthase
PFK-1?

A

increase
decrease
decrease

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63
Q

What are glucagon’s effects on:
Frc-1-6-BP
Pyruvate kinase
Triacylglycerol lipase

A

increase
decrease
increase

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64
Q

Insulin has 1/2 life of 5 minutes. How can we more easily measure insulin release clinically?

A

C-peptide from the “Prepro” hormone

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65
Q

Describe insulin’s effects on target cells.

A

Insulin binds outside

Tyrosine Phosphorylated

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66
Q

After phosphorylation, what is the most important downstream effect of Insulin binding?

A

Translocation of GLUT4 to the membrane

this allows Glc to enter cell

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67
Q

What is one of the effectors of GLUT4 inside the cell after Insulin binding?

A

P13-kinase

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68
Q

T/F

Insulin features prominently in the uptake of ions such as K+ and PO4-3.

A

True

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69
Q

What senses glucose in the pancreas?

A

GLUT2 (ferrari)

Glucokinase

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70
Q

What is the pathway leading to insulin release at a Beta cell?

A 
Glc enters through GLUT2
Glycolysis creates ATP
ATP shuts down K+ channel
depolarization opens Ca++ channel
Calcium stimulates insulin release
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71
Q

What is the insulin and glucagon response following a high carbohydrate meal?
a high protein meal?

A

carb: Insulin up, glucagon down
protein: Insulin AND glucagon up

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72
Q

What 3 Amino Acids stimulate the release of Insulin?

A

AGR
alanine
glycine
arginine

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73
Q

How do A, G, and R AA’s depolarize Beta cells?

A

Alanine & Glycine - Na+ symport depolarizes

R (arginine) - dedicated transport protein. Arg is a cation and depolarizes cell directly

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74
Q

What class of substances is responsible for the greater insulin response when taken orally?

A

Incretins

remember: GLP-1 and the Gila monster

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75
Q

What is the coenzyme in catecholimine rate limiting step?

epinepherine

A

Tetrahydrobiopterin > Dihydrobiopterin

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76
Q

What is the function of GLP-1 in the liver?

remember: this comes from Proglucagon

A

Enhances Insulin effects

also Gila monster drug - (Incretins)

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77
Q

What are the body’s priorities after a meal?

A
  1. Replenish glycogen stores
  2. store fat
  3. increase protein reserves
78
Q

What are the body’s 2 biggest goals when hungry?

A
  1. Brain and CNS (GNG, etc)

2. Conserve protein

79
Q

What are the 2 main sources of fuel during fasting (1 hr after meal)?

A

Liver glycogenolysis - glc

Adipose Lypolysis - fat

80
Q

In a progression of fasting (beyond a few hours), what does the liver also make (besides breaking down glycogen)?

A

GNG pathways are activated

81
Q

If a fast continues for 2 or more days, what occurs in the muscle and brain?

A

Muscle switches off ketone bodies (oxidizes fatty acids) so they can go to the brain.

82
Q

When is glc not the sole fuel for the brain?

A

prolonged starvation

83
Q

Why does skeletal muscle produce lactate when actively contracting?

A

Glycolysis much faster than CAC so buildup of product.

84
Q

What does resting muscle preferentially metabolize?

A

Fatty acids

85
Q

T/F

Heart has glycogen reserves

A

false

86
Q

What is the main source of fuel for the heart?

A

fatty acids

ketone bodies/lactate CAN fuel the heart

87
Q

What is the glycolytic intermediate in adipose tissue necessary for synthesis of TAG’s?
(somehow leads to CoA derivative transfer to glycerol-3-P)

A

dihydroxyacetone phosphate

88
Q

Why are Fatty Acids released into the blood if glucose levels are low?

A

No glycerol-3-Phosphate for TAG synth

89
Q

What organ provides half GNG during starvation?

A

Kidney

90
Q

What are the main precursors to GNG in liver?

A

Lactate and Alanine from muscle
glycerol from adipose
glucogenic AA’s from diet

91
Q

What does the liver make ketone bodies out of in the fasting state?

A

Fatty Acids

92
Q

What prevents Fatty acids from entering the mitochondrial matrix?

A

Malonyl CoA

this is fed state and FA’s exported to adipose

93
Q

What allows the passage of Fatty Acids into the mitochondrial matrix to make ketone bodies under low energy conditions?

A

Low levels of Malonyl CoA

94
Q

The liver absorbs most of the AA’s from the blood. What is the priority for use?

A

Protein synthesis

rather than catabolism

95
Q

What three AA’s are processed in muscle rather than liver?

A

Leucine, Isoleucine, and Valine

LIV

96
Q

What does the liver use as its main energy source?

A

Alpha-Ketoacids

glycolysis are building blocks and ketogenics are exported

97
Q

Does Adipose tissue undergo Beta-oxidation?

A

Negative

exports FA’s for breakdown in other tissues

98
Q

T/F

Glucagon inhibits Insulin (but not vise versa)

A

FALSE
Insulin inhibits glucagon

Glucagon does not inhibit insulin
(if glucagon levels are high reasonable to assume meal is just around the corner)

99
Q

How long do glycogen stores last?

A

12-18 (maybe 24) hours

100
Q

What does muscle preferentially use for energy if Glucagon is high?

A

FAT

101
Q

What does skeletal muscle use for energy in the first few days of not eating?

A

Fat, Ketone bodies (reach highest level at Day 3), Fat

this allows ketone bodies to go to the brain
(GNG decreases and spares muscle)

102
Q

What 2 energy sources remain constant in fasting Day 3 to 40?

A

Adipose lypolysis

Ketone body formation

103
Q

Why does urea excretion go down with prolonged fasting?

A

Preserve water and muscle (as much as possible)

104
Q

Why does the liver lag in the uptake of Glc after a meal?

A

leaves it for peripheral tissues

stays in GNG mode for glycogen synth

105
Q

What is the Master Switch (energy sensor enzyme)?
What activates?
What does it do?

A

AMPK

high levels AMP

produces ATP
(and shuts down processes using ATP)
106
Q

What, specifically, does AMPK do?

A

phosphorylates rate-limiting enzymes in energy using/producing pathways

(senses cellular energy levels)

107
Q

Define:
polyuria
polydipsia
polyphagia

A

Lots of urine
thirsty
hungry

108
Q

What part of insulin can be detected longer?

A

C-peptide

109
Q

What lipid enzyme does insulin stimulate?

A

Acetyl CoA Carboxylase

110
Q

Why are you sleepy after a meal?

A

Insulin actually makes blood slightly hypoglycemic

111
Q

Frequency of Ketosis in Type 1 vs Type 2 diabetes?

A

Type 1 - common

Type 2 - rare

112
Q

Why is Type 1 diabetes unresponsive to oral drugs treating hypoglycemia?

A

No insulin whatsoever

113
Q

What cells are totally eliminated (eventually) in Type 1 diabetes?

A

Beta cells

114
Q

What cell receptor needs insulin for fat uptake?

A

Lipoprotein Lipase

115
Q

What two states characterize type 2 diabetes?

A

insulin secretion deficit

insulin resistance

116
Q

The curve of insulin output in Type 2 diabetes is due to:

A

Burnout of Beta cells

117
Q

Why is ketoacidosis less of an issue with Type 2 diabetes?

A

There’s still a little insulin

118
Q

How is hyperglycemia measured?

A

Hemoglobin A1c

119
Q

What 3 conditions must be met for sorbitol to do real damage?

A
  1. Diabetic
  2. tissue must be able to take up glc without insulin
  3. tissue lacks ability to take sorbitol to fructose
120
Q

What enzyme makes sorbitol from glucose?

A

Aldose reductase

121
Q

What comprises metabolic syndrome?

A

Hyperglycemia
low HDL
Apple fat
high TAG’s

122
Q

Preproinsulin is synthesized in the:

Proinsulin breaks down to Insulin and C-peptide in the:

A

ER

Golgi

123
Q

What makes up insulin structurally?

A

Alpha and Beta chains attached by two disulfide bonds

124
Q

What type of adipocytes are more hormonally responsive and have a greater impact on the liver?

A

Abdominal

125
Q

What receptor increases with the amount of fat you store?

A

Lipoprotein Lipase

note: this sticks around after losing weight so more efficient at storing fat

126
Q

Obesity is a disease of chronic…

A

Inflammation

127
Q

Name 3 Adipokines that increase with obesity and one that does not.

A

Leptin, TNf-alpha, IL-6

Adiponectin

128
Q

What two Adipokines induce insulin resistance?

A

TNF-alpha

IL-6

129
Q

Does leptin increase with weight?

A

It should be proportional to adipose tissue.

130
Q

What does a lot of leptin signal?

What does low levels of leptin signal?

A

Leptin signals the brain and tells you you’re full, so low amounts signals to slow down, don’t eat, stay on the couch.

131
Q

What suggests human obesity isn’t related to the amount of Leptin?

A

Trials negative (positive with mice and that kid in Turkey)

This suggests the brain’s resistance to Leptin

132
Q

What adipokine decreases inflammation?

A

Adiponectin

133
Q

What structure in the brain is responsible for integrating hunger/satiety signals?

A

Hypothalamus

134
Q

What structure in the brain is associated with overeating and obesity?

A

Damage to
Ventromedial or
Paraventricular nuclei

(VM and P of the hypothalamus)

135
Q

What part of the hypothalamus is often damaged in weight loss and anorexia?

A

Lateral Hypothalamic

136
Q

What two types of neurons in the hypothalamus regulate appetite?

A

Orexigenic (go eat)

Anorexigenic

137
Q

Name 2 Orexigenic neurons:

A 
Neuropeptide Y (NPY)
Agouti related protein  (AgRP)

(these nerves signal the proteins they’re named for)

138
Q

What are the two Anorexigenic neurons in the hypothalamus?

One has an important derivative:

A

POMC (pro-opiomelanocortin)
CART (cocaine/amphetiamine regulated transcript)

note: POMC processed to alpha-MSH (melanocyte stimulating hormone)

139
Q

What does Leptin stimulate and inhibit in the hypothalamus?

A

stimulates anorexigenics:
POMC/MSH

inhibits orexigenics:
NPY/AgPR

140
Q

What acts in a similarly to Leptin in the hypothalamus?

A

Insulin

can’t go far wrong thinking Insulin and Leptin do the same thing

141
Q

Name 2 molecules in the intestine that act as satiety signals to the brain?

A

CCK
GLP-1

(note: GLP-1 signals brain and pancreas)

142
Q

What are the functions of GLP-1?

A

acts as satiety signal to the brain
incretin for insulin and pancreas

(increases insulin secretion, biosynth, B-cell proliferation, B-cell survival)

143
Q

What is the peptide hormone that acts as an appetite stimulant originating in the stomach?
What are its actions on the brain?

A

Ghrelin

binds/stimulates NPY/AgPR/GABA neurons

(orexigenic = glucagon-like)

144
Q

Under normal circumstances what occurs in cells in response to weight gain?

A

Cells grow larger (hypertrophy)

145
Q

Under what circumstances do we see new adipocytes forming instead of just increasing in size?

A

Severe obesity

146
Q

Where is alcohol generally oxidized?

A

80-90% in the liver

147
Q

What part of the GI tract absorbs alcohol?

What part is most effective?

A 
All parts 
small intestine (because of large surface area)
148
Q

Does alcohol require a transporter to enter cells?

A

NO

149
Q

T/F

15% alcohol eliminated in sweat, urine, feces, breath, saliva, and lactation.

A

False

10%

150
Q

What is the main enzyme used by “naive” alcohol consumption?

Where does this occur?

A

Alcohol dehydrogenase

Cytosol

151
Q

What system is used in habitual drinkers to metabolize alcohol?

Where does this take place?

A

Cytochrome P450
(MEOS)

Smooth ER

152
Q

What are the major and minor routes of ethanol oxidation?

A

Major:
Alcohol dehydrogenase in cytosol
Cytochrome P450 (MEOS) in Smooth ER

Minor:
Catalase dependent oxidation in Peroxisome
Gastric Oxidation (first pass) in stomach

153
Q

What do the metabolic routes of ethanol processing have in common for both habitual and “naive” drinkers?

A

Both seriously deplete NAD+

154
Q

dehydrogenase =

A

redox

155
Q

What are the two main steps of ethanol metabolism?

Where do they occur?

A

cytosol:
Ethanol > Acetaldehyde
(Alcohol dehydrogenase)

mitochondria:
Acetaldehyde > Acetate
(Aldehyde dehydrogenase - ALDH2)

156
Q

Why is acetaldehyde damaging to the cell?

A

creates many adducts

increases ROS

157
Q

What does ethanol consumption do to the following rxn:

pyruvate + NADH > lactate + NAD+

A

Le Chat pushes toward lactate due to 10 fold increase in NADH

158
Q

What is the product Acetate (from ethanol met.) converted into?

A

Acetyl CoA

*requires GTP

159
Q

Cytochrome P450 aka:

A

CYP2E1

160
Q

What can ROS/Acetaldehyde from ethanol metabolism damage?

A

proteins
causes lipid peroxidation
Mutagenic/Carcinogenic
DNA repair

161
Q

What cofactor does Alcohol Dehydrogenase carry?

A

Zinc metalloprotein

162
Q

How many genes code for how many classes of Alcohol Dehydrogenase and which one has the lowest Km?

A

7 genes
5 classes

lowest Km (highest affinity) is Class I in the liver
*this is the major one
163
Q

What is a major contributor to the variation we see in ability to metabolize alcohol?

A

ALDH2 variants

164
Q

Pretty much all the biochemical downstream side effects of ethanol ingestion is due to:

A

Decreased NAD+/NADH ratio

165
Q

Why does alcohol cause hypoglucemia?

A

excess NADH prevents GNG in liver

166
Q

What are 4 major consequences of decreased NAD+/NADH ratio?

A

Hypoglicemia (GNG suppressed)
Lactic Acidemia
Ketonemia (lots Acetyl CoA, no glycogen, no GNG)
Hyperuricemia (ketones/lactate compete with uric acid for renal pump)

167
Q

Why does alcohol cause dehydration?

A

inhibits ADH

168
Q

How does alcohol affect protein trafficking?

4 ways

A

Fatty liver (acetaldehyde adducts tubulin)
Protein secretory/plasma mem. assembly impaired
VLDL export decreased
*receptor mediated endocytosis affected

169
Q

What does alcohol consumption do to the major excitatory and inhibitory neurotransmitters?

A 
Inhibits Glutamate (excitatory)
 - uncoordination, speech, memory
Enhances GABA (inhibitory)
 - anxiety reduction and sleep
170
Q

Are most alcoholics malnourished?

A

no

171
Q

What 3 vitamin deficiencies do alcoholics often have?

A

Thiamin (B1)
Folic Acid
Vitamin A

172
Q

What syndrome is associated with decreased thiamin levels due to alcohol consumption?

A

Wernicke-Korsakoff syndrome

173
Q

Folic acid depletion leads to…

A

anemia

174
Q

Why is Vitamin A deficiency seen upon alcohol consumption?

A

Retinol (Vitamin A) degraded by MEOS

resembles alcohol just enough

175
Q

T/F

Alcohol has a greater overall effect on women

A

True

176
Q

Which vitamins are water soluble?

A

B and C

total of 9

177
Q

What are the fat soluble vitamins?

A

ADEK

178
Q

What is the most important Vitamin?

A

D

*calcium and bloot clotting

179
Q

What is Vitamin A important for?

A

growth, immune system, vision

180
Q

What is Vitamin C important for?

A

Collagen/scurvy

*hydroxylation step in collagen synth

181
Q

Vitamin B1:
name
pathology

A

Thiamine

Beriberi, Wernicke Korsikoff

182
Q

Vitamin B2
name
pathology

A

Riboflavin

mouth lesions and dermatitis

183
Q

B5
name
pathology

A

Pantothenate

Hypertension

184
Q

B6
name
pathology

A 
Pyridoxal phosphate
(*aminotransferases)

Depression, confusion, convulsions

185
Q

B7
name
pathology

A

Biotin

rare rash/fatigue

186
Q

B9
name
pathology

A

Folate

anemias

187
Q

B12
name
pathology

A

Cobalmin

anemias

(*Odd Homo Meth)

188
Q

B3
name
pathology

A

NAD - Niacin

Pellagra (dermatitis, depression, diarrhea)

189
Q

Vitamin A
name
pathology

A

Retinol

Night blindness

190
Q

Vitamin D
name
pathology

A

Calcitriol

Rickets, osteomalacia

191
Q

Vitamin E
name
pathology

A

tocopherol

Erythrocyte hemolysis (newborns)

192
Q

Vitamin K
function
pathology

A

synth prothrombin and clotting factors

difficulty in blood coagulation (takes a long time)

Tim's Cards (140 decks)

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