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Biochemistry 2019 > Lecture 33 > Flashcards

Lecture 33 Flashcards

1
Q

State the 3 metabolism molecules where the cell makes “a decision”.

A
  1. Glucose-6-phosphate:
  2. Pyruvate:
  3. Acetyl-CoA
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2
Q

For Glucose-6-phosphate, explain the 2 available “decisions” the cell can make in terms of where to go with metabolism from here.

A

glucose-6-phosphate:
1. Enter glycolysis and become Fructose-6-phosphate

  1. Enter gluconeogenesis and become Glucose-1-phosphate
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3
Q

For Pyruvate, explain the 4 available “decisions” the cell can make in terms of where to go with metabolism from here.

A

Pyruvate:
1. Enter TCA cycle (to make energy) and become Acetyl-CoA

  1. Enter Fermentation (to make less energy) and become Lactate
  2. Enter Gluconeogenesis and become OAA
  3. Enter AA synthesis and become Alanine
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4
Q

For Acetyl-CoA, explain the 3 available “decisions” the cell can make in terms of where to go with metabolism from here.

A

Acetyl-CoA:
1. Enter TCA cycle and Ox-Phos and become CO2 + H2O

  1. Enter Ketone body Synthesis and become a ketone (Acetoacetate, Acetone, or Beta-Hydroxybutyrate)
  2. Enter FA synthesis and become a FA (TAG)
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5
Q

Describe what the following organ does in terms of fuel reserves it may have and energy pathways it may conduct.

Liver

A

Fuel reserves: TAGs and Glycogen

Pathways: 
Glycolysis
Gluconeogenesis
Beta-oxidation
FA synthesis
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6
Q

Describe what the following organ does in terms of fuel reserves it may have and energy pathways it may conduct.

Muscle

A

Fuel Reserves: Glycogen and Protein

Pathways: 
Beta-oxidation
Glycolysis
Proteolysis
TCA cycle
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7
Q

Describe what the following organ does in terms of fuel reserves it may have and energy pathways it may conduct.

GI (intestines)

A

Fuel Reserves: none

Pathways: none

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8
Q

Describe what the following organ does in terms of fuel reserves it may have and energy pathways it may conduct.

Brain

A

Fuel Reserves: none

Pathways:
Glycolysis
TCA cycle

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9
Q

Describe what the following organ does in terms of fuel reserves it may have and energy pathways it may conduct.

Heart

A

Fuel Reserves: none

Pathways:
Beta-oxidation
TCA cycle

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10
Q

Describe what the following organ does in terms of fuel reserves it may have and energy pathways it may conduct.

Adipose tissue

A

Fuel Reserves: TAGs

Pathways:
Beta-oxidation
TAG synthesis

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11
Q

State the 3 tissues that store energy molecules and the 3 that make energy molecules

A 
Store energy molecules:
Skeletal Muscle (at rest), Adipose, and Liver
Make energy molecules:
Skeletal Muscle (during exercise), Adipose, and Liver
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12
Q

For Brain tissue, state its
Fuel Reserves:
Preferred Fuel: (include it normally and during starvation)
Fuel sources exported:

A

Fuel Reserves: none

Preferred Fuel: Glucose (ketone bodies during starvation)

Fuel sources exported: none

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13
Q

For Skeletal Muscle tissue at rest, state its
Fuel Reserves:
Preferred Fuel:
Fuel sources exported:

A

Fuel Reserves: Glycogen and Protein

Preferred Fuel: FAs

Fuel sources exported: none

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14
Q

For Skeletal Muscle tissue during exercise, state its
Fuel Reserves:
Preferred Fuel:
Fuel sources exported:

A

Fuel Reserves: none

Preferred Fuel: glucose

Fuel sources exported: Lactate

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15
Q

For Heart Muscle tissue, state its
Fuel Reserves:
Preferred Fuel:
Fuel sources exported:

A

Fuel Reserves: none

Preferred Fuel: FAs

Fuel sources exported: None

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16
Q

For Adipose tissue, state its
Fuel Reserves:
Preferred Fuel:
Fuel sources exported:

A

Fuel Reserves: TAGs

Preferred Fuel: FAs

Fuel sources exported: FAs (TAGs) and Glycerol

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17
Q

For Liver tissue, state its
Fuel Reserves:
Preferred Fuel:
Fuel sources exported:

A

Fuel Reserves: TAGs and Glycogen

Preferred Fuel: Glucose, FAs, or AAs

Fuel sources exported: FAs, Glucose, and Ketone Bodies

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18
Q

State the fuel that is produced by these 3 fuel producers of the body.

Liver:
Adipocytes:
Kidney:

A

Liver: Glucose

Adipocytes: FAs

Kidney: Glucose (during starvation only)

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19
Q

State the fuel molecules in order of most preferred to least preferred for the following tissues.

Skeletal Muscle:
Brain:
Heart:

A

Skeletal Muscle: Glycogen then Creatine Phosphate then Lactate

Brain: Glucose then Ketone bodies

Heart: FAs then Lactate/Ketone bodies

20
Q

True or False:

The Primary fuel for Liver tissue is Glucose. explain.

A

False.

The primary fuel for Liver tissue is FAs, however it can use Glucose or even AA’s if it needs to

21
Q

Explain how fed and fasting states affect the reaction rate of glucokinase in in the liver and what the liver is synthesizing.

A

Fed State: increases the glucokinase reaction rate
FA’s (TAGs) are synthesized

Fasting State: decreases the glucokinase reaction rate
Ketone Bodies are synthesized

22
Q

Glucokinase, and enzyme only found in the liver and kidneys, has a _____Km value than Hexokinase which is found in the liver, kidneys and even muscle tissues. Explain what this difference in Km value means.

A

Higher

Since Glucokinase has a higher Km value, it takes a very large amount of glucose in the liver to reach the Vmax of glucokinase, whereas Hexokinase is almost always at it’s Vmax bc it takes small levels of glucose to reach it.

23
Q

True or False:

The liver can produce Ketone Bodies but is unable to use them as fuel. explain.

A

True:

It can make Ketone bodies from AA’s but it LACKS CoA Transferase, so it is unable to make Acetyl-CoA from Ketone bodies (therefore it cannot use Ketone bodies as fuel)

24
Q

State the 2 enzymes that are unique to the Liver and Kidneys only.

A

glucose-6-phosphatase (allows them to “complete” gluconeogenesis)

Urea Cycle Enzymes

25
Q

Describe the effect that Etoh consumption has on NAD+ levels. What pathways are affected by these low levels of NAD+ that can occur from Etoh consumption?

A

Etoh consumption decreases NAD+ levels

This decreases the activity of the following pathways
Gluconeogenesis
Glycolysis
TCA cycle
Beta-oxidation
26
Q

An increase in what 2 molecules is responsible for your hangover after drinking Etoh?

A

increased lactate and Ketone bodies (causing acidosis)

27
Q

State the time it takes to achieve the following metabolic states and the main mechanism/goal of each state

Fed:
Fasting:
Starvation:

A

Fed: begins at the conclusion of a meal
Energy production and storage

Fasting: begins 1 hr after a meal
uses PREFERRED metabolic fuel stores to provide energy (like making glucose from glycogen)

Starvation: begins around 4-5 days without food intake
uses fat stores (TAGs) and Derivatives (Ketone Bodies) to provide energy

28
Q

For the following cholesterol-containing molecules, state the origin, destination, and function of it.

Chylomicrons

A

Chylomicrons
Origin: Intestine (basically come straight from food)

Destination: Adipocytes

Function: TAG transport

29
Q

For the following cholesterol-containing molecules, state the origin, destination, and function of it.

VLDLs

A

VLDLs
Origin: Liver

Destination: Adipocytes

Function: TAG transport

30
Q

For the following cholesterol-containing molecules, state the origin, destination, and function of it.

IDLs

A

IDLs
Origin: VLDL’s

Destination: Liver and Adipocytes

Function: Intermediate molecule

31
Q

For the following cholesterol-containing molecules, state the origin, destination, and function of it.

LDLs

A

LDLs
Origin: VLDLs

Destination: All cells

Function: Cholesterol Distribution

32
Q

For the following cholesterol-containing molecules, state the origin, destination, and function of it.

HDLs

A

HDL
Origin: Liver (empty when they leave)

Destination: Liver (full when they return)

Function: Cholesterol Collection

33
Q

Explain how IDLs and LDLs are created from VLDLs

A

VLDLs are purged (TAGs are removed from them) until they form IDLs and can eventually form LDLs after more purging past the IDL stage

34
Q

Compare LDLs with HDLs in terms of “good and bad” and the protein to cholesterol composition of them

A

HDLs are the “good cholesterol” with more protein and less cholesterol in them
(these will circulate and “fill up” with excess cholesterol and return it to the liver)

LDLs are the “bad cholesterol” with less protein and more cholesterol composing them
(these circulate and deposit cholesterol throughout the body)

35
Q

What type of metabolic condition does diabetes mimic? explain how.

A

Diabetes mimics starvation conditions because during both diabetes and starvation, glucose cannot be used to provide the body with energy

(in starvation it is bc there is not glucose around to be used)
(indiabetes its bc insulin issues do NOT bring glucose into the cell)

36
Q

State the 3 enzymes that are considered master regulator molecules of metabolism. Then state the 7 Hormones that are considered master regulator molecules of metabolism

A

Enzymes: “SAM” mnemonic
Sirtuins
AMPK
mTOR

Hormones: "I Get Lost PAGE"
Insulin
Glucagon
Leptin
PYY3-36
Adiponectin
Ghrelin
Epinephrine
37
Q

State 2 Serine/Threonine kinases with opposite functions that regulate metabolism. Which of these is active in the fed state and which is inactive in the fed state?

A

AMPK and mTOR

mTOR is active in the fed state (bc it triggers anabolic activity)

AMPK is inactive in the fed state (bc it triggers catabolic activity)

38
Q

For AMPK and mTOR, state what molecules activate and inhibit each of them.

A

AMPK:
Increased AMP activates it
Increased ATP Inhibits it

mTOR:
Insulin activates it
AMPK (on) Inhibits it

39
Q

AMPK is a heterotrimeric protein. State the 3 subunits that compose AMPK and give their functions (one of the subunits serves 2 functions)

A

Alpha:
N-terminus is the active site with a kinase domain
C-terminus is the regulatory site that is phosphorylated when the protein is “activated”

Beta: structural component

Gamma: Binds 4 AMPS

40
Q

How are AMPK and PPAR (Peroxisome Proliferator-Activated Receptor) related? Describe the function of PPAR

A

Activated AMPK activates PPAR

PPAR has 4 isozymes that serve slightly different purposes in different tissues but all of them regulate metabolism of FAs and lipid synthesis

41
Q

State what the following hormones signal

Insulin:
Glucagon:
Epinephrine:

A

Insulin: Signals fed state

Glucagon: Signals fasting state

Epinephrine: Signals stress

42
Q

Leptin and Insulin work together in order to determine what? Compare the 2 in terms of what releases them, what type of sensor they serve as, and what they “signal” in terms of metabolic states.

A

They work together to determine what molecules are available to be used for energy

Insulin:
Released from Pancreas
Blood glucose sensor
Actions signal fed state

Leptin:
Released from Adipocytes
TAG storage sensor
Actions signal full state

43
Q

State 2 hormones that signal the full state, much like leptin, but their action is much more brief than leptin. Why is their action so much shorter?

A

CCK (Cholecystokinin) and GLP1 (Glucagon-like peptide 1)

Their action is shorter than leptin because they are peptide hormones (short duration of action by nature)

44
Q

State the 3 hormones that activate Anorexigenic neurons and state what occurs when these neurons are stimulated. Do the same for the 2 hormones that stimulate Orexigenic neurons.

A 
Anorexigenic neurons: signal fed/full state when stimulated
1. Leptin
2. Insulin
3. PYY3-36
("LIP" mnemonic)

Orexigenic neurons: signal “hungry” state when stimulated

  1. Ghrelin
  2. Adiponectin
45
Q

True or False:

Cortisol is a fast-acting hormone that is derived from cholesterol. explain.

A

False

Cortisol is not a fast acting hormone (most cholesterol derived hormones are not fast acting)

Cortisol is a SLOW-acting hormone that is derived from cholesterol

46
Q

State the effect that cortisol has on the following tissues.

Adipocytes:
Skeletal Muscle:
Liver:

A

Adipocytes: release FAs

Skeletal Muscle: Protein degradation and export AAs

Liver: Increase in pyruvate carboxylase, leading to an increase in gluconeogenesis

Biochemistry 2019 (32 decks)

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