L30: Nutritional Status and Utilization Flashcards
Which molecules are allosteric effectors? What are their signals and affects?
Which molecules are inducers of covalent modifications (aka phosphorylations)? Signals and affects?
What molecules are regulators of gene expression? Signals? Affects?
Fuel preferences / energy needs of RBCs, muscles, brain, adipose and liver
- 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
Describe metabolism of glucose, AAs and FAs in well-fed state
In what cells does insulin have a function? What response?
- Muscle: uptake of glucose, production of glycogen - Liver: production of glycogen, production of TAG - Adipose: uptake of glucose
Objectives of well-fed state?
- 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
Objectives of early fast?
- 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
Describe metabolism of early fast.
In what cells does glucagon have a function? What response?
- Liver: stimulates degradation of glycogen, stimulates gluconeogenesis from AA sources, stimulates energy production from AA sources - Adipose: stimulates lipolysis
Role of urea cycle during early fast?
- 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
Describe transition from early to late fast
- 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
Describe problems associated with refeeding and causes of refeeding syndrome. Consider what starvation leads to? How to refeed?
- 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)
Why obese pts can experience starvation?
- ?
Metabolic changes that occur during exercise?
- 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