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4 Clinical Physiology > L3 Fat and Protein Metabolism > Flashcards

L3 Fat and Protein Metabolism Flashcards

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1
Q

How do we optimize movement as a PT?

A

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

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2
Q

What are the limiting factors in any cell’s ability to produce energy?

A
  1. Availability of O2 to breakdown fuel
  2. Availability of appropriate fuel/energy stores
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3
Q

What determines any cell’s availability of oxygen?

A

Blood supply to the cell
Amount of O2 in the blood
Oxygen uptake from lungs
Oxygen partial pressure in environment

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4
Q

What energy stores are available in the body?

A

ATP (limited stores)
Creatine phosphate (muscle)
Glucose (not stored)
Glycogen (liver, muscle)
Protein (not used as energy)
Fat (limitless supply)

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5
Q

Creatine Phosphate

A

Considered high energy phosphate intramuscular reservoir
4-6x greater concentration than ATP

CP –> C + P + energy, ADP + P + energy –> ATP

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6
Q

What activities rely exclusively on ATP and CP?

A

Short duration, high intensity exercise
Brief bursts of max power output

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7
Q

Normal fasting blood concentration

A

70-99 mg/dl

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8
Q

Glycogen stores

A
  1. Hepatocytes, highest concentration per cell. 90-100 g total
  2. Skeletal muscle cells, lower concentration, total exceeds liver @ 325 g
  3. Very small amounts in kidney
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9
Q

Glycogen catabolism

A

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

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10
Q

Glycogen anabolism

A

condensation reaction
occurs when there is enough energy in the cell, so PFK activity decreases, which slows glycolysis.

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11
Q

Functions of Fat

A

adipocytes either synthesize or catabolize triglycerides

Endocrine organ

Adipocytes release adipokines that act on brain, muscle, liver

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12
Q

Obesity and adipokines

A

increased leptin
decreased adiponectin
increased resistin

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13
Q

Leptin

A

suppresses hunger, increases energy metabolism, improves insulin sensitivity, regulates puberty/reproduction, promotes anti-inflammatory effects in CV system

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14
Q

Adiponectin

A

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

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15
Q

Resistin

A

stimulates inflammation and impairs vascular relaxation

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16
Q

Obesity and leptin

A

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

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17
Q

Adipokines promote a state of _____ _______ in obesity

A

chronic inflammation

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18
Q

Lipid Catabolism (Big steps)

A

Lipolysis
FFA transport
Beta oxidation

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19
Q

Lipolysis

A

breakdown of triglycerides into glycerol and free fatty acids, performed by lipases.

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20
Q

Lipases

A

under hormonal control
LIPOLYSIS IS THE ONLY STEP OF FAT BREAKDOWN THAT IS REGULATED

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21
Q

What increases lipolysis rate?

A

epinephrine, cortisol, low level of insulin

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22
Q

What decreases lipolysis rate?

A

normal or high levels of insulin

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23
Q

Free fatty acid transport

A

FFA move from the blood to the cells that need energy

must be transported to the mitochondria where beta oxidation occurs

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24
Q

Beta oxidation of FFA Steps

A

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

25
Q

Beta Oxidation general

A
  1. Occurs inside the mitochondrial matrix
  2. FFA are major energy source b/c oxidation yields large amounts of energy
  3. due to complexity of chemical reactions, oxidation is slow
26
Q

ATP produced with 1 FFA

A

146 ATP
sooo much more carbon vs glucose

27
Q

What determines the % of your body’s energy needs being derived from lipid?

A

30-80% energy is derived from lipids

  1. Nutritional Status
  2. Intensity of exercise
  3. Duration of exercise
  4. Level of fitness
  5. Mode of exercise
  6. Carb intake before exercise
  7. BMR
28
Q

Carbs as metabolic primer

A

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

29
Q

Ketone bodies

A

liver’s solution to the accumulation of Acetyl-CoA is to make ketones

30
Q

Ketogenesis

A

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

31
Q

Ketosis

A

abnormally high level of ketones in blood

Ketones can be used as a mechanism of energy generation, like in the brain

Ketones are ACIDS

32
Q

Ketoacidosis

A

can lead to coma and death, body is no longer buffering the acids

sweet-smelling breath of person in ketosis is due to acetone

33
Q

Epilepsy

A

some cases can improve on a ketogenic diet

34
Q

Lipid utilization ______ with ______ exercise INTENSITY

A

decreases
increasing

mostly endurance exercises are going to use lipids as energy source

35
Q

Lipid utilization _______ with ________ exercise DURATION

A

increases
increasing

36
Q

Conditions that will increase lipid utilization

A

Fasted
moderate intense exercise
long duration of exercise
fit individuals
running (vs cycling)
decreased carb intake before exercise

37
Q

Lipogenesis

A

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

38
Q

Protein Catabolism

A

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

39
Q

Protein and amino acid catabolism steps

A
  1. Proteases break peptide bonds between AA
  2. Amino acids can be catabolized to provide ATP or intermediates for fat and carb synthesis after nitrogen removal
40
Q

How does the body remove nitrogen from AAs?

A
  1. Oxidative deamination
  2. Transamination
41
Q

Oxidative deamination

A

amino group gives rise to ammonia and is replaced by oxygen to form a keto acid (kreb cycle intermediate)
catabolic process

42
Q

Transamination

A

amino group is transferred from one amino acid to a keto acid to form another/different amino acid
anabolic process

43
Q

Ammonia

A

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

44
Q

Urea

A

Liver MAKES urea
Kidneys EXCRETE urea

major nitrogenous waste product of protein catabolism and is excreted into urine
2NH3 + CO2 = urea

45
Q

How and why is urea clinically measured?

A

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

46
Q

Reasons for increased BUN

A

high protein intake
kidney dysfunction
excessive protein breakdown

47
Q

Reasons for decreased BUN

A

Liver failure, causes accumulation of ammonia
malnutrition

48
Q

How does the body actually make the nonessential amino acids?

A

from carbohydrates/ketoacids and other amino acids via transamination

reason behind why calorimeter value is higher than the actual kcals protein provides

49
Q

Amino acids come from…

A
  1. ingested proteins
  2. synthesis of nonessential amino acids via transamination
  3. continuous catabolism of our own body protein
50
Q

Healthy adults and nitrogen

A

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

51
Q

Negative nitrogen balance

A

not enough protein
severe injury or illness
wasting

52
Q

Positive nitrogen balance

A

kids in growth spurts

53
Q

What group LACKS protein intake?

A

elderly women

54
Q

Protein intake in athletes

A

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

55
Q

Gluconeogenesis

A

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

56
Q

Substrates for gluconeogenesis

A

Lactate via cori cycle
Pyruvate (major input!!)
Glycerol
Amino Acids

57
Q

“detours” in glycolysis

A

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)

58
Q

Gluconeogensis from glycerol

A

only the glycerol backbone of lipids can be used
FFA canot b/c carbons are lost as CO2

4 Clinical Physiology (9 decks)

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