biochem exam 3

fatty acid roles

fuel, building phospho and glycolipids, membrane proteins, derivatives

derivatives of fatty acids

hormones and intracellular messages

triacylglycerols

uncharged esters, adipose, muscle energy

adipose

fuel, white, subcutaneous, visceral

adipocytes

site of triacylglycerol accumulation

lipids are digested by

by pancreatic lipases

triacylglycerol into

into fatty acids and monoglycerol

stomach emulsion

triacylglycerol surrounded by cholesterol

formation of bile acids

by cholesterol in liver

bile is secreted by

secreted by gallbladder

function of bile

orients ester bonds to make accessible to lipase digestion

colipase

protein that binds lipases for degradation

colipases is secreted by

secreted by pancreas

lipids are transported in

in chylomicrons

chylomicron pathway

chylomicrons to blood to triacylglycerols absorbed by tissues

free fatty acids and monoacylglycerol into

into plasma membrane by micelles

free fatty acids and monoacylglycerol packed into

packed into chylomicrons

fatty acid transport proteins

bring free fatty acids and monoacylglycerols into membrane

fatty acid binding proteins

proteins to move from cytosol to smooth ER and resynthesis of triacylglycerols

degrading chylomicrons

degraded by membrane lipases at adipose and muscle

3 steps of fatty acid processing

mobilization, activation/transport, breakdown

mobilization

triacylglycerol degradation from adipose for energy

lipid activation and transport

activate free fatty acids into mitochondria

lipid breakdown

into acetyl coA and krebs

controlling lipases

glucagon and epinephrine receptors activate pkA to perilipin and hormone sensitive lipase

perilipin

fat-droplet protein that restructures fatty so triacylglycerols are more accessible to mobilization

perilipin mechanism

phosphorylate perilipin activates adipose triglyceride lipase to start mobilization by releasing fatty acids and form diacylglycerol to bond to ATGL

lipid transport

carnitine into acyl carnitine via acyl carnitine translocate to enter mitochondrial matarix

B oxidation

shorten by 2 C per cycle, makes acetyl coA, NADH, FADH2

unsaturated and odd chain fatty acid oxidation

b-oxidation, isomerize to propynyl coA then sucinyl coA for oxaloacetate or krebs

unsaturated even oxidation

b oxidation, isomerize, acyl coA dehydrogenase then continue with normal breakdown

ketone bodies are derived

derived from fats

fasting/diabetes state

oxaloacetate to glucose and acetyl coA to oxaloacetate and d-3-hydroxybutrate

making ketone bodies

acetoacetate + D-3-hydroxybutyrate + acetone

characteristics of ketone bodies

water soluble, transportable acetyl units, high amounts because of untreated diabetes

ketone transport

liver to peripheral tissues

locations of fatty acid synthesis

liver and adipocytes

fatty acid synthesis formation

in cytoplasm the thiol group of acyl carrier protein causes malonyl ACP to malonyl coA

acetyl coA to malonyl coA

uses acetyl coA carboxylase

degradation of fatty acids

in mitochondrial matrix, that releases acetyl coA, NAD+ and FAD

saturated synthesis

condense malonyl acyl + acetyl ACP to acetoacetyl ACP to butyrl ACP to malonyl ACP until into palmitate

acetyl coA + oxaloacetate transport

using citrate using ATP citrate lyase into cytoplasm to acetyl coA+ oxaloacetate to malate to pyruvate for mitochondria

lipoproteins types

chylomicrons, VLDL,LDL,IDL,HDL

chylomicron characteristics

high lipid, low protein, GI to liver

VLDL

in liver endogenous lipids to peripheral tissues, high lipid, low protein

LDL

high lipid, low protein

IDL

HDL into this when it collects peripheral cholesterol

HDL

clears peripheral cholesterol, liver into plasma

familial hypercholesteremia

defective LDL receptors, autosomal dominate

Tay-sachs disease

no hexosaminidase S that breaks down gangliosidases, high lipids in brain

Gaucher’s disease

no glucocerebrosidase, autosomal recessive

krabbe disease

mutation of GALC leading to low glucocerebrosidase, autosomal recessive

G3P + fatty acyl coA

to monoacylglycerol 3P to phosphatidate

fate of phosphatidate

membrane phospholipids or diacylglycerol for triglycerides

cholesterol removal

elimination by feces, LDL pathway and receptor-mediated endocytosis for cholesterol into hepatocytes

in liver cholesterol

into bile and bile salts

bile characteristics

high polarity, exit via bile duct

enteroheptatic cycling

gut microbiome removes conjugated metabolism leading to 95% of cholesterol being reabsorbed

amino acid fates

into protein synthesis, gluconeogenesis, ketogenesis

essential amino acids

cannot be humanly synthesized

reason for amino acid degradation

damage, misfolding, changing metabolic needs

pepsin characteristic

proteolytic, in stomach, pH 2

emulsion release causes

stimulates release of sodium bicarbonate and pancreas proteolytic enzymes

aminopeptidases

increase digestioin

transporting amino acids

specific transporter for different amino acids

absorbed amino acids

into blood by Na-amino acid antiporters

oligopeptide absorption

through peptidases to interstitial cell, peptidase to go into blood

steps of amino acid degradation

amino removed, carbon skeleton metabolized in glycolysis or acetyl coA for krebs

location of amino acid degradation

mostly in liver

amino acid degradation in muscle

can degrade Leu,Ile,Val

transfers amino to glutamate

uses aminotransferases making alpha ketoglutarate

vitamin B derivative

derivative of PLP coenzyme

aspartate aminotransferase

amino of aspartate to alpha ketoglutarate

alanine aminotransferase

amino of alanine to alpha ketoglutarate

serine to pyruvate

serine dehydrogenase

threonine to alpha ketobutyrate

threonine dehydrogenase

removing amino of glutamate

glutamate dehydrogenase

characteristics of glutamate dehydrogenase

in mitochondria, uses NAD+/NADP+

inhibits glutamate dehydrogenase

inhibited by GTP

stimulates glutamate dehydrogenase

stimulated by ADP

types of amino acids

ketogenic and glycogenic

ketogenic

degraded to acetyl coA, ketone bodies, fattty acids

examples of ketogenic amino acids

leucin, lysine

glucogenic

degraded into pyruvate and kreb cycle intermediates

both of keto and glucogenic

isoleucine, phenylalanine, tryptophan, tyrosine

aquatic direct ammonia excretion

ammonotellic

ammonia + bicarbonate to carbamoyl phosphate

using carbamoyl phosphate synthetase 1

carbamoyl phosphate synthetase 1 characteristic

needs n-acetylglutamate regulator

carbamoyl phosphate synthetase 1 inhibition

inhibited by acetylation

carbamoyl phosphate synthetase 1 stimulation

stimulated by deacetylation

acetyl coA + glutamate to N-acetylglutamate

using n-acetylglutamate synthase

n-acetylglutamate synthase characteritics

activated by arginine-urea intermediate

carbamoyl phosphate + ornithine to citrulline

using ornithine transcarbamoylase

citrullin to arginineosuccinate

orgininosuccinate synthetase using ATP and amino aspartate

citrullin to arginineosuccinate locations

into cytoplasm

arininosuccinate to fumate or arginine

using argininosuccinase

fumarate pathway in urea cycle

to malate to oxaloacetate to either gluconeogenesis or aspartate

arginine pathway in urea cycle

using arginase into ornithine or urea

mutate of urea cycle enzymes

causes high ammonia, physical and mental disabilities

alkaptonuria

no homogentisate oxidase causing dark urine and arthritis