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51 Cards in this Set
- Front
- Back
Lactose: bond? enzyme? made of? |
lactase, beta 1-4, galactose and glucose |
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Sucrose: bond? Enzyme? Made of? |
sucrase, alpha 1-2, glucose and fructose |
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maltose and isomaltose: bond? Enzyme? Made of? |
maltose: alpha 1-4, maltase |
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alpha endoglycosidases |
digests alpha 1-4 bonds |
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what are disaccharides? |
lactose, sucrose and maltose |
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bonds in amylose vs amylopectin |
amylose: alpha 1-4 |
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What is digested in the mouth? and by what? Broken down into what? |
Starch, salivary alpha amylase, a type of alpha-endoglycosidases, alpha dextrins, maltose and matotriose |
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What digestion of carbohydrates in stomach? |
nothing! |
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What does pancreatic alpha amylase act on? where is it released? |
alpha 1-4 bonds aka alpha dextrins, released in duodenum |
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panreatic alpha amylase makes what? |
oligosaccharides, disaccharides (maltose and isomaltose) and trisaccharides |
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Alpha glucosidases: breaks down what? found where? breaks down into? |
1) hydrolyze oligosaccharides, trisaccharides and disaccharides AT THE ENDS! |
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What happens in the mucosal lining of the upper jejunum? |
final digestion, disaccharides attached to brush border and broken down by alpha glucosidases (isomaltase, maltase, etc) |
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Where do undigested carbs go? What happens to them? |
into the colon, colon bacteria metabolizes saccharides via fermentation |
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What do undigested carbs become? |
gas (H2, CO2,CH3), short chain fatty acids, lactate |
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What happens to the gas from colon bacteria? |
they are osmotically active = increased retention of water in colon, water rushes into the lumen = diarrhea. |
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A carbos? |
inhibits alpha glucosidase therefore glucose is not being broken down, treats type 2 diabetes mallitus |
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Site of monosaccharide absorption |
duodenum, upper jejunum |
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SGLT-1 |
secondary active carrier, glucose, Na+/K+ pump creates Na+ gradient, and glucose goes against its gradient |
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Glut 5 |
- fructose, glucose, galactose - sodium independent monosaccharide transporter - facilitated diffusion - intestinal epithelium and spermatazoa |
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Glut 2 |
- glucose, galactose, fructose - liver and pancreatic beta cells, low affinity for glucose = functions at high concentrations of glucose - works with glut 5 and SGLT 1 |
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GLUT 1 |
red blood cells, all barriers (blood-brain, blood-retina, blood placental, blood testes), high affinity |
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GLUT 3 |
Brain, neurons, high affinity |
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GLUT 4 |
- adipose tissue, skeletal muscle, cardiac muscle - insulin sensitive receptor; in presence of insulin, lots of receptors - high affinity for glucose |
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What is a cytoplasmic pathway? |
glycolysis |
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anaerobic glycolysis |
pyruvate ---> lactate via lactate dehydrogenase (makes NADH into NAD+ to allow continuation of glycolysis) |
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Hexokinase/Glucokinase Step |
Glucose to Glucose-6-Phosphate - ATP to ADP - irreversible |
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Phosphofructokinase-1 Step |
Fructose-6-Phosphate to Fructose-1,6-bisphosphate - Rate limiting enzyme - irreversible |
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Glyceraldehyde-3-Phosphate Dehydrogenase |
Glyceraldehyde-3-Phosphate to 1,3-bisphosphoglycerate - oxidation reduction reaction - arsenic metal ion competes with Pi here |
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Phosphoglycerate Kinase |
1,3-bisphosphoglycerate to 3-Phosphoglycerate - substrate level phosphorylation |
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enolase |
2-Phosphoglycerate to Phosphoenolpyruvate - bacterial enolate inhibited by fluoride |
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Pyruvate Kinase |
Phosphoenolpyruvate to Pyruvate - irreversible - substrate level phosphorylation - deficiency = hemolytic anemia |
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Hexokinase |
- Km is 0.05mM - low Vmax and low Km = high affinity - substrates early - active at low concentrations of glucose - in cells other than liver and pancreatic beta - allows for redistribution of glucose |
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Glucokinase |
- Km is 5mM - High Km, High Vmax - Low affinity for glucose - active at high concentrations of glucose - in liver and pancreatic beta cells - induced by insulin |
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Maturity onset diabetes of the young (MODY) |
- type of type 2 diabetes - mutation in pancreatic glucokinase - Glut 2 uptakes glucose = Glucokinase engulfs it into G-6-P - no glucokinase = no insulin released = lots of glucose in blood = hyperglycemia - symptoms: polydipsia and polyuria |
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PFK-1: inhibited by? stimulated by? |
- inhibited by: ATP, citrate - stimulated by: AMP, Fructose-2,6-bisphosphate - insulin stimulates, glucagon inhibits |
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Arsenic Poisoning |
Glyceraldehyde-3-phosphate dehydrogenase, arsenic binds to organic phosphate, skips to 3-Phospholycerate and Net ATP is 0 |
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2,3-Bisphosphoglycerate |
binds to Hemoglobin A = decreases affinity for oxygen = allows release of oxygen, made from mutase from 1,3-bisphosphoglycerate, |
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Enzymes induced by insulin and repressed by glucagon |
glucokinase, phosphofructokinase and pyruvate kinase |
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pyruvate kinase and glucagon |
glucagon inhibits the enzyme =phosphorylates=inactive, activated by F-1,6-bp, inhibited by: ATP, acetyl co-A, alanine, long chain fatty acids, |
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pyruvate transporter |
How pyruvate enters mitochondria |
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pyruvate converted to acetyl coA |
- pyruvate dehydrogenase complex |
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Pyruvate Dehydrogenase complex |
- 5 enzymes: Thiamine pyrophosphate (TPP) Lipoate (lipoic acids) NAD+ (niacin derivative) FAD (riboflavin rerivative) Reduced Coenzyme A (CoASH) (pantothenic acid derivative) |
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What does arsenate bind to in the PDH complex? |
E2 - lipoate |
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Aconitase |
- citrate to isocitrate - fluoroacetate (rat poison) competes here - fluoroacetyl coA + oxaloacetate = flurocitrate |
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isocitrate deyhdrogenase |
- isocitrate to alpha-ketoglutarate - rate limiting enzyme - oxidative decarboxylation |
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alpha-ketoglutarate dehydrogenase complex |
- alpha-ketoglutarate to succinyl coA - oxidative decarboxylation - similar to PDH complex - succinyl coA has a high energy thioester bond - coASH used here |
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succinate thiokinase |
- Succinyl CoA to succinate - substrate level phosphorylation - GDP to GTP - coASH exits |
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succinate dehydrogenase |
- succinate to fumarate - in the inner mitochondrial membrane - complex 2! - FAD to FADH2 |
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malate dehydrogenase |
malate to oxaloacetate - regenerates oxaloacetate |
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Net ATP from Anaerobic glycolysis |
2 ATP |
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Net ATP from aerobic glycolysis |
7 ATP |