nutr 455 exam 2

Oligosaccharide

3-10 monosaccharides linked by glycosidic bonds.

in beans, peas, bran, and whole grain

composed of glucose, galactose, fructose

Oligosaccharide examples

raffinose, stachyoses, verbascose

cellulose

glucose units rotated 180\* relative to next residue and linked by beta bonds

very limited ability to digest in humans

amylose

linked by alpha bonds and face each other

polysaccharides

starch

glycogen

cellulose

starch

in plant; grains, potatoes, legumes

starch amylose

linear, glucose alpha 1→4 glycosidic bonds

starch amylopectin

branched alpha 1→6 glycosidic bonds

glycogen

storage form in animal (liver and skeletal muscle)

high branched and readily available

regulated by glycogen synthesis/glycogenolysis

what is cellulose

major component of plant cell walls

beta 1→4 glycosidic bonds

__**indigestible**__ by mammals

amino sugars

chitin

glycoprotein hormones

beta-D-glucosamine → chitin

anti inflammatory

beta-D-glucosamine → glycoprotein hormones

toxic

digestion CHO mouth

amylose AND amylopectin salivary glands release alph amylase to hydrolyze alpha 1→4 glycosidic bonds;

forms dextrins

digestion CHO stomach

amylose AND amylopectin; acidity of gastric juice destores enzymatic activity of alpha amylase so dextrins pass unchanged to small intestine

digestion CHO small intestine amylose

pancreas release pancreatic alpha amylase to hydrolyze alpha 1→4 glycosidic bonds; dextrins broken down to maltose

digestion CHO small intestine amylopectin

pancreas release pancreatic alpha amylase to hydrolyze alpha 1→4 glycosidic bonds; produce limit dextrins, maltotriose, isomaltose, and maltose.

hydrolysis stops 4 residues away from alpha 1→6 bond

digestion CHO brush border amylose

maltose hydrolyzed by maltase (in border) to form free glucose

digestion CHO brush border amylopectin

maltose, maltrotriose, and isomaltose further hydrolyzed in brush border by maltase or isomaltse (alpha dectrinase) to glucose

alpha dextrinase sole carbohydrate that can hydrolise alpha 1→6 glycosidic bonds

salivary alpha amylase

alpha 1→4 bonds in starch = dextrins

pancreatic alpha amylase

alpha 1→ 4 bonds in starch = maltotriose

alpha dextrinase or iosmaltase

alpha 1→6 bonds in dextrins = oligosaccharides

small intestine

glucoamylase, glucosidase, and surase

alpha 1→4 bonds in maltase = maltotriose

small intestine

trehalase

trehalose small intestine

sucrase

sucrose

maltase

maltose

lactase

lactose

only intestinal enzyme that will hydrolyze alpha 1→6 glycosidic bonds during digestion of carbohydrates (CHO) is?

alpha dextrinase

absorption of glucose and galactose into cell

active transport by sodium glucose transporter 1 (SGLT1)

mutation associated with GLU/GAL malabsorption

absorption of glucose and galactose into blood

diffusion, GLUT2

especially utilized after high CHO meals

absorption of fructose into cell

facilitated transport- GLUT5

absorption of fructose into blood

GLUT2

absorption of fructose

limited in 60% of adults

typically no fructose beyond portal vein (efficiently absorbed by liver)

transport of monosaccharide into enterocytes step 1

active transport of glucose and galactose requiring ATP and NA+

transport of monosaccharide into enterocytes step 2

facilitated transport of glucose and galactose into enterocyte by GLUT 2

intestinal lumen glucose levels high

transport of monosaccharide into enterocytes step 3

fructose entering the enterocyte via transport facilitated by GLUT 5 and leaves cell via transport by GLUT 2

absorption in small intestine

SGLT1 (sodium glucose transporter 1)

GLUT2 (Glucose transporter 2)

GLUT5 (Glucose transporter 5)

Catalytic proteins (enzymes)

functionality depends on protein and prosthetic group or coenzyme

maximum velocity

enzyme velocity at substrate saturation

Km (michaelis constant)

concentration of substrate when reaction is at 1/2 maximum velocity

Vmax graph

glucose transporters

used because glucose is hydrophilic so can not diffuse on own

GLUT1

glucose, galactose, mannose, glucosamine

in erythrocytes, central nervous system, blood brain barrier, placenta, fetal tissues

GLUT2

glucose, galactose, mannose, glucosamine, fructose

in liver, beta cells of pancreas, kidney, small intestine

GLUT3

glucose, galactose, mannose, xylose, dehydroascorbic acid

GLUT4

insulin dependent

glucose, glucosamine, dehydroascorbic acid

in muscle, heart, brown and white adipocytes

GLUT5

fructose, but not glucose

in intestine, kidney, brain, skeletal muscle, adipose tissue, and hepatocytes

Insulin

binds to membrane receptor to stimulate GLUT4 to move to membrane

maintence of blood glucose levels

allows glucose in

translocation of GLUT4 to membrane 1

biosynthesis of GLUT4 stored in GSVs is stimulated

translocation of GLUT4 to membrane 2

GSV transports to membrane through microtubules and actin

translocation of GLUT4 to membrane 3

interaction between GVS, plasma membrane through tethering

translocation of GLUT4 to membrane 4

GVS docks in plasma membrane for fusion

translocation of GLUT4 to membrane 5

lipid bilayers fuse

translocation of GLUT4 to membrane 6

GLUT4 becomes a part of membrane and able to transport glucose in

GRB2

most important

glycemic index (GI)

increase in blood glucose during 2-hour period after comsuming certain amount of CHO compared with equal CHO from reference food

glycemic load

considers quantity and quality of CHO in food

GI x g of CHO in 1 serving

OGTT

Oral glucose tolerance test

determine how well body is able to absorb glucose after ingesting a certain amount

OGTT slow

more glucose resistant

calculation of GI

glycemic index calculated by dividing area under curve for test food by area under curve for reference food and multiplying by 100

OGTT fast

more glucose tolerant

glycogenesis

synthesis of glycogen

glycogenolysis

breakdown of glycogen

glycolysis

oxidation of glucose

gluconeogenesis

production of glucose from non carbohydrate intermediates

pentose phosphate pathway

production of 5 carbon monosaccharides and NADPH

tricarboxylic acid (TCA) cycle

oxidation of pyruvate and acetyl-CoA to CO2 and H2O

the biochemical pathway of glucose synthesis from non carbohydrate sources like amino acids and protein during starvation time points is referred as ___

gluconeogensis

glycogenesis liver

\~7% of tissue weight

maintains systemic glucose homeostasis

glycogenesis skeletal muscle

\~1% tissue weight

energy source, cannote release free glucose to the blood

Hexokinase Types 1 and 2

in muscle, allosterically inhibited by glucose-6-P, low Km functions are max velocity at fasting blood glucose concentrations.

not induced by insulin

Hexokinase Type 4 (glucokinase)

liver and pancreas not inhibited by G-6-P (liver has high levels)

high Km and functions at max velocity __**only**__ when glucose levels are high

induced by insulin in normal but not in insulin resistant

the peptide hormone that activates glucose absorption and glycogenesis is __

glucagon

glycogenolysis cleaved

from non reducing end (systematically)

synthesis when

high glucose levels

phosphorylase

cleaves

allosteric regulation

allosterically regulated positively by AMP and negatively by ATP and G-6-P

phyophorylase b kinase

stimulated by hormones glucagon and epinephrine and cAMP

glucagon stimulates glycogenolysis

with enzymes

epinephrine

is high when stressed

glucagon

created in starvation

insulin increases

glycogen synthesis

insulin decreases

glycogenolysis

glycogen synthase

dephosphorylated form is active

insulin causes dephoshorylation

activates PP1 (protein phosphatase 1)

glycogen phosphoylase deactivated by

PP1

glucagon can stimulate glycogenolysis by activating ___ which inactivates glycogen synthase via phosphorylation and activates phosphorylase kinase via phosphorylation

protein kinase A

muscle phosphorylase

activated by AMP, inhibited by G-6-PO4, ATP, and glucose

hormonal regulation by covalent modication via PP1

liver phosphorylase

less sensitive allosteric regulation by intercellular ligand

hormonal regulation

what will happen if we have mutation or deficiency in the enzymes involved in glycogenolysis pathway?

glycogen accumulates in liver and results in development of glycogen storage diseases

phenotype of deficiency in liver?

mainly found in liver and kidney to maintain blood glucose for other cells in obyd

Von Gierke

in liver and kidney, Glucose-6-phopshatase or transport system

increase glycogen and theres a massive enlargement of the liver

Pompe

all organs, alpha 1,4-glucosidase (lysosomal)

massive increase in glycogen

cardiorespiratory failure causes death, usually before 2 years old

Cori

muscle and liver

amylo-1,6-glucosidase (debranching enzyme)

increased glycogen with short outer branches

enlargement of liver

Anderson

liver and spleen

branching enzyme (alpha 1,4→ alpha 1,5)

normal glycogen but very long outer branches

progressive cirrhosis of liver; failure and death before age 2

McArdle

muscle

phosphorylase

moderately increase glycogen

limited ability to perform strenuous exercise, painful muscle cramps

Hers

liver

phosphorylase

increase glycogen

enlargement of liver

The enzyme that converts pyruvate into oxaloacetate is

pyruvate carboxylase

anomeric carbon

during cyclization, carbonyl carbon forms 2 diasteriomers. the new stereocenter is the anomeric carob

locate anomeric carbon

locate oxygen then carbons on either side. carbon without CH2OH group