Lecture 27 - 031111

Lecture 27 - 031111 - Final exam Mar. 18, 3:00pm-5:59pm...

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Unformatted text preview: Final exam Mar. 18, 3:00pm-5:59pm CENTR 101 and 115 Sit one seat apart Fill in the entire bubble Bring ID Fill in ID in scantron bubbles (replace A by 1) Write names on all sheets of exam No calculator 1 Lecture 27 Integration of Metabolism (II) Insulin secretion from a pancreatic cell Plasma membrane Biochemical response to physiological conditions: hormones 2 3 Starved-fed cycle Insulin signals storage of fuels Glucose uptake by liver An isozyme of hexokinse --- glucokinase Glucokinase has high K M and not inhibited by G6P Higher [glucose] in blood -> form G6P more rapidly glucose Branched-chain amino acids (Val, Ile, Leu) Protein synthesis GAP 4 Starved-fed cycle Glucagon and epinephrine signal production of energy Keep blood-glucose level: 1. Mobilization of glycogen and the release of glucose by the liver 2. Release of fatty acids by adipose tissue 3. Shift in the fuel used from glucose to fatty acids by muscle and the liver 5 6 Starved-fed cycle Refed state (after breakfast): Fat processed as the normal fed state Glucose different: Peripheral tissues absorb glucose first Liver remains gluconeogenesis to replenish livers glycogen stores Then, liver takes glucose for fatty acid synthesis 7 Prolonged starvation Provide enough glucose to brain and other tissues (like red blood cells) Preserve proteins by shifting to fatty acids and ketone bodies 8 Decreased insulin and increased Glucagon and epinephrine Prolonged starvation: First day Liver: Gluconeogenesis and fatty acid oxidization Glycerol used for glucose synthesis Adipose tissue: mobilization of triacylglycerols Muscle: switch to fatty acids completely (no glucose use) -> [acetyl CoA]...
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Lecture 27 - 031111 - Final exam Mar. 18, 3:00pm-5:59pm...

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