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How long does ingested glucose last in body? When does glycogenolysis begin? End? When does GNG begin? Peak?
- 4 hrs.
- 4-6 hrs after meal. 10-18 hrs after meal if fasting.
- Begins at 4 hrs. Peaks at ~30 hrs.
Wha limits survival during starvation? What hormones are released during fasting mode? (4)
Loss of body protein(serum glucose) = limiting survival factor. Can only use 1/3 of protein stores before you die.
Glucagon, ACTH, epinephrine, cortisol
What happens in early fasting? Stage I? (3)
Low insulin - high glucagon
- 1. Liver, muscle, peripheral tissues rely heavily on FAs and ketone bodies for energy
- 2. Liver increases GNG
- 3. Brain, RBCs, WBCs, still use glucose for energy
- Net result: Though many organs switch to FAs and ketones and serum glucose levels fall, glucose demand still high.
What happens in stage II of starvation?
1. Adipose? (3)
2. Muscle? (2)
3. Brain? (2)
- Adipose tissue:
- 1. Lipolysis is activated via Glucagon/epinephrine.
- 2. FAs --> liver for oxidation to power GNG and to (3) provide ketones which spares glucose.
Muscle: (1) Protein degradation to provide substrates for GNG (2) Uses ketones for energy - glucose sparing.
Brain: (1) Begins to adapt to using ketones (2) reduces glucose use and spares proteins somewhat
What happens in stage III aka trend to hypometabolism? BMR? Liver? (3)
- 1. Decrease in basal metabolic rate preserves fuel stores (contrasted with stress)
- 2. Liver: Glycogenolysis, GNG, FA oxidation in liver --> ketone bodies.
What happens after decrease in hypometabolic rate?
Changes in fluids & electolytes? (3). Why?
Changes in fuel supply with reduced BMR? (3)
Muscle? How does rate change? Does body make distinctions bt essential & nonessential? What is the major gluconeogenic AA? What is the result of using more protein?
How does major fuel source change? When does death come?
- Fluids & electrolytes:
- 1. low circulating volume & hemo-concentration
- 2. decreased cardiac output
- 3. depleted water-sol vitamins.
Increased ketone excretion increases water needs.
Change in fuel supply with reduced BMR: decrease in GNG, ketones become primary source of fuel, protein degradation is limited but not absent.
Protein breakdown initially enhanced, then slowed. No distinction between essential & nonessential!!!!!
Excess N is disposed of as urea.
Protein hydrolysis is major source of glucose during fasting. Death come when 1/3 of body protein is used.
What are the 2 undesired effects in using very low calorie diets for weight loss?
- 1. Loss of essential protein stores
- 2. Need for incrased water to dispose of urea safely
What wer ethe findings of the minnesota starvation experiment? 7
Anemia, fatigue, apathy, extreme weakness, irritability, neurological deficits, leg edema
Apart from brain, muscle, and liver, how do other organs adapt to starvation?
Kidney (2), BMR (3) heart rate (2), Overall activity? (1)
- 1. Kidney - GNG, glutamine = significant GNG AA, excess N is excreted as urea & ammonium (increasing water needs)
- 2. Basal metabolic rate - reduces energy requirements and slows loss of lean muscle mass and fat stores.
- 3. Heart rate - decreases leading to impaired physical performance.
- 4. Overall, activity is lowered.
What are 5 problems associated with starvation?
- 1. Body cannot breakdown fat w/o breaking down protein.
- 2. Body can't distinguish b/t essential & nonessential protein - heart, vital organs (liver, kidney), immune system, and anemia occurs.
- 3. Water and electrolyte losses are excessive due to increased water needs to dispose of ketones, urea and ammonium - hypertension, cardiac arrthymias
- 4. Excess ketones and NH4+ can cause problems - ketoacidosis and hyperammonemia can cause neural damage especially to fetal brain - rapidly changes pH of blood.
- 5. Serum uric acid concentration rises (ketone bodies compete w/ uric acid for same transporter)
Why does liver become fatty during starvation?
Incrase in FFAs from adipose tissue from lipolysis due to low energy.
How does one recover from starvation - why would one recommend a gradual increase in calories? (4) Expand on each one.
- 1. Heart muscle weakened - should not put extra strain on heart.
- 2. Thiamine deficiency - needed for PDH and a-ketoglutarate dehydrogenase. High carb intake can rapidly use up last traces of thiamine. Can lead to Beriberi heart disease.
- 3. Potassium deficiency - refeeding leads to uptake of serum K+ by cells, resulting low K+ in serum can lead to fatal cardiac arrhythmia.
- 4. Impaired digestion & absorption of carbs, lipids, proteins - lack of digestive enzymes and lack of inducible enzymes in liver and kidney.
What are the differences b/t stress and starvation?
- Glucose uptake
- Protein breakdown
- Metabolic rate
How do hormones change in starvation vs. trauma or stress?
3. Stress hormones - Epinephrine, NE, Cortisol
5. Insulin resistance.
How does energy expenditure change in stress vs. starvation- name 2 reason why.
How does loss of body protein compare?
What are 3 ex of stressors?
Energy expenditure increases much more in stress vs. starvation - increased respiratoin and increased body temp.
Body protein loss in stress is MUCH higher.
Trauma, surgery, sepsis
How do insulin & glucagon change in response to stress? What other hormones are released? (3) What insulin-like protein is released?
Insulin and glucagon levels both increase, but ratio favors glucagon.
Cortisol, catecholamines, growth factor. ILF-1 binding protein.
What happens to glucose levels & insulin sensitivity during stress? What happens to carbohydrate metabolism? (4)
What happens to glucose uptake? (2)
Hyperglycemia paired with insulin resistance.
- 1. More lactate produced
- 2. Increased GNG
- 3. Impaired glycogen synthesis
- 4. High glucose oxidation
Increased GLUT 1 & 2 glucose uptake (insulin independent) and decreased GLUT 4 uptake (heart, muscle, adipose tissue)
What sorts of signaling molecules are released during stress for sepsis or trauma? (4) What do the first two do? (3) What does this lead to? (3) What does THAT lead to? (3)
Chemokines, pro-inflammatory cytokines and production of reactive oxygen and N species.
1. Inflammatory People: PUFA derived eicosanoids & thromboxanes (produced by COX) cause: reduce heart function, blood flow in peripheral vessels, and blockages in blood vessels.
This leads to tissue hypoperfusion, inadequate oxygenation, and organ failure.
Thus, membrane function is impaired and may result in amplified production of reactive oxygen species, chemokines, and cytokines.
What are the caloric and nutrient needs during stress and trauma? (3)
- 1. Increase in protein intake to make up for wound/urinary losses.
- 2. Do not increase carb intake - liver hepatic output is doubled.
- 3. Dietary lipids/overfeeding should be limited bc adipose tissue is geared towards lipolysis, so TAGs will pile up in liver & muscle --> insulin resistance.
Name similarities between starvation and stress? (3)
- 1. Both have breakdown in body protein & fat
- 2. Both have one arrow increase in glucagon
- 3. Both have increases in stress hormones, but under stress, they are MUCH higher.
- 4. Both have decreased glucose uptake, but stress is much less glucose uptake.
Name differences between stress and starvation? (5)
- 1. Insulin: decreases dramatically in starvation, but increases slightly in stress.
- 2. Glucose uptake: Increases in starvation, decreases a lot in starvation due to insulin res
- 3. Ketogenesis - starving has it, stress doesn't.
- 4. Metabolic rate: starvation - decreases, stress increases.
- 5. Insulin resistance.