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54 Cards in this Set
- Front
- Back
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What are the 2 priorities during periods of starvation?
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1. Glucose to the brain -- and other tissue dependent on glucose (ie: RBC)
2. Preserve protein -- done by shifting fuels from glucose to FA and ketone bodies |
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Stage I of Starvation
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- FASTING
- Exogenouse glucose used by all tissues - gluconeo NOT active - Glucose - major fuel for brain |
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Stage 2 of Starvation
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- 4-16 hours
- insulin low, glucagon HIGH so glycogen breakdown starts - HEPATICE gluconeo starts -- sources for gluconeo are pyruvate, alanine, glycerol - brain still uses glucose |
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Stage 3 of Starvation
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-16-24 hours
- glycogen low, hepatic gluconeo up - glycogen breakdown and hepatic gluconeo sources for glucose - Brain still uses glucose |
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Stage 4 of Starvation
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2-24 DAYS
- kidney begins gluconeo - brain begins using ketone bodies |
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Stage 5 of Starvation
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24-40 DAYS
- liver, kidney - gluconeo - Brain now mainly using ketone bodies since not a lot of glucose around |
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Muscle protein degradation
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3 days: 75g consumed; 40th day: 20 g
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Initial sources of protein
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rapid turnover proteins
ie: intestinal epithelium and secreted proteins from pancreas |
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Proteins after day 3 of starvation
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Liver forms ketone bodies which become main form of energy --> preventing protein degradation
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Proteins after 40 days
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TAG stores are depleted; ketone bodies depleted
- protein degradation INCREASES = DECREASE heart, liver, kidney fxn = DEATH |
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Why and where are ketone bodies made?
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Made in the liver from Free FA that come from adipose tissue
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How are Ketone bodies made?
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During low glucose -- ie: fasting/starvation
1. OAA level drops in liver 2. CAC slows --> A-Coa taken from CAC diverted to make KB IN liver 3. FA taken and broken down to make KB via B-oxidation 4. KB in blood transported to other tissue 5. Converted to A-CoA and used for energy |
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How are ketone bodies used for energy?
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Under normal conditions, FA are releaed from adipose and broken down in B-oxidation to make acetyl-coA, which is further oxidized and its energy is transfered as electrons in CAC.
Fasted/starvation state: If CAC slows and OAA decreases, acetyl-CoA is taken to make KB, and then these ketone bodies are used in the liver and to other tissues to be re-converted to A-CoA via CAC. |
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What are the 3 key junction molecules of metabolism?
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What are the fates of glucose 6-phosphate?
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What are the fates of pyruvate?
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What are the fates of acetyl CoA?
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Know the role of Liver in carbohydrate metabolism? Lipid metabolism? amino acid metabolism?
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What 2 fuels does the brain use?
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Know the difference in resting, moderately active muscle, and active muscle in terms of fuel use.
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Understand the cori cycle and the glucose-alanine cycle (this is review from previous lectures)
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What are your fuel sources for muscle during exercise?
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What fuels can the heart use?
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How is lactate utilized as fuel in the heart?
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What functions do the kidneys serve in metabolism?
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What are the 3 functions of adipose tissue?
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What are Islets of Langerhans?
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What are the functions of insulin in liver, muscle, and adipose?
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What are the functions of glucagon in liver and adipose? Why not muscle?
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What are the functions of epinephrine in liver, adipose, and muscle?
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How does AMPK serve as a fuel sensor at the level of the cell?
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What is the effect of AMPK in hypothalamus, muscle, liver, and adipose tissue?
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What is the general mechanism of PPAR activation?
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What is the function of PPARα during periods of starvation?
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What is the function of PPARδ? How does it differ than PPARα?
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Which PPAR sensitizes muscles to the effects of insulin?
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Why is PPARγ considered the master regulator of adipogenesis?
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What is the role of UCP/thermogenin in metabolism?
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How is activation of UCP beneficial?
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What is the “set point” theory?
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What is the role of the arcuate nucleus of the hypothalamus (lateral hypothalamus) in metabolism?
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What are adipokines? Where are they produced?
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What are 2 general functions of adipokines?
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What is leptin and how does it function to maintain levels of fat reserves?
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What is α-MSH and NPY? How do they function?
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What are the consequences of being leptin deficient (ob/ob mouse)?
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How do leptin injections act to decrease obesity in leptin deficient mice?
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Understand why increased leptin levels in obese patients have no effect
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What are parabiosis experiments?
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What is adiponectin and how does it function? What are the consequences of not having adiponectin?
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What are Ghrelin and PYY? Where are they produced and what do they do?
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Understand how leptin signals the hypothalamus to eat less and metabolize more (schematic on slide 54)
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Understand the fed and fasted state – what’s happening in the liver, fat, and muscle?
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How are blood glucose levels maintained during an overnight fast?
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