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28 Cards in this Set
- Front
- Back
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The liver: storage fuel? preferred fuel? exported fuel?
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- storage: glycogen, triglycerides
- preferred: glucose, FA, AA - exported: glucose, FA, ketones |
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skel muscle (rest vs working): storage fuel? preferred fuel? exported fuel?
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- storage fuel: glycogen (resting)
- preferred fuel: FA (resting), glucose (working) - exported fuel: alanine, lactate (working) |
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adipocyte: storage fuel? preferred fuel? exported fuel?
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- storage: TG
- preferred: FA - exported: FA, glycerol |
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The heart: storage fuel? preferred fuel? exported fuel?
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- stored: nothing
- preferred: FA - exported: nothing |
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The brain: storage fuel? preferred fuel? exported fuel?
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- stored: nothing
- preferred: glucose (ketones in starvation) - exported: nothing |
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What are 4 ways to regulate metabolism?
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1) allosteric inhibition or stimulation
2) covalent modification 3) regulation of amount of enzyme 4) compartmental separation |
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fructose-2,6 bisphosphate balancing glycolysis and gluconeogenesis, glucose 6-phosphate activation of glycogen synthetase, or glucose inhibition of phosphorylase are all examples of what kind of regulation?
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- allosteric
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Explain the example of covalent modification by phosphorylation of hormone-sensitive lipase?
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- glucagon --> cAMP --> PKA --> phosphorylation of HSL = activation: TGs --> FAs + gycerol
- insulin --> dephosphorylation of HSL = inactive |
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How is fatty acid oxidation an example of compartmental separation?
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- Fatty acid oxidation happens in mito - blocked by malonyl coA (first step in building FAs)
- high levels of AMP stimulates kinases which make acetyl coA out of malonyl CoA therefore not blocking FAs into mito |
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What does insulin do?
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- promotes fuel storage after a meal
- stimulates amino acid uptake/protein synthesis - FA synthesis & storage - storage of glucose as glycogen (liver + skeletal muscle) |
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what does glucagon do?
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- mobilizes fuel
- activates gluconeogensis & glycogenolysis - activates FA release from adipocytes - CANNOT ACT ON MUSCLE |
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What does epinephrine do?
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- mobilizes fuel during stress
- produces glucose from glycogen - stimulates FA release from adipose tissue - similar to glucagon but CAN ACT ON MUSCLE |
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what does cortisol do?
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- changes for long-term
- stimulates amino acid mobilization - stimulates gluconeogensis - stimulates FA release from adipose tissue - works at level of transcription - steroid hormone - antagonist to insulin |
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What happens in the cAMP cascade? Which hormones act through this?
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- receptor activated --> G protein --> adenylate cyclase --> cAMP --> PKA --> phosphorylation of things
- epi & glucagon |
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Explain the receptor structure that activates cAMP. Which hormones act on these?
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- 7 transmembrane receptor
- extracellular domain provides specificity - same G protein intracellularly - epi & glucagon |
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Explain the G-protein cycle
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- heterotrimer w/ inhibitory beta/gamma subunits
- receptor (guanine nucleotide exchange factor GEF) causes dissociation of subunits & GDP allowing GTP to bind - Gsa then activates adenylate cyclase - Gsa then hydrolyzes GTP to GDP with GAP shutting off process - binds to beta/gamma again |
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what do cholera & pertussis toxins do?
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- inhibit hydrolysis of GTP during G-protein cycle keeping constitutively active cAMP
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______ causes the synthesis of cAMP whereas _____ degrades it. What does caffeine do?
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- adenylate cyclase
- phosphodiesterase - caffeine inhibits phosphodiesterase |
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how does cAMP work on PKA?
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- cAMP causes dissociation of the regulatory subunits and liberates the catalytic subunits
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How does PKA regulate glycogen breakdown and synthesis?
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- PKA phosphorylates phosphorylase kinase activating it to phosphorylate phosphorylase which breaks down glycogen
- PKA also phosphorylates glycogen synthase making it inactive |
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How does cortisol receptor work?
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- cytoplasmic steroid receptor released from hsp90 when cortisol enters --> translocates to the nucleus to act on transcription
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Where do you get fuel from in the postabsorptive phase? early starvation? intermediate? prolonged?
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- glycogen
- early starvation: 16 hrs coming from gluconeogenesis - intermediate: gluconeogenesis - prolonged: gluconeogensis |
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Why is gluconeogenesis higher in early starvation than in intermediate or prolonged starvation?
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- because you stop doing as much gluconeogenesis when you switch over to ketone bodies as fuel
- don't want to keep burning your protein |
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What is the difference in glucose metabolism (specific to liver exporting) just after a meal vs when you start to fast? What is your liver using as fuel during this time?
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- just after a meal: glucose coming in from blood, LDL being excreted, liver is using glucose from blood
- when start to fast: fat from adipocytes used by liver & liver breaks down glycogen to export glucose into the blood |
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What happens between early & intermediate/prolonged starvation in terms of protein use?
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- in early starvation you are using more protein
- in middle/late there is a big drop in protein utilization |
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During a prolonged fast the brain switches from _____ to ______ for fuel
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- glucose
- ketone bodies (derived from FA breakdown) |
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What happens to urinary nitrogen & urinary ammonia during a prolonged fast?
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- amount of nitrogen being excreted (primarily as urea) decreases
- total amount of ammonia increases to conserve cations that would be excreted with excess ketone bodies |
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what happens in refeeding?
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- electrolytes will suffer
- phosphate will rapidly drop which is important, can kill someone via this |
