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51 Cards in this Set

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  • Back

Lactose: bond? enzyme? made of?

lactase, beta 1-4, galactose and glucose

Sucrose: bond? Enzyme? Made of?

sucrase, alpha 1-2, glucose and fructose

maltose and isomaltose: bond? Enzyme? Made of?

maltose: alpha 1-4, maltase
isomaltose, alpha 1-6, isomaltase
- 2 glucose

alpha endoglycosidases

digests alpha 1-4 bonds

what are disaccharides?

lactose, sucrose and maltose

bonds in amylose vs amylopectin

amylose: alpha 1-4
amylopectin: alpha 1-6

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

What digestion of carbohydrates in stomach?


What does pancreatic alpha amylase act on? where is it released?

alpha 1-4 bonds aka alpha dextrins, released in duodenum

panreatic alpha amylase makes what?

oligosaccharides, disaccharides (maltose and isomaltose) and trisaccharides

Alpha glucosidases: breaks down what? found where? breaks down into?

1) hydrolyze oligosaccharides, trisaccharides and disaccharides AT THE ENDS!
2) small intestine
3) glucose, monosaccharides

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)

Where do undigested carbs go? What happens to them?

into the colon, colon bacteria metabolizes saccharides via fermentation

What do undigested carbs become?

gas (H2, CO2,CH3), short chain fatty acids, lactate

What happens to the gas from colon bacteria?

they are osmotically active = increased retention of water in colon, water rushes into the lumen = diarrhea.
SYMPTOMS: diarrhea, bloating, bad breath

A carbos?

inhibits alpha glucosidase therefore glucose is not being broken down, treats type 2 diabetes mallitus

Site of monosaccharide absorption

duodenum, upper jejunum


secondary active carrier, glucose, Na+/K+ pump creates Na+ gradient, and glucose goes against its gradient

Glut 5

- fructose, glucose, galactose

- sodium independent monosaccharide transporter

- facilitated diffusion

- intestinal epithelium and spermatazoa

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


red blood cells, all barriers (blood-brain, blood-retina, blood placental, blood testes), high affinity


Brain, neurons, high affinity


- adipose tissue, skeletal muscle, cardiac muscle

- insulin sensitive receptor; in presence of insulin, lots of receptors

- high affinity for glucose

What is a cytoplasmic pathway?


anaerobic glycolysis

pyruvate ---> lactate via lactate dehydrogenase (makes NADH into NAD+ to allow continuation of glycolysis)

Hexokinase/Glucokinase Step

Glucose to Glucose-6-Phosphate

- ATP to ADP

- irreversible

Phosphofructokinase-1 Step

Fructose-6-Phosphate to Fructose-1,6-bisphosphate

- Rate limiting enzyme

- irreversible

Glyceraldehyde-3-Phosphate Dehydrogenase

Glyceraldehyde-3-Phosphate to 1,3-bisphosphoglycerate

- oxidation reduction reaction

- arsenic metal ion competes with Pi here

Phosphoglycerate Kinase

1,3-bisphosphoglycerate to 3-Phosphoglycerate

- substrate level phosphorylation


2-Phosphoglycerate to Phosphoenolpyruvate

- bacterial enolate inhibited by fluoride

Pyruvate Kinase

Phosphoenolpyruvate to Pyruvate

- irreversible

- substrate level phosphorylation

- deficiency = hemolytic anemia


- 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


- 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

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

PFK-1: inhibited by? stimulated by?

- inhibited by: ATP, citrate

- stimulated by: AMP, Fructose-2,6-bisphosphate

- insulin stimulates, glucagon inhibits

Arsenic Poisoning

Glyceraldehyde-3-phosphate dehydrogenase, arsenic binds to organic phosphate, skips to 3-Phospholycerate and Net ATP is 0


binds to Hemoglobin A = decreases affinity for oxygen = allows release of oxygen, made from mutase from 1,3-bisphosphoglycerate,

Enzymes induced by insulin and repressed by glucagon

glucokinase, phosphofructokinase and pyruvate kinase

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,

pyruvate transporter

How pyruvate enters mitochondria

pyruvate converted to acetyl coA

- pyruvate dehydrogenase complex
- oxidative-decarboxylation

Pyruvate Dehydrogenase complex

- 5 enzymes:

Thiamine pyrophosphate (TPP)

Lipoate (lipoic acids)

NAD+ (niacin derivative)

FAD (riboflavin rerivative)

Reduced Coenzyme A (CoASH) (pantothenic acid derivative)

What does arsenate bind to in the PDH complex?

E2 - lipoate


- citrate to isocitrate

- fluoroacetate (rat poison) competes here

- fluoroacetyl coA + oxaloacetate = flurocitrate

isocitrate deyhdrogenase

- isocitrate to alpha-ketoglutarate

- rate limiting enzyme

- oxidative decarboxylation

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

succinate thiokinase

- Succinyl CoA to succinate

- substrate level phosphorylation

- GDP to GTP

- coASH exits

succinate dehydrogenase

- succinate to fumarate

- in the inner mitochondrial membrane

- complex 2!

- FAD to FADH2

malate dehydrogenase

malate to oxaloacetate

- regenerates oxaloacetate

Net ATP from Anaerobic glycolysis


Net ATP from aerobic glycolysis