Week 3 Biochemistry Flashcards

1
Q

Gluconeogenesis enzyme activity is activated by ______ and slowed down by _________

A

Gluconeogenesis is turned on by glucagon and slowed down by insulin.

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2
Q

Where does gluconeogenesis occur?

A

LIVER (95%) and kidney.

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3
Q

Gluconeogenesis activity is highest when _______

A

Fasting

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4
Q

What molecules inhibit Complex IV in the ETC? This inhibits the reduction of _____ to _______

A

Cyanide (CN-) and carbon monoxide (CO) poisoning. It inhibits the reduction of 1/2 O2 to H2O and cell cannot generate ATP.

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5
Q

What do uncoupling agents in the ETC inhibit?

A

Uncoupling agents inhibit the formation of a proton gradient so H+ does not go through ATP synthase.

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6
Q

Which of the following is NOT a substrate of gluconeogenesis?

  • lactate
  • glycerol
  • acetyl CoA
  • alanine
  • aspartate
  • glutamate
A

Acetyl coA is NOT a substrate for gluconeogenesis. You cannot use fatty acids (acetyl coA precursors) to form glucose through this pathway.

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7
Q

Signaling from _________ and __________ can increase gene expression for gluconeogenesis enzymes (i.e. PEP carboxykinase) when starving or stressed.

A

Glucagon when starving, and cortisol when stressed

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8
Q

95% of gluconeogenesis takes place in what organ?

A

95% in Liver. 5% in kidneys

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9
Q

What molecules are used to form gluconeogenesis?

A

Lactate, glycerol, and glucogenic amino acids

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10
Q

Can acetylCoA form glucose?

A

NO! It is part of the TCA/Kreb cycle

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11
Q

Within the liver, what enzyme cleaves what molecule to form glucose?

A

glucose-6-phosphatase cleaves glucose-6-phosphate to make glucose

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12
Q

What does a deficiency in glucose-6-phosphatase cause?

A

It prevents the glucose-6-phosphate from being cleaved to make free glucose. This is known as Van Gierke’s disease.

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13
Q

When muscles use glucose to form ATP what is the byproduct and where does it go once it is formed?

A

The byproduct is lactate and it goes to the liver to become part of gluconeogenesis.

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14
Q

Within the pentose phosphate pathway, glucose-6-phosphate dehydrogenase (G6PDH) is responsible for forming what molecule?

A

NADPH!

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15
Q

Why is a deficiency in glucose-6-phosphate dehydrogenase in red blood cells bad?

A

Bc it causes the RBC to be more susceptible to damage by reactive oxygen species due to it’s inability to produce NADPH which reduces GSSG to GSH so it can give up electrons to free radicals (preventing H2O2’s conversion to water).

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16
Q

Transketolase, an enzyme in the PP pathway, requires what special cofactor? And its activity within RBC’s is reflected by the status of what vitamin?

A

Cofactor: Thiamine pyrophosphate (TPP)

Vitamin: B1

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17
Q

What are the two main functions of pentose phosphate pathway (PPP)?

A

To produce:

  1. NADPH (a reducing agent)
  2. Ribose-5-phosphate (for nucleotide biosynthesis)
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18
Q

Where is glucose stored?

A

You just fell for the oldest trick in the book! Glucose cannot be stored bc it is so-o-o water soluble, so it must be converted to the insoluble polymer GLYCOGEN. The most important storage spaces for GLYCOGEN are the liver and skeletal muscles.

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19
Q

When do you want glycogen synthase to be active?

A

After a mean when insulin is high to promote glycogen synthesis.

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20
Q

Glucagon promotes the phosphorylation of what molecule to make glucose?

A

Glycogen synthase

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21
Q

Where does alpha-amylase hydrolyze glycogen or starch?

A

In the mouth and small intestine (from the pancreas)

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22
Q

Which enzyme within the human body breaks down cellulose?

A

Trick question. What do you think we are cows? We can’t break down the beta-1,4 linkages in cellulose!

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23
Q

What will happen if we do not have the enzyme lactase in our bodies?

A

The gut is unable to break down lactose in the small intestine. Instead it is transported to the large inestine where it will be broken down by bacteria which will cause bloating, diarrhea, and dehydration.

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24
Q

Describe the flow of glucose into the cell.

A

Glucose is driven against its concentration gradient by coupling to Na+. Once glucose enters, Na+ is driven out of the cell as K+ enters the cell driven by the dephosphorylation of ATP. This allows glucose to also leave the cell and go into the blood stream.

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25
Q

Name the disaccharides that can be absorbed.

A

Trick question. Only MONOsaccharides can be absorbed by the by.

26
Q

What priming enzyme helps turn glucose into glucose-6-phosphate within glycolysis?

A

Hexokinase

27
Q

What priming enzyme helps turn fructose-6-phosphate into fructose-1,6, bisphosphate?

A

Phosphofructokinase

28
Q

What are the products of glycolysis?

A

4 ATP, 2 NADH, & 2 Pyruvate

29
Q

What happens to glycolysis under anaerobic conditions?

A

NADH is produced but it is unable to be used for phosphorylation which causes a build up of NADH. The build up of NADH prevents glycolysis so NADH is converted to NAD+ to allow glycolysis to ensue and pyruvate is reduced to lactate then sent to the liver.

30
Q

What three hormones control blood glucose levels?

A

Insulin, glucagon, and epinephrine.

31
Q

High amounts of what molecule(s) will down regulate glycolysis?

A

ATP! and others include H+, citrate, and alanine

32
Q

High amounts of what molecule(s) will up regulated glycolysis?

A

F-1,6-BisP, F-2,6-BisP, and AMP

33
Q

What enzymes can be used to phosphorylate glucose into G-6-P within the liver? Which one is specific to the liver?

A

Hexokinase and glucokinase

Glucokinase is specific to the liver.

34
Q

For glucokinase to be active, it needs _______ concentration of glucose bc it has a ________ affinity to glucose.

A

It needs HIGHER concentration of glucose bc it has a LOWER affinity to glucose.

35
Q

When is glucokinase active?

A

Only after a meal when glucose concentration is high.

36
Q

High insulin to glucagon ratio (after a meal) stimulates the liver to _________

A

To store glucose as glycogen

37
Q

Low insulin to glucagon ratio (fasting) stimulated the liver to __________

A

To degrade glycogen and release glucose into the blood stream.

38
Q

What is the role of glucagon?

A

To oppose insulin and turn glycogen into glucose

39
Q

Where does aerobic/oxidative glucose catabolism take place?

A

Mitchondria

40
Q

Where does the ETC occur?

A

In the inter-membrane space of the mitochondria

41
Q

Where does the TCA (Kreb) cycle occur?

A

In the matrix of the mitochondria

42
Q

Name the two key enzymes of the TCA (Kreb) cycle?

A
  1. Pyruvate dehydrogenase complex (turning pyruvate –> acetyl-CoA)
  2. Alpha ketoglutarate dehydrogenase complex (turning alpha ketoglutarate –> succinyl-CoA
43
Q

What are the required cofactors for the key TCA enzymes?

A
  1. Thiamine pyrophosphase (TPP) (vit B1)
  2. Lipoic acid
  3. CoenzymeA
  4. NAD+/NADH
  5. FAD/FADH2
44
Q

Which molecules regulated the TCA?

A

Activate: NAD+ and ADT
Inhibit: NADH and APT

45
Q

What are the two main molecules the TCA produces?

A

ATP and NADH

46
Q

GPCRs are ________ plasma membrane proteins with 7 ___________ transmembrane segments

A

Integral membrane proteins with 7 alpha helical transmembrane segments.

47
Q

________—> GPCR —> ________ —–> 2nd messengers —-> many intracellular effectors

A

Ligand —> GPCR —> G Protein —–> 2nd messengers —-> many intracellular effectors

48
Q

T/F: When G protein alpha is bound to GDP it is active

A

False. It is activated after a nucleotide exchange (NOT phosphorylation) and it is bound to GTP.

49
Q

How does G alpha become inactivated?

A

G alpha acts as a timer and enzyme (GTPase) and slowly cleaves the bound GTP to give GDP (loses Pi).

50
Q

What is the 2nd messenger in the Gs pathway?

A

cAMP is the second messenger that starts the signaling cascade.

51
Q

_______ activates PKA which then __________ proteins.

A

cAMP activates PKA which then phosphorylates proteins

52
Q

What is the target of the cholera toxin? How does this cause diarrhea?

A

G alpha-GTP is target, it cannot be hydrolyzed, remains active inducing cAMP production thus PKA activation. PKA overstimulated, opens CFTR protein causing loss of Cl- and so water as well.

53
Q

Pertussis targets the _______ which turns it (on/off).

A

Pertussis targets G alpha i/o which turns it off.

54
Q

What is the equation for t1/2?

A

t1/2 = 0.693 x Vd / CL

Where Vd = volume of distribution
CL = clearance

55
Q

What is the equation for dosing rate?

A

dosing rate= CL x Cp

Where CL = clearance
Cp = plasma drug concentration

56
Q

What is the equation for loading dose?

A

loading dose = Vd x Cp

Where Vd = volume of distribution
Cp = plasma drug concentration

57
Q

What are chylomicrons? Where do they first circulate, then where do they go?

A

After a meal, when digest fatty acids (FA) and absorb them into the cells, chylomicrons are the particles that pick up and transport the FA. They first circulate through the lymph then into the blood stream.

58
Q

What is the job of lipoprotein lipase?

A

Lipoprotein lipase breaks down the triglyceride to form fatty acids and glycerol.

59
Q

Where will fatty acids be used as energy and where will it be stored?

A

Muscles use fatty acids for energy and fatty acids get stored in adipocytes.

60
Q

What is the pathway of lipoproteins from the liver to the peripheral cells?

A

Liver (FA –> TG –> VLDL) –> Blood stream (VLDL –> Broken down to FA & Glycerol –> IDL –> LDL) –> peripheral cell.

61
Q

Name the location of fatty acid biosynthesis? Where are they degraded (oxidized)?

A

Biosynthesized in the cytosol and degraded in the mitochondria.