Mobilization/oxidative Degradation Of Fa

Front 1

What is a monoacylglycerol, diacylglycerol, and triacylglycerol?

Back 1

They consist of 1,2,3 FA connected to a glycerol by an ester linkage.

Front 2

What is an emmulsion droplet?

Back 2

When a fat droplet is attacked by ACID-STABLE LIPASE it is broken down to FA, mono-, and diacylglycerols and is converted into an emmulsion droplet. The process helps increase the surfact to volume ratio.

Front 3

How are emulsion droplets processed?

Back 3

They are attacked by PANCREATIC LIPASE-this cleaves them in FA+monogly. PHOSPHOLIPASE A2 cleaves glycerol into a FA+lysophosphate.

Front 4

What are bile acid/salts?

Back 4

Bile acid-devivative of cholesterol, acts as detergent (1 hydrophil end & 1 hydrophob end).

Front 5

What are micelles?

Back 5

~Tiny pancake like structures formed from release of lipids from emulsion droplets (when they are processed w/bile)
~diameter 40-600 A
~high surface:volume ratio (makes absorbtion easier)
~contain FA, monogly, lysophospholipids, cholesterol, and fat-sol vitamens

Front 6

What is a chylomicron?

Back 6

~kind of lipoprotein
~tri+other lipoproteins are put into chylomicron
~secreted into blood where attacked by LIPOPROTEIN LIPASE
~releases tri and glycerol...fats carried by serum albumin to adipose and other tissue

Front 7

What are the actions of lipase?

Back 7

lipase is a water soluable enzyme that breaks the ester bond of lipids.

Front 8

What is the structure of palmitic acid?

Back 8

Saturated straight chain 16 C

Front 9

How are trigly digested in the intestine?

Back 9

~attacked by PANCREATIC LIPASE>Tri+ 2 FA
~PHOSPHOLIPASE A2 cleaves gly phospholipids>FA + lysophosphatide
~lipids from emulsion drops react w/bile>its detergent properties from pancake micelles (they cont:FA, mono, lysophospho, cholest, and fat sol vit)
~micelles absorbed by intestinal cells
~short/med FA released direct to blood where bind to albumin
~long FA made into tri, combined with lipoproteins into chylomicrons, secreted into lymph then blood

Front 10

How are tri broken down in adipose cells?

Back 10

~TRIACYLGLYCEROL LIPASE(aka hormone sensitive lipase) removes FA
~other lipases break down digly into gylcerol + 3 FA
(triacylglycerol lipase is the highly regulated RXN)

Front 11

How is TRIACYLGLYCEROL LIPASE regulated?

Back 11

~very carefully...
~+ by adrenaline, glucagon, ACTH...when activated gets Phosphorylated
~- by insulin...gets dephos to be deactivated
(remember insulin wants low blood sugar...if not use FA then will use glucose and lower it in blood, vise versa for glucagon, and adrenaline and ACTH are stress hormones...we want to mobilize good, fast NRG so they increase activity of breakdown)

Front 12

How are FA transported in the blood?

Back 12

bound non-covalently to serum albumin...when reach target the are activeted by binding to coenzyme A (via ACYL COA SYNTHETASE)...RXN costs 2 ATP!!

Front 13

How are FA transported into the mitochondria?

Back 13

~if less than 10 C, diffuse directly and are bound to CoA .
~if more than 10 C, bound to Carnitine by CARNITINE ACYLTRANSFERASE I...looks like this...
FACoA+Carnitine}FA Carnitine+CoASh
~then FACar transported across membrane
~then CARNITINE ACYLTRANSFERASE II undoes it...
FACar+CoASH}FACoA + Carnitine

Front 14

From what AA is carnitine derived?

Back 14

lysine

Front 15

What is the cycle of B-oxidation?

Back 15

1. FACoA + FAD } Enoyl Coa+ FADH2
~catalyzed by ACYL COA DEHYDROGENASE (several kinds...LCAD for 12 +, MCAD for 6-12, SCAD for 4-6) Basically a double bond added @ B C
2. Enoyl CoA + H2O } L-3-Hydroxyacyl CoA
~catalysed by ENOYL COA HYDRATASE (note only produces L steroisomer)...basically double bond removed and OH added at G C.
3. L-3-Hydroxyacyl CoA + NAD+} Ketoacyl CoA + H+ + NADH
~catalyzed by L-3-HYDROXYACYL DEHYDROGENASE...basically replaces OH with a double bonded O
4. Ketoacyl CoA + CoASH}FACoA + FA minus 2 Carbon
~cleaved by THIOLASE...basically chops off 2 carbons and the shorter FA will go throught cycle agian until finished.

Front 16

What are the different types of FattyAcyl CoA Dehydrogenases?

Back 16

LCAD for 12 +, MCAD for 6-12, SCAD for 4-6

Front 17

What is the energy yeild for B Oxidation?

Back 17

For each cycle your get Acetly CoA, FADH2 and NADH. For something like Palmitic Acid (w/16 C) you get 8 Acyl CoA, 7 FADH2 and 7 NADH which yeilds 8x10+7x1.5+7x2.5=108. Since we used 2 ATP to join our FA to CoA, the net yeild is 106.

Front 18

Hoew does the B oxidation NRG yeild differ from that of glucose breakdown?

Back 18

the ATP:Molecular Weight is much more productive. Ex: Palmitic acid gives 106 ATP/weighs 256. Glucose gives 30 ATP/weighs 180. Do the math and the FAT:Glucose ratio is 2.48 so Fats are more than 2 times as fattening by weight.

Front 19

Where are very long chain FA degraded and what is the by-product?

Back 19

In peroxisomes and H2O2 is produced because of a very different acyl dehydrogenase RXN.

Front 20

What is the pathway for ketogenesis?

Back 20

1. 2 Acetyl CoA ->(via enzyme Thiolase)->Acetoacetyl CoA + CoA
2.Acetoacetyl CoA + Acetyl CoA + H2O->(via Hydroxymethylglutary CoA)-> 3-Hydroxy-3-methylglutaryl CoA + CoA
3. 3-Hydroxy-3-methylglutary CoA->( via hydroxymethylglutary CoA lyase)->Acetoacetate + Acetyl CoA
4. Acetoacetate + NADH + H -> (via 3-hydroxybutyrate dehydrogenase)->D-3-Hydroxybutyrate + NAD+

Front 21

What is the role of ketogenesis?

Back 21

When FA are oxidized the majority of the NRG obtained comes from their entry into the TCA cycle, which requires oxaloacetate (from glycolysis). When oxaloacetate is low, the acetyl CoA form FA oxidation builds up (b/c remember it cannot move freely on its own). It is broken into ketone bodies via ketogenesis into acetoacetate and D-3-hydroxybutyrate, which can both diffuse freely out of the liver mitochondria and int the blood...yeah!

Front 22

What are the pathways for Ketone use by tissue?

Back 22

1. D-3-Hydroxybutyrate + NAD+->(via 3-hydroxybutyrate dehydrogenase)->Acetoacetate + NADH + H ->
2. Acetoacetate+ Succinate CoA->(via acetoacetate:succinate CoA transferase)->Acetoacetyl CoA + Succinate
4. Aceoacetyl CoA + CoA->(thiolase)->2 Acetyl CoA
Basically the opposite of ketogenesis w/ some small differences

Front 23

What is ketoacidosis and how does it occur?

Back 23

A buildup of + charges in the blood. In uncontrolled diabetes and starvation, there is no oxaloacelate b/c glucose is exhausted. So ketogenesis makes tons of ketone bodies, whice cannot not be broken down. They are acidic and buildup in the blood-causing a fall in pH=acidosos. Can lead to coma :(

Front 24

What are the steps of B oxidation of FA w/ odd # Carbons?

Back 24

B Oxidation proceedes normally until last step when get acetyl CoA and propinyl CoA. Propional CoA is converted to Succinyl CoA...
1. Propionyl CoA->D-Methylmalonyl CoA
*cat by propionyl CoA carboxylase which requires biotin
2. D-Methylmalonyl CoA->L-Methylmalonyl CoA
*cat by Methylmalonyl CoA racemase
3. L-Methylmalonyl CoA->Succinyl CoA
*cat by Methylamonyl CoA mutase which req Vit B12
Succinyl CoA then can enter TCA cycle.

Front 25

What is LCAT deficiency?

Back 25

A disorder of lipoprotein metabolism in which lecithin cholesterol acyltransferase, which catalyzes the formation of cholesterol esters in lipoproteins, is deficient. The deficiency causes accumulation of unesterified cholesterol in certain body tissues. Symptoms of the familial form include diffuse corneal opacities, target cell hemolytic anemia and proteinuria with renal failure.

Front 26

What is hyperbetalipoproteinemia?

Back 26

High levels of beta-lipoproteins and cholesterol in the blood, can lead to atherosclerosis at an early age.

Front 27

What is hyporbetalipoproteinemia?

Back 27

abnormally low level of LDL cholesterol.

Front 28

What is abetalipoproteinemia?

Back 28

There is an absence of apolipoprotein B so patients unable to breakdown fats into chylomicrons and consequently are unable to absorb fats.