Metabolism: Overview Flashcards
What fuel sources can the brain use/store?
Brain primarily uses glucose, and uses a lot of it! It can also use ketone bodies in times of starvation
What fuel sources can muscles use/store?
Muscles are the main store of glycogen in the body. They use glucose, fatty acids, and ketone bodies as fuel. They’re able to send lactate back to the liver to form more glucose (cori cycle) and can send alanine to the liver to form more glucose (glucose-alanine cycle) in the case of muscle protein breakdown
What fuel sources does the liver use/store?
The liver pulls the majority of glucose from the blood supply for manufacture of fatty acids, glycogen, ketone bodies. The liver processes a lot of the body’s glucose. The liver produces glucose from glycogen stores for the rest of the body, and generates NADPH from the pentose phosphate pathway
What fuel sources do fat tissues use/store?
Fat tissues mostly store triacylglycerides (fatty acids + glycerol). Glycerol can be used to form glycogen or broken down into glucose for glycolysis depending on needs. Fatty acids are degraded to acetyl CoA to produce energy.
What fuel sources do RBCs use/store?
Red blood cells don’t have mitochondria, so they can only produce energy from the steps of glycolysis. They use glucose
Are GLUT transporters passive or active?
Passive. Glucose has to be passed along the concentration gradient.
What are the differences between GLUT 1, 2, 3, & 4?
Glut 1 has a low Km (high binding affinity) and is seen in all cells. It accommodates the basic glucose needs of a cell.
Glut 2 has a higher Km (low binding affinity) and is only found in the liver. Glut 2 is bidirectional, it can pass glucose into and out of the liver.
Glut 3 is like Glut 1 but found only in neurons (extra glut 3 in neurons for extra glucose needs). It has a slightly lower Km.
Glut 4 is used in muscle cells, and can be increased in number from aerobic exercise over time. Subject to insulin regulation.
What is insulin’s mechanism of action?
Insulin binds to a receptor tyrosine kinase dimer and activates protein kinases. these kinases deactivate glycogen synthase kinase (which is trying to deactivate glycogen synthase by phosphorylating it) and allows glycogen synthase to remain active. In other pathways insulin activates a phosphatase to pull phosphates off of enzymes.
What is glucagon’s mechanism of action?
Glucagon binds to a GPCR, which goes to activate adenylate cyclase, which produces cAMP from ATP. cAMP activates PKA (protein kinase A), which phosphorylates phosphorylase kinase, which phosphorylates phosphorylase (which causes glycogen breakdown)
What is epinephrine’s mechanism of action?
Epinephrine binds to a GPCR, which goes on to activate adenylate cyclase, which causes cAMP to activate PKA.
What are acini?
Small clusters of cells around a duct used for secretion or absorption.
What are islets of langerhans?
Pancreatic clusters of alpha and beta cells, where secretion of insulin (beta) and glucagon (alpha) actually occurs.
Where is epinephrine made? What stimulates secretion of epinephrine? What does it do?
Epinephrine is made in the adrenal medula. Its secretion is boosted during stressful moments, or during exercise. Epinephrine is key in the “fight or flight” response of the body to stress. It pushes homeostasis towards the breakdown/use of energy bearing molecules (glucose, fatty acids)
Does insulin cause an increase or decrease in blood glucose levels?
Decrease! Insulin leads to the stimulation of glycolysis, which consumes glucose for energy. Insulin activates phosphoprotein phosphatase-I which takes a phosphate off of pyruvate kinase and pushes it into the active state, which encourages glycolysis.
Insulin activates phosphoprotein phosphatase-I which takes a phosphate off of glycogen synthase (activating it in this case) and encourages glycogen production
Does glucagon cause an increase or decrease in blood glucose levels?
Increase! Glucagon leads to stimulation of the gluconeogenesis pathway, which leads to the production of glucose. Glucagon activates protein kinase A, which phosphorylates (deactivates in this case) PFK2. PFK2 normally turns F6P into F26bP, which stimulates PFK1 and glycolysis, but is inhibited. So blood glucose is not being used up in glycolysis. In the glycogen pathway, glucagon causes PKA to phosphporylate (activate in this case) phosphorylase kinase, which phosphorylates (activates) glycogen phosphorylase. Glycogen phosphorylase cuts G-1Ps off of glycogen. Gluconeogenesis is not necessarily boosted by glucagon, but since glycolysis has been inhibited gluconeogenesis is able to predominate.
What happens in the fed state (general)?
Glycolysis begins, glycogen synthesis begins, fatty acid synthesis begins. Proteins are broken down, digested in the urea cycle.
What happens in the fasting state (general)?
Energy reserves are released. Glycolysis is inhibited. Gluconeogenesis begins.
What happens in the stressed state (general)?
Epinephrine is released. The body releases any stored energy so the muscles can be maximally active. Glycolysis continues
What are VLDLs?
Denser (than chylomicrons) fatty acid storage molecules used to transport triacylglycerides from the liver to fat cells.
What are chylomicrons?
Fatty acid storage molecules used to transport triacylglycerides from the intestine to fat cells and muscle cells.
Draw the framework of human metabolism
glycolysis & gluconeogenesis, glycogen synthesis & breakdown, amino acid breakdown & synthesis, fatty acid breakdown & synthesis, Krebs & electron transport chain, urea cycle. Pentose phosphate pathway, lactate production,
