L30: Nutritional Status and Utilization Flashcards

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1
Q

Which molecules are allosteric effectors? What are their signals and affects?

A
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2
Q

Which molecules are inducers of covalent modifications (aka phosphorylations)? Signals and affects?

A
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3
Q

What molecules are regulators of gene expression? Signals? Affects?

A
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4
Q

Fuel preferences / energy needs of RBCs, muscles, brain, adipose and liver

A
  • RBCs: glucose, anerobic metabolism - Non-cardiac muscle: glucose-anaerobic/aerobic, FFAs - Cardiac muscle: glucose aerobically only, FFAs - Brain: glucose aerobically, ketone bodies after serious period of starvation - Adipose: glucose, TAG – FAs - Liver: FAs, glucose, AAs and lactate
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5
Q

Describe metabolism of glucose, AAs and FAs in well-fed state

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6
Q

In what cells does insulin have a function? What response?

A
  • Muscle: uptake of glucose, production of glycogen - Liver: production of glycogen, production of TAG - Adipose: uptake of glucose
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7
Q

Objectives of well-fed state?

A
  • Glucose stored directly in liver and muscles. Excess glucose converted into VLDL for storage in adipose - AAs used for protein synthesis, excess converted into glucose or FAs by liver - TAGs present in chylomicrons are broken down for energy by most cells of body
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8
Q

Objectives of early fast?

A
  • Overall: nutrients stored in well-fed are mobilized - Glucose released into circulation from glycogen stores in liver. Muscle uses endogenous glycogen - FAs and glycerol released from adipose for consumption by muscle cells - Ketone bodies produced from FAs by liver - AAs from breakdown of protein released by muscle. Liver converts to glucose and ketone bodies - Urea cycle enzymes induced
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9
Q

Describe metabolism of early fast.

A
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10
Q

In what cells does glucagon have a function? What response?

A
  • Liver: stimulates degradation of glycogen, stimulates gluconeogenesis from AA sources, stimulates energy production from AA sources - Adipose: stimulates lipolysis
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11
Q

Role of urea cycle during early fast?

A
  • AAs are broken down from muscle and enter the liver to take part in gluconeogenesis or production of ketone bodies/ATP. - To cope with ammonia generation, urea cycle is induced during this period to rid body of this
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12
Q

Describe transition from early to late fast

A
  • Occurs after several days of fasting - Glycogen stores become exhausted and brain uses ketone bodies (generated primarily by liver, also minorly by kidney) to reduce glucose consumption - BMR drops
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13
Q

Describe problems associated with refeeding and causes of refeeding syndrome. Consider what starvation leads to? How to refeed?

A
  • Starvation: 1.) leads to degradation of digestive enzymes, 2.) depletes intracellular phosphate pools and 3.) depletes potassium stores - Problems: 1.) digestion is impaired and feeding leads to diarrhea and dehydration, 2.) glycolysis starting soaks up phosphate from serum leading to life-threatening hypophosphatemia and 3.) sudden insulin release (insulin moves K into cells) lowers serum potassium further - Watch electrolytes (esp. phosphate and K)
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14
Q

Why obese pts can experience starvation?

A
  • ?
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15
Q

Metabolic changes that occur during exercise?

A
  • Muscles powered by FAs and glucose - Glycogen depletes more rapidly than fat deposits - After 1 hour of exercise, 50% of glycogen is spent - After 2 hours of exercise, glycogen is depleted and energy comes from FA oxidation
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