during the starved state, what become the major sources of glucose?
glycerol and lactate
during the starved state, what does the brain eventually start using?
ketone bodies
what does the body stop breaking down in a prolonged starvation state?
where do ketone bodies go during overnight fasting?
to the muscle
how does glucagon affect adipose tissue?
glucagon/epinephrine phosphorylates hormone sensitive lipase which removes fatty acids from stored triglycerides
what inactivates hormone sensitive lipase and how?
insulin through activation of a phosphatase
where is hormone sensitive lipase found?
adipose tissue
what are the products of triglyceride catabolism?
3 fatty acids and a glycerol
what happens to fatty acids when they are released from adipose tissue?
they are carried on albumin to tissues, (liver, muscle) in need of them
what does the liver do with acetyl CoA during gluconeogenesis?
the liver turns acetyl CoA into ketone bodies, which are transported out and sent to other tissues as an energy form
how many carbons does acetyl CoA have?
where are ketone bodies made?
the mitochondria
what is the first step of ketone body synthesis?
combination of 2 acetyl CoAs to produce a 4 carbon acetoacetyl-CoA
what is the second step of ketone body synthesis? what is the product of this step called/used for?
addition of another acetyl CoA to acetoacetyl-CoA, by HMG synthetase, (induced during a fast) (6 carbons total, composed of 3 acetyl-CoAs). this product is called HMG-CoA, and is used in the cytosol to make cholesterol by HMG-CoA synthase
what happens to HMG-CoA in the production of ketone bodies?
HMG-CoA is catabolized by HMG-lyase to give acetoacetate, the first ketone body. this rxn gives off 2C and a CoA
what are the second and third ketone bodies that are produced from HMG-CoA?
beta-hydroxybutyrate is the second formed if there is enough NADH around, (from fatty acid catabolism), to reduce the C=O, (adds a little more energy). acetone is the third which can be produced spontaneously, giving off a CO2
what product is formed from both ketone bodies, betahydroybutyrate and acetoacetate?
betahydroybutyrate is oxidized to form acetoacetate again, (NADH can be used to make ATP in the muscle), and then a CoA needs to be added. the CoA added comes from succinyl-CoA, which is pulled off from the TCA cycle, (=one less GTP produced), giving acetoacetatyl-CoA
what happens to the 4C acetoacetatyl-CoA in the utilization of ketone bodies?
acetoacetatyl-CoA is broken in half and another CoA is added, giving 2 2C acetyl-CoAs
can acetyl CoA or ketone bodies be used to make glucose?
no, acetyl CoA is needed for the TCA, net 4C are given off as CO2 and no carbons are left to be made into glucose
what are the major users of ketone bodies?
heart, muscle, and brain
which has more energy, betahydroybutyrate or acetoacetate?
what brings fatty acids into the mitochondria?
carnitine transferase
what are the 4 effects of beta oxidation of fatty acids?
increased NADH, (which in turn increases ATP), increased acetyl CoA, the liver spares itself and makes ketone bodies from acetyl CoA, and these products also drive gluconeogenesis
what ketogenic enzyme is induced during fasting?
HMG synthetase
when are ketone bodies formed?
periods of high acetyl CoA, (due to beta oxidation/idling TCA cycle). HMG synthetase is also induced during fasting
can the liver use ketone bodies?
how can diabetes TYPE I cause ketoacidosis?
no insulin = high glucagon, (activates hormone sensitive lipase) = ketoacids, this can build up = ketoacidosis. lack of insulin prevents glucose absorption -> hyperglycemia. dehydration is also a factor.
how can alchol induce ketoacidosis?
alcohol is broken down to acetyl CoA and acetate, which can be made into high levels of KBs. alcohol also blocks the first steps of gluconeogenesis and causes osmotic movement of water -> urine (dehydration)
can starvation cause ketoacidosis?
why does the ketogenic diet seem to help children with epileptic seizures?
increased brain energy, (these pts may be less able to get KBs), increased mitochondrial #, (don’t know why this would be), “slower” energy from KBs though TCA), the GABA shunt hypothesis, (intermediates of TCA can be used as NTs, glutamate, succinate, etc), ketone bodies also seem to have direct anticonvulse effects on the brain
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