Lecture 33 Flashcards
State the 3 metabolism molecules where the cell makes “a decision”.
- Glucose-6-phosphate:
- Pyruvate:
- Acetyl-CoA
For Glucose-6-phosphate, explain the 2 available “decisions” the cell can make in terms of where to go with metabolism from here.
glucose-6-phosphate:
1. Enter glycolysis and become Fructose-6-phosphate
- Enter gluconeogenesis and become Glucose-1-phosphate
For Pyruvate, explain the 4 available “decisions” the cell can make in terms of where to go with metabolism from here.
Pyruvate:
1. Enter TCA cycle (to make energy) and become Acetyl-CoA
- Enter Fermentation (to make less energy) and become Lactate
- Enter Gluconeogenesis and become OAA
- Enter AA synthesis and become Alanine
For Acetyl-CoA, explain the 3 available “decisions” the cell can make in terms of where to go with metabolism from here.
Acetyl-CoA:
1. Enter TCA cycle and Ox-Phos and become CO2 + H2O
- Enter Ketone body Synthesis and become a ketone (Acetoacetate, Acetone, or Beta-Hydroxybutyrate)
- Enter FA synthesis and become a FA (TAG)
Describe what the following organ does in terms of fuel reserves it may have and energy pathways it may conduct.
Liver
Fuel reserves: TAGs and Glycogen
Pathways: Glycolysis Gluconeogenesis Beta-oxidation FA synthesis
Describe what the following organ does in terms of fuel reserves it may have and energy pathways it may conduct.
Muscle
Fuel Reserves: Glycogen and Protein
Pathways: Beta-oxidation Glycolysis Proteolysis TCA cycle
Describe what the following organ does in terms of fuel reserves it may have and energy pathways it may conduct.
GI (intestines)
Fuel Reserves: none
Pathways: none
Describe what the following organ does in terms of fuel reserves it may have and energy pathways it may conduct.
Brain
Fuel Reserves: none
Pathways:
Glycolysis
TCA cycle
Describe what the following organ does in terms of fuel reserves it may have and energy pathways it may conduct.
Heart
Fuel Reserves: none
Pathways:
Beta-oxidation
TCA cycle
Describe what the following organ does in terms of fuel reserves it may have and energy pathways it may conduct.
Adipose tissue
Fuel Reserves: TAGs
Pathways:
Beta-oxidation
TAG synthesis
State the 3 tissues that store energy molecules and the 3 that make energy molecules
Store energy molecules: Skeletal Muscle (at rest), Adipose, and Liver
Make energy molecules: Skeletal Muscle (during exercise), Adipose, and Liver
For Brain tissue, state its
Fuel Reserves:
Preferred Fuel: (include it normally and during starvation)
Fuel sources exported:
Fuel Reserves: none
Preferred Fuel: Glucose (ketone bodies during starvation)
Fuel sources exported: none
For Skeletal Muscle tissue at rest, state its
Fuel Reserves:
Preferred Fuel:
Fuel sources exported:
Fuel Reserves: Glycogen and Protein
Preferred Fuel: FAs
Fuel sources exported: none
For Skeletal Muscle tissue during exercise, state its
Fuel Reserves:
Preferred Fuel:
Fuel sources exported:
Fuel Reserves: none
Preferred Fuel: glucose
Fuel sources exported: Lactate
For Heart Muscle tissue, state its
Fuel Reserves:
Preferred Fuel:
Fuel sources exported:
Fuel Reserves: none
Preferred Fuel: FAs
Fuel sources exported: None
For Adipose tissue, state its
Fuel Reserves:
Preferred Fuel:
Fuel sources exported:
Fuel Reserves: TAGs
Preferred Fuel: FAs
Fuel sources exported: FAs (TAGs) and Glycerol
For Liver tissue, state its
Fuel Reserves:
Preferred Fuel:
Fuel sources exported:
Fuel Reserves: TAGs and Glycogen
Preferred Fuel: Glucose, FAs, or AAs
Fuel sources exported: FAs, Glucose, and Ketone Bodies
State the fuel that is produced by these 3 fuel producers of the body.
Liver:
Adipocytes:
Kidney:
Liver: Glucose
Adipocytes: FAs
Kidney: Glucose (during starvation only)
State the fuel molecules in order of most preferred to least preferred for the following tissues.
Skeletal Muscle:
Brain:
Heart:
Skeletal Muscle: Glycogen then Creatine Phosphate then Lactate
Brain: Glucose then Ketone bodies
Heart: FAs then Lactate/Ketone bodies
True or False:
The Primary fuel for Liver tissue is Glucose. explain.
False.
The primary fuel for Liver tissue is FAs, however it can use Glucose or even AA’s if it needs to
Explain how fed and fasting states affect the reaction rate of glucokinase in in the liver and what the liver is synthesizing.
Fed State: increases the glucokinase reaction rate
FA’s (TAGs) are synthesized
Fasting State: decreases the glucokinase reaction rate
Ketone Bodies are synthesized
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.
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.
True or False:
The liver can produce Ketone Bodies but is unable to use them as fuel. explain.
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)
State the 2 enzymes that are unique to the Liver and Kidneys only.
glucose-6-phosphatase (allows them to “complete” gluconeogenesis)
Urea Cycle Enzymes
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?
Etoh consumption decreases NAD+ levels
This decreases the activity of the following pathways Gluconeogenesis Glycolysis TCA cycle Beta-oxidation
An increase in what 2 molecules is responsible for your hangover after drinking Etoh?
increased lactate and Ketone bodies (causing acidosis)
State the time it takes to achieve the following metabolic states and the main mechanism/goal of each state
Fed:
Fasting:
Starvation:
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
For the following cholesterol-containing molecules, state the origin, destination, and function of it.
Chylomicrons
Chylomicrons
Origin: Intestine (basically come straight from food)
Destination: Adipocytes
Function: TAG transport
For the following cholesterol-containing molecules, state the origin, destination, and function of it.
VLDLs
VLDLs
Origin: Liver
Destination: Adipocytes
Function: TAG transport
For the following cholesterol-containing molecules, state the origin, destination, and function of it.
IDLs
IDLs
Origin: VLDL’s
Destination: Liver and Adipocytes
Function: Intermediate molecule
For the following cholesterol-containing molecules, state the origin, destination, and function of it.
LDLs
LDLs
Origin: VLDLs
Destination: All cells
Function: Cholesterol Distribution
For the following cholesterol-containing molecules, state the origin, destination, and function of it.
HDLs
HDL
Origin: Liver (empty when they leave)
Destination: Liver (full when they return)
Function: Cholesterol Collection
Explain how IDLs and LDLs are created from VLDLs
VLDLs are purged (TAGs are removed from them) until they form IDLs and can eventually form LDLs after more purging past the IDL stage
Compare LDLs with HDLs in terms of “good and bad” and the protein to cholesterol composition of them
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)
What type of metabolic condition does diabetes mimic? explain how.
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)
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
Enzymes: “SAM” mnemonic
Sirtuins
AMPK
mTOR
Hormones: "I Get Lost PAGE" Insulin Glucagon Leptin PYY3-36 Adiponectin Ghrelin Epinephrine
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?
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)
For AMPK and mTOR, state what molecules activate and inhibit each of them.
AMPK:
Increased AMP activates it
Increased ATP Inhibits it
mTOR:
Insulin activates it
AMPK (on) Inhibits it
AMPK is a heterotrimeric protein. State the 3 subunits that compose AMPK and give their functions (one of the subunits serves 2 functions)
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
How are AMPK and PPAR (Peroxisome Proliferator-Activated Receptor) related? Describe the function of PPAR
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
State what the following hormones signal
Insulin:
Glucagon:
Epinephrine:
Insulin: Signals fed state
Glucagon: Signals fasting state
Epinephrine: Signals stress
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.
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
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?
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)
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.
Anorexigenic neurons: signal fed/full state when stimulated
1. Leptin
2. Insulin
3. PYY3-36
("LIP" mnemonic)
Orexigenic neurons: signal “hungry” state when stimulated
- Ghrelin
- Adiponectin
True or False:
Cortisol is a fast-acting hormone that is derived from cholesterol. explain.
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
State the effect that cortisol has on the following tissues.
Adipocytes:
Skeletal Muscle:
Liver:
Adipocytes: release FAs
Skeletal Muscle: Protein degradation and export AAs
Liver: Increase in pyruvate carboxylase, leading to an increase in gluconeogenesis
