metabolism of triacylglycerols

how are fatty acid stored for future use

triacylglycrides (TAG)

where are triacylglycerides stored

adipocytes of adipose tissue

the FAs present in tags are primarily

saturated

the FAs incorporated into TAGs are

all activated to acyl-CoAs through the action of various acyl-coa synthetases

where does triacylglycerol synthesis occur by a different pathway and becomes a component of chylomicrons

in intestinal epithelial cells

where does glycerol-3-phosphate provide the glycerol moiety that reacts with two fatty acyl-CoAs to form phosphatidic acid

in the liver and adipose tissue

how is a triacylglycerol formed

the phosphate group is cleaved to form a diacylglycerol that reacts with another fatty acyl-CoA

how does the liver use glycerol

to produce glycerol-3-phosphate by a reaction that requires ATP and is catalyzed by glycerol kinase

what tissue lacks glycerol kinase

adipose tissue

why cant adipose tissue generate glycerol-3-phosphate from glycerol

because it lacks glycerol kinase

what tissues can convert glucose through glycolysis to DHAP

adipose and liver

what is DHAP reduced by to form glycerol-3-phosphate

NADH

where is triacylglycerol incorporated into VLDL to enter the blood

in the liver

adipose tissue

specialized connective tissue designed for synthesis, storage and hydrolysis of TAGs

• main site for long-term storage of energy that is widely distributed in the body (under skin, around deep blood vessels, and in abdominal cavity)

what does adipose tissue consist of

adipocytes

what percentage of mass does adipose tissue make up in a young adult human

15%

• 65% of this mass is in the form of TAGs

what state do triacylglycerols in adipocytes exist

dynamic

dynamic state

being continuously hydrolyzed and re-esterified under the control of hormones

• insulin

• glucagon

• epinephrine

highly reduced FA that contains more than twice as much energy as carbohydrates and proteins

TAGs

how are TAGs stored

unhydrous

unhydrous

no marked effect on body weight as compared to glycogen

how is TAG synthesized in adipose tissue

from excess fuels (mainly glucose)

obtained from glucose

glycerol and fatty acids

in the fed state when there is high glucose level

insulin is released and it enhances glucose uptake in adipocytes by GLUT4

where is most of the glucose converted to TAG

in adipocytes

what 3 sources in the fed state allow us to get TAG in adipose tissue

1. dietary TAG

2. adipocytes

3. TAG synthesis in liver

how is dietary TAG transported

to adipocytes via chylomicrons

how do adipocytes uptake blood glucose

insulin action

how is TAG synthesized in liver transported to adipose tisse

VLDL

3 sources of TAG in adipose tissue in fed state

1. chylomicron

2. blood glucose

3. VLDL

enhances uptake and synthesis

insulin

how is VLDL released

in the circulation to reach the adipose tissue and muscles where we have LPL to hydrolyze TAG in the same way as the for CM

what is VLDL converted to

IDL

what is IDL converted to

LDL

where does VLDL go

1. converted to IDL

2. converted to LDL in circulation

1. liver to be further processed

when do fatty acids and glycerol get released from adipose triacylglycerol stores and serve as a source of fuel for other tissues

during fasting

what hormones rise and fall during fasting

glucagon: rise

insulin: fall

what does the rise of glucagon and fall of insulin during fasting cause

the activation of hormone sensitive lipase by cAMP-dependent mechanism

hormone-sensitive lipase

initiates the conversion of adipose triacylglycerols to fatty acids and glycerol which are released into the blood

how are fatty acids transported

in the blood complexed with albumin

how are fatty acids uptaken

by various tissues to be oxidized for energy

where are fatty acids converted to ketone bodies and glycerol converted to glucose

in the liver

fuels such as ketone bodies and glucose

serve as energy sources for other tissues

regulation of triacylglycerol synthesis

key regulatory enzymes in the pathway are activated and a high carbohydrate diet causes their induction

glycolytic enzymes that are active

glucokinase

PFK-1

pyruvate kinase

dephosphorylated and active

pyruvate dehydrogenase

inducible

citrate lyase

activated by citrate and converted to its active dephosphorylated state by a phosphatase that is stimulated by insulin

acetyl-CoA carboxylase

fatty acid synthase complex

active

provides the reducing equivalents for fatty acid synthesis

NADPH

how is NADPH produced

1. by inducible malic enzyme

2. inducible enzymes of the PPP

• glucose-6-phosphate dehydrogenase

• 6-phosphogluconate dehydrogenase

the product of acetyl-CoA carboxylase that inhibits carnitine acyltransferase I

malonyl-CoA

malonyl-CoA

prevents newly synthesized fatty acids from entering the mitochondria and undergoing b-oxidation