L3 Fat and Protein Metabolism Flashcards
How do we optimize movement as a PT?
to have optimal movement, a person must have adequate oxygen and fuel sources supplied to their muscles
PT should recognize this as a prerequisite to optimal movement
What are the limiting factors in any cell’s ability to produce energy?
- Availability of O2 to breakdown fuel
- Availability of appropriate fuel/energy stores
What determines any cell’s availability of oxygen?
Blood supply to the cell
Amount of O2 in the blood
Oxygen uptake from lungs
Oxygen partial pressure in environment
What energy stores are available in the body?
ATP (limited stores)
Creatine phosphate (muscle)
Glucose (not stored)
Glycogen (liver, muscle)
Protein (not used as energy)
Fat (limitless supply)
Creatine Phosphate
Considered high energy phosphate intramuscular reservoir
4-6x greater concentration than ATP
CP –> C + P + energy, ADP + P + energy –> ATP
What activities rely exclusively on ATP and CP?
Short duration, high intensity exercise
Brief bursts of max power output
Normal fasting blood concentration
70-99 mg/dl
Glycogen stores
- Hepatocytes, highest concentration per cell. 90-100 g total
- Skeletal muscle cells, lower concentration, total exceeds liver @ 325 g
- Very small amounts in kidney
Glycogen catabolism
requires several enzymes, results in glucose-6-phosphate
GSP can be broken down to pyruvate in glycolysis
ONLY liver (and some kidney) can produce free glucose from glycogen
Glycogen anabolism
condensation reaction
occurs when there is enough energy in the cell, so PFK activity decreases, which slows glycolysis.
Functions of Fat
adipocytes either synthesize or catabolize triglycerides
Endocrine organ
Adipocytes release adipokines that act on brain, muscle, liver
Obesity and adipokines
increased leptin
decreased adiponectin
increased resistin
Leptin
suppresses hunger, increases energy metabolism, improves insulin sensitivity, regulates puberty/reproduction, promotes anti-inflammatory effects in CV system
Adiponectin
released from subcutaneous fat
strong anti-inflammatory effect in vasculature, sensitizes tissue to insulin
ultimately increases fatty acid oxidation and glucose uptake into skeletal muscles
Resistin
stimulates inflammation and impairs vascular relaxation
Obesity and leptin
very few obese people have leptin mutations
most obese people produce plenty of leptin, but fail to respond to it.
Obesity is usually due to leptin resistance
Adipokines promote a state of _____ _______ in obesity
chronic inflammation
Lipid Catabolism (Big steps)
Lipolysis
FFA transport
Beta oxidation
Lipolysis
breakdown of triglycerides into glycerol and free fatty acids, performed by lipases.
Lipases
under hormonal control
LIPOLYSIS IS THE ONLY STEP OF FAT BREAKDOWN THAT IS REGULATED
What increases lipolysis rate?
epinephrine, cortisol, low level of insulin
What decreases lipolysis rate?
normal or high levels of insulin
Free fatty acid transport
FFA move from the blood to the cells that need energy
must be transported to the mitochondria where beta oxidation occurs
Beta oxidation of FFA Steps
Catabolism of fatty acids
1. Enzymes remove 2 carbon units and their Hs from the acid end of FFA
2. Continues until entire FFA is converted into acetyl CoA, which goes to the Krebs Cycle
Beta Oxidation general
- Occurs inside the mitochondrial matrix
- FFA are major energy source b/c oxidation yields large amounts of energy
- due to complexity of chemical reactions, oxidation is slow
ATP produced with 1 FFA
146 ATP
sooo much more carbon vs glucose
What determines the % of your body’s energy needs being derived from lipid?
30-80% energy is derived from lipids
- Nutritional Status
- Intensity of exercise
- Duration of exercise
- Level of fitness
- Mode of exercise
- Carb intake before exercise
- BMR
Carbs as metabolic primer
More lipid is mobilized that can be used for energy when carb breakdown is limited
happens because carb intake triggers insulin release. Low or absent insulin increases rate of lipolysis
more FFA that can be used, ketones are produced
Ketone bodies
liver’s solution to the accumulation of Acetyl-CoA is to make ketones
Ketogenesis
Synthesis of ketone bodies by the liver
Insulin deficiency > Increased mobilization of FFA > Increased FFA delivery to liver > increased oxidation of FFA by liver > accelerated production by liver
Ketosis
abnormally high level of ketones in blood
Ketones can be used as a mechanism of energy generation, like in the brain
Ketones are ACIDS
Ketoacidosis
can lead to coma and death, body is no longer buffering the acids
sweet-smelling breath of person in ketosis is due to acetone
Epilepsy
some cases can improve on a ketogenic diet
Lipid utilization ______ with ______ exercise INTENSITY
decreases
increasing
mostly endurance exercises are going to use lipids as energy source
Lipid utilization _______ with ________ exercise DURATION
increases
increasing
Conditions that will increase lipid utilization
Fasted
moderate intense exercise
long duration of exercise
fit individuals
running (vs cycling)
decreased carb intake before exercise
Lipogenesis
Fat anabolism
once fatty acids are formed, triglyceride is made by linking that fatty acid chain to glycerol
occurs in the cytosol of fat and liver cells
formation of FFA requires 8 ATP
Protein Catabolism
Protein is not generally considered a major energy source
Critical in maintaining blood glucose levels during starvation, prolonged intense exercise
before protein can be used for energy, nitrogen has to be removed
Protein and amino acid catabolism steps
- Proteases break peptide bonds between AA
- Amino acids can be catabolized to provide ATP or intermediates for fat and carb synthesis after nitrogen removal
How does the body remove nitrogen from AAs?
- Oxidative deamination
- Transamination
Oxidative deamination
amino group gives rise to ammonia and is replaced by oxygen to form a keto acid (kreb cycle intermediate)
catabolic process
Transamination
amino group is transferred from one amino acid to a keto acid to form another/different amino acid
anabolic process
Ammonia
produced with oxidative deamination
gas that passes through cell membranes into the blood
can be highly toxic if it accumulates
Urea is produced to negate accumulation
Urea
Liver MAKES urea
Kidneys EXCRETE urea
major nitrogenous waste product of protein catabolism and is excreted into urine
2NH3 + CO2 = urea
How and why is urea clinically measured?
in a test called blood urea nitrogen. Should be between 6-25 mg/dL
increased urea is toxic and can cause cognitive problems.
High urea is much more common than low urea
Reasons for increased BUN
high protein intake
kidney dysfunction
excessive protein breakdown
Reasons for decreased BUN
Liver failure, causes accumulation of ammonia
malnutrition
How does the body actually make the nonessential amino acids?
from carbohydrates/ketoacids and other amino acids via transamination
reason behind why calorimeter value is higher than the actual kcals protein provides
Amino acids come from…
- ingested proteins
- synthesis of nonessential amino acids via transamination
- continuous catabolism of our own body protein
Healthy adults and nitrogen
Healthy individuals are in nitrogen balance, so amount of nitrogen ingested is equal to the amount of nitrogen excreted
individuals that are healing from injury, surgery, illness need more protein than athletes
Negative nitrogen balance
not enough protein
severe injury or illness
wasting
Positive nitrogen balance
kids in growth spurts
What group LACKS protein intake?
elderly women
Protein intake in athletes
primary nutritional problem with most athletes is ingesting excessive protein and not enough carbs
in trained athletes, excessive protein intake isn’t helpful, but can cause renal failure.
those in weight restricting sports may lack protein intake
Gluconeogenesis
biosynthesis of new glucose from intermediates derived from other fuel molecules, not from glucose
occurs in the liver
it is ABSOLUTELY CRITICAL to maintain normal blood glucose levels
Substrates for gluconeogenesis
Lactate via cori cycle
Pyruvate (major input!!)
Glycerol
Amino Acids
“detours” in glycolysis
used for liver cells to produce pyruvate or lactate when it lacks it
only possible in gluconeogenic cells that have necessary enzymes (like liver cells)
Gluconeogensis from glycerol
only the glycerol backbone of lipids can be used
FFA canot b/c carbons are lost as CO2
