chpt 12. Lipid Metabolism.

The rate of B-oxidation in the liver is dependent on.. (where FA's are also used in the synthesis of TG's and phospholipids)

how quickly these molecules are transported into the mitochondria. When glucose levels are high and excess glucose is being converted into fatty acids, malonyl-CoA (the product of the first committed step in FA synthesis) prevents a futile cycle by inhibiting CAT-I.

Pancreatic Lipase

hydrolyzes TG's to free two fatty acids, leaving a monoacylglycerol.

Butyric acid, a simple four-carbon FA, is oxidized by B-oxidation. Calculate the number of FADH2 and NADH molecules produced in this oxidation. How many acetyl-CoA molecules are also produced.

in the oxidation of butyric acid by the B-oxidation pathway, 1 mole each of FADH2 and NADH and two moles of acetyl-CoA are produced.

How does Carnitine transport acyl-CoA into the matrix?

it forms an ester bond with the fatty acyl group and carries it into the matrix.

Draw a cholesterol molecule and indicate the isopentenyl units.

(student handbook pg 219)

Determine how many ATP equivalents are obtained by the oxidation of oleic acid.

(student hb pg 219)

There are three basic sources of fatty acids in animals that can be used for energy conversion processes:

*1.* Fatty acids present in TG's obtained from diet *2.* fatty acids stored as TG's in adipose tissue that are released by hydrolysis following hormone stimulation *3.* FA's synthesized in the liver from excess carbs & exported as TG's.

Brief description of fatty acid synthesis (in mito matrix)

*Activation* by acyl-CoA synthetase (in outer mito membrane) *Transport* through inner membrane to matrix 3. *B-Oxidation*

Describe the role of insulin in lipid metabolism.

it promotes TG synthesis and the storage and uptake of FA's. Specifically, it inactivates hormone-sensitive lipase to prevent hydrolysis of fats to glycerol and FA's, and stimulates the release of VLDL from the liver, and activates lipoprotein lipase synthesis and transport to endothelial cells serving fat and muscle tissue.

What happens to the glycerol produced by lipoprotein lipase?

it returns to the liver and is converted to dihydroxyacetone phosphate.

The amount of FA that is transported into cells is dependent on...

its concentration in the blood and the relative activity of the FA transport mechanism.

The absorption of TG's in the small intestine is an energy-requiring process that involves hydrolytic reactions to yield monoacylglyercol and fatty acids. After their transport into enterocytes, FA's and monoacylglycerol are reconverted into triacylglycerols. Suggest a reason why triacylglycerols are not absorbed direction without the hydrolytic reactions.

In the small intestine, TG's mix with bile salts and are emulsified (solubilized). The size of the TG's and their emulsification with bile salts prevent them from crossing the enterocytes' cell membranes.

Many processed and fast foods contain trans fatty acids. Explain why these molecules are a problem for the body.

It contains trans double bonds. The body can only process FA's w/ cis. Poses a risk for C.V. disease b/c lipoprotein lipoase can only bind molecules w/ cis. As a result, trans fat remains in the blood for long periods of time and likely to contribute to plaque formation.

Glyceroneogenesis is an abbreviated form of gluconeogenesis, and a major source of G3P required for TG synthesis. Substrates include

lactate, pyruvate, and glucogenic amino acids such as alanine.

Mechanism of Fatty acid Synthase:

linking malonyl-CoA to acyl carrier protein, followed by decarboxylation & condensation rxn that extends the hydrocarbon chain.

What does CAT-I catalyze in fatty acid metabolism? "commitment step"

links fatty acyl-CoA molecules to hydroxyl group of carnitine.

G3P is rewuired for new (de novo) synthesis of triacylglycerols in the _________ and reassembly of triacylglycerols (storage) in _______.

liver, adipose tissue

Tissues depending on fatty acids for energy:

liver, heart, skeletal muscle (except in severe exercise), kidney cortex

What inhibits CAT-I?

malonyl-CoA, which signals that glucose levels are high and FA synthesis is favored. (product of acetyl-CoA carboxylase rxn)

How do cells adjust the fluidity of their membranes?

membrane remodeling - phospholipases & acyl transferases alter the fatty acid composition. - replacement of saturated fatty acids w/ unsaturated fatty acids increases fluidity.

Sex Hormones: Progesterone, Testosterone, 17-B-estradiol

molecules that regulate the development of primary and secondary sex characteristics and various reproductive behaviors.

Apolipoprotein C-II: (fig. 4)

on the surface of chylomicrons; binds to and activates *lipoprotein lipase* - leads to release of FA's and glycerol.

B-oxidation spiral:

a process where the B-oxidation cycle is repeated until, in the last cycle, a four carbon acyl-CoA is cleaved to form two molecules of acetyl-CoA.

In human triacylglycerols, _____ is often attached at C-1 and ______ at C-2.

palmitate, oleate

What are the products of oxidation of the molecules in question #12?

pg 216 handbook

An experimenter using acetyl-CoA with a 14C label on the carbonyl group traces the label in a cell synthesizing cholesterol. On what atoms of mevalonate will the label appear?

pg 220 of handbook

Glyceroneogenesis

abbreviated version of gluconeogenesis where G3P (required for TG synthesis) is synthesized from substrates other than glucose or glycerol.

Ketone bodies

acetoacetate, B-hydroxybutyrate, and acetone. produced within the mito when excess acetyl-CoA is available. (usually only small amounts produced)

Ketosis

acetone is formed by spontaneous decarboxylation of acetoacete when conc. is high. occurs during starvation and in uncontrolled diabetes. heavily relies on fat stores and B-oxidation of fatty acids for energy.

Determine the position of 14C in isopentenylpyrophosphate

pg 221 of handbook

The condensation product of glycerol-3-phosphate and two acyl-CoA's is...

phosphatidic acid (used in phospholipid synthesis)

What happens when you eat too many "non-fat" labeled foods?

activates the FA synthesis pathway, converting acetyl-CoA to FA's stored as TG's.

Hormone signaling releases fatty acids from adipose tissue that bind to an abundant transport protein in serum called

albumin

Pyruvate is converted to OAA in the mitochondria by..

pyruvate carboxylase (PC)

In the liver, chylomicron remnants are removed from the blood via

receptor-mediated endocytosis.

What is the role of CAT-II?

regenerates acyl-CoA in step 3 of B-oxidation

The rate of B-oxidation in the muscle is dependent on ..

availability of substrate (conc. of FA's in blood) and the tissue's current energy requirements. When NADH/NAD+ ratios are high, B-hydroxyacyl-CoA dehydrogenase (step 3 enzyme) is inhibited. High acetyl-CoA levels depress the activity of thiolase.

Why are triacylglycerols (fats) the most abundant source of energy, which provide twice as much as carbs and protein?

because the FA's present in triacylglycerols are already in the reduced form.

Some cells cannot use fatty acids as fuel. An example would be...

brain and red blood cells

Muscle cells are made up of which tissues?

cardiac and skeletal

Some cells rely on FA's for a significant portion of their energy requirements. An example would be..

cardiac muscle.

Fatty Acid Synthase:

catalyzes a series of rxns that adds C2 units to a growing FA chain covalently attached to the enzyme complex.

Acetyl-CoA carboxylase: "commitment step"

catalyzes biotin-mediated rxn mechanism that carboxylates acetyl-CoA to form C3 compound malonyl CoA. activity of acetyl-CoA is regulated by both reversible phosphorylation and allosteric mechanisms. (citrate binding stimulates, palmitoyl-CoA inhibits)

Fatty acids in dietary triacylglycerols are transported from the intestines to the rest of the body by large lipoprotein particles called

chylomicrons

Pancreatic Lipase: (fig. 3)

cleaves ester bond at C-1 and C-3 carbons to release two FFA's and monoacylglycerol (other intestinal lipases cleave at the C-2 carbon to generate glycerol and FA)

Bile Acid: Cholic Acid

converted into bile salts. produced in the liver, in the absorption of dietary fats and fat-soluble vitamins in the intestine.

In the liver, glycerol is converted to ______, catalyzed by glycerol kinase. this product is used in the synthesis of TG's, phospholipids, or glucose.

glycerol-3-phosphate (G3P)

DHAP is reduced by _________ to glycerol 3 phosphate, which is then utilized in TG synthesis.

glycerol-3-phosphate dehydrogenase

The FA's provide a rich source of energy for tissues throughout the body when...

glycogen stores have been depleted (especially during endurance exercise and dieting)

Fatty acids stored in adipose cells are released into the blood in response to..

hormone signaling by activation of cellular lipases (which cleave stored TG's)

Fatty acids are degraded by B-oxidation. What is this?

removal of two-carbon fragments from the carboxyl end of FA's. During this, the B-carbon (2nd carbon from carboxyl group) is oxidized and acetyl-CoA is released as the bond between the a&B carbons is cleaved. (process is repeated until entire fatty acid chain has been processed)

Where are bile acids secreted from and what is their function?

secreted from bile duct; function as detergents to promote formation of micelles.

Citrate Shuttle:

shipping acetyl CoA out of the mitochondria using citrate and OAA.

The acetyl-CoA molecule can enter the citric acid cycle to give 3 NADH, 1 FADH2, and 1 GTP.

so [(3 NADH x 2.5 ATP/NADH) + (1 FADH2 x 1.5 ATP/FADH2) + 1 ATP] = 10 ATP per acetyl-CoA

Lipogenesis

stores TGs when energy is high

#22 pg 458

the hydrophobic portions of the molecule are the long hydrocarbon tails. The hydrophilic portion is the phosphate ester functional group. The hydrocarbon tails are within the bilayer and the phosphate head group is on the surface of the membrane.

What happens to fatty acids after their transport across the adipocyte plasma membrane in lipolysis?

they bind to serum albumin. The albumin-bound FA's are carried to tissues throughout the body, where they are released from albumin and taken up by cells.

Pamitate: (1.5 x 7 FADH2) + 2.5 x 7 NADH) + 10 x 8 acetyl-CoA = 108 ATP

*subtract 2 ATP from the total ATP for final answer. those two were the "activation fee"* (energy cost to activate the FA)

The number of ATP produced from each molecule in B-oxidation..

- 1.5 ATP per FADH2 - 2.5 ATP per NADH - 10 ATP per acetyl-CoA

What are the key enzymes in FA metabolism?

- Acyl-CoA Synthetase - CAT-I (carnitine acyltransferase 1) - Acetyl-CoA carboxylase - Fatty acid synthase

What purpose does fatty acid metabolism serve in animals?

- FA oxidation in mito provides energy when glucose levels are low. - TG's stored in adipocytes in humans can supply energy to the body for ~3 months during starvation. - FA synthesis rxns in cytosol of liver and adipose cells converts excess acetyl-CoA that builds up in mito matrix when glucose levels are high into FA's that can be stored or exported as TG's.

In the liver:

-Glycerol (via glycerol kinase) converts to G3P, which is used in the synthesis of TG's, phospholipids, and glucose. -Chylomicron remnants are removed from the blood via receptor-mediated endocytosis. - VLDLs are synthesized.

How are fatty acids transported into cells?

-by a protein in the plasma membrane -process linked to the active transport of sodium.

Composition of fatty acid-binding proteins:

-water-soluble -function is to bind/transport hydrophobic fatty acids

Each cycle of B-oxidation produces:

1 FADH2, 1 NADH, and 1 acetyl-CoA. (*Note*: the last cycle produces 2 acetyl-CoA)

Fatty Acid Degradation (in the mito matrix)

1. *Activation* by acyl-CoA synthetase (outer mito membrane) 2. *Transport* (through inner membrane to matrix) 3. *B-Oxidation*

Before B-Oxidation (inside mitochondria) starts, each FA is activated in a reaction with ATP and CoASH, catalyzed by acyl-CoA synthetase (found in outer membrane).Because the inner membrane is impermeable to most acyl-CoA molecules, carnitine is used as a carrier to transport acyl groups in. This carnitine-mediated transfer of acyl groups into the matrix is accomplished through the following mechanism:

1. Acyl-CoA is converted to an acylcarnitine derivative, catalyzed by CAT-I. 2. inner membrane carrier protein transfers acylcarnitine into matrix. 3. Acyl-CoA regenerated by CAT-II 4. Carnitine transported back into intermembrane space by carrier protein. Then reacts with another acyl-CoA.

Five steps of the absorption and transport of dietary triacylglycerols:

1.) emulsification of TG's by bile acids 2.) hydrolysis of FA's by intestinal lipases 3.) re-synthesis of TG's inside intestinal epithelia cells 4.) packaging of TG's into large lipoprotein particles - *chylomicrons* 5.) export of chylomicrons to lymphatic system.

List three differences between fatty acid synthesis and B-oxidation.

1.) they take place in different cell compartments. Synthesis in cytoplasm & B-oxidation in mitochondria. 2.) the intermediates of fatty acid synthesis and B-oxidation are linked through thioester linkages to ACP and CoASH, respectively. 3.) Electron carrier for fatty acid synthesis is NADPH; for B-oxidation NADH and FADH2.

The oxidation of each FADH2 during the ETC and oxidative phosphorylation yields approx. 1.5 molecules of ATP. The oxidation of each NADH yields approx. ____ molecules of ATP.

2.5

The yield of ATP from the oxidation of palmitoyl-CoA generates what to form CO2 and H2O?

7 FADH2, 7 NADH, and 8 acetyl-CoA molecules

Describe the difference between IDLs and LDLs

After the TG content of VLDL (very low density lipoproteins) has been depleated, the lipoprotein is referred to as an IDL (intermediate density) lipoprotein.

Oxidation of fatty acids occurs in what 3 stages?

B-oxidation, resulting acetyl groups participate in Kreb's cycle to form NADH & FADH2, the reduced coenzymes (NADH & FADH2) are oxidized by giving up the protons and electrons present in the mitochondria to synthesize ATP by oxidative phosphorylation in the ETC.

Before B-oxidation, FA's are converted to their CoASH derivatives. Explain why this rxn is necessary.

B/c they are transported into the mito matrix by conversion to their CoASH derivatives. B-oxidation takes place in mito matrix. To cross both inner and outer membrane, these derivatives are needed. (first acyl-CoA synthase catalyzes the formation of the FA acyl-CoA, which is released into the inner membrane space. the acyl group is then transferred to carnitine for transport across the inner membrane into the matrix)

Lipolysis

Breakdown of triglycerides into glycerol and fatty acids

Describe the possible effects of low levels carnitine on a person's metabolism.

Carnitine is required for the transport of FA's into the mitochondria where they are oxidized to generate energy. When carnitine levels are low, fat metabolism is impaired. Although glucose metabolism accelerates, an energy deficit occurs. In addition, accumulating acyl-CoA molecules become substrates for competing processes such as peroxisome B-oxidation and TG synthesis.

PEP is then converted via gluconeogenesis to ______.

DHAP

Fatty acids are: - a major source of energy in muscle tissue (skeletal and cardiac) - used minimally in nervous tissue

During fasting, many tissues use fatty acids or ketone bodies for energy. Target issue: primarily muscle cells & adipocytes; also lactating mammary gland cells. All of these synthesize lipoprotein lipase, transferred to the endothelial surface of capillaries.

B-oxidation of naturally occurring monosaturated fatty acids requires an additional enzyme. What is this enzyme, and how does it accomplish its task?

Enoyl-CoA isomerase converts the naturally occusing cis double bond at ^3 to a trans double bond at ^2, the correct position for the next round of B-oxidation.

Explain the intracellular separation of FA metabolic processes (i.e. fatty acid biosynthesis in cytoplasm and degradation in mitochondria and peroxisomes)

FA biosynthesis occurs in the cytoplasm, where as FA catabolism takes place in mitochondria and peroxisomes so that these pathways may be regulated independently and energy-wasting futile cycles can be prevented.

In the absence of oxygen, cells can produce small amounts of ATP from the anaerobic oxidation of glucose. This is not true for fatty acid oxidation, why?

FA oxidation, which involves the citric acid cycle and ETC, cannot operate without O2.

Provide an explanation for the fact that most FA's are 16 or 18 carbons long.

FA's are assembled from two carbon acid synthase which ends the process at C-16. Although there is a robust capacity to elongate FA's, the most abundant FA's are C16 and C18, the product of one round of elongation process.

Degrading fatty acids requires enzymatic rxns inside the mitochondria.

FA's need to be activated by co-enzyme A on outer membrane, then transported into matrix by a carrier system.

Carnitine transports acyl-CoA into the matrix in fatty acid degradation. Why is this necessary?

Fatty acid catabolism occurs inside the matrix. Fatty acyl-CoA cannot cross the inner membrane, but carnitine can.

Lipogenesis

Glucose conversion to Fatty Acids (REMEMBER, THE OPPOSITE DOES NOT HAPPEN)

Describe the fate of glycerol generated from TG hydrolysis in adipocytes.

Glycerol (generated from the lipolysis of adipocyte TG's) is released into the blood and transported to the liver, where glycerol kinase converts it to glycerol-3-phosphate, which is a substrate for the synthesis of glucose, phospholipids, and TGs.

insulin induces LPL enzyme. and GLUT4 transporters on the surface to ensure glucose will be made into sugar backbone. now have TG stores you can use later during a fast.

If APO-C2 or LPL is defective, you will have high TGs in the blood from chylomicrons. (hypertriglyceridemia)

After OAA is reduced by _____, the product, _____, is transported out of the mitochondria where the reaction is reversed to form OAA.

NADH, Malate

Review the steps in B-oxidation and determine which ones are actually oxidation reactions.

Only reactions 1 & 3. 1.) Acyl-CoA + FAD --> trans-a,B-Enoyl-CoA + FADH2 3.) L-B-Hydroxyacyl-CoA + NAD+ --> B-Ketoacyl-CoA + NADH + H+

OAA is then phosphorylated and decarboxylated by _________ in a GTP-requiring reaction to form __________.

Phosphoenolpyruvate carboxykinase (PEPCK-C), phosphoenolpyruvate (PEP)

Key enzymes for Glyceroneogenesis

Pyruvate Carboxylase (PC) and cytoplasmic isoform of phophoenolpyruvate carboxykinase (PEPCK-C). (these are found in lipogenic tissues and in the brain, heart, and adrenal glands)

When the production of acetyl-CoA exceeds the body's capacity to oxidize it, acetoacetate, B-hydroxybutyrate, and acetone accumulate. When generated in large amounts, these substances can exceed the blood's buffering capacity. As the blood pH falls, the ability of red blood cells to carry oxygen is affected. Subsequently, the brain can be starved for oxygen, and a fatal coma can result. Explain how severe dieting can produce this condition.

Severe dieting (less than 600 cal a day) causes the oxidation of large amounts of FA's from the body's TG reserves. Ketone body production increases dramatically with the effect of causing acidosis. Brain cells are damaged by the acidosis and by the ketone bodies themselves, especially the organic solvent acetone.

Explain how hormones act to modify the metabolism of fatty acids in both the short and long term. Give examples.

Short term: hormones alter the activity of pre-existing regulatory enzyme molecules. Ex: the binding of glucagon inhibits acetyl-CoA carboxylase. Long term: changes in the pattern of enzyme synthesis in target cells. Ex: insulin promotes the synthesis of the enzymes involved in lipogenesis.

When CO2 is used in the synthesis of malonyl-CoA from acetyl-CoA, no label appears in the eventual FA products. Explain.

Since the CO2 that is added to acetyl-CoA is removed in the reaction of malonyl-ACP with acetyl synthase to form acetoacetyl-ACP, no 14C label appears in the eventual FA products.

Chylomicrons transport...

TG's to adipose tissue for storage, and to muscle cells for energy conversion processes.

In exogenous pathway, TG's are absorbed and distributed to tissues by chylomicrons.

TGs are constantly being synthesized and hydrolyzed to yield FAs and glycerol. The recycling rate is stimulated by epinephrine and norephinephrine and depressed by insulin.

Describe the exogenous pathway (fig 12.1) http://www.cengage.com/biology/discipline_content/animations/digestion_absorption.html

TGs are digested within the lumen of the small intestine. Dietary fats mix with bile salts, and TGs are digested by pancreatic lipase to form fatty acids and monoacylglycerol. These are then transported across the plasma membrane of intestinal cell walls (enterocytes)

You have just consumed a cheeseburger. Trace the fat molecules (TGs) from the cheeseburger to your adipocytes (fat cells).

The TG's are emulsified in the small intestine by bile salts. Then digested by lipases (pancreatic lipase). The products are fatty acids and monoacylglycerol, which are transported into the enterocytes and reconverted to TG. TG is then incorporated into chylomicrons, which are then transported into lymph via exocytosis, and finally into the bloodstream for transport to the fat cells.

Membranes that contain a significant proportion of cis unsaturated FA's are more fluid then similar membranes with higher levels of saturated FA's. Explain.

The kink in a cis-unsaturated FA partially disrupts the otherwise close packing. They have lower M.P. than saturated FA's b/c less heat energy is required to disrupt the packing. In lipid bilayers w/ cis-alkenes, the amphipathic nature of the phospholipid helps prevent bilayers from melting. (however, more cis causes increased fluidity within bilayer, resulting in more facile lateral motion w/in the bilayer.)

The adaptations of desert animals to their environment include water conservation mechanisms. A number of these organisms conserve water so successfully that they never actually drink it. They depend instead on water generated during metabolism. Determine how much water can be obtained by the oxidation of one mole of palmitic acid.

The reaction for the oxidation of one mole of palmitic acid is: CH3(CH2)14COOH + 23 O2 --> 16 CO2 + 16 H20 one mole of palmitic acid produces a yield of 16 moles of water molecules. From this number must be subtracted 8 moles of water of which 7 are used in the hydration reaction in each round of the B-oxidation spiral and 1 mole is used for the hydrolysis of pyrophosphate, the reaction that drives the activation of the palmitic acid molecule to completion. The net reaction, therefore, yields a total of 8 molecules of metabolic water.

Compare the energy content of a stearic acid molecule compared with glucose.

The yield of ATP from the oxidation of stearic acid is 122 (8 FADH2 x 1.5 ATP, 8 NADH x 2.5 ATP and 9 acetyl-CoA x 10 ATP) Since the formation of stearoyl-CoA requires two ATP equivalents and the net synthesis is 120 ATP. Stearic acid yields 120/18 or 6.6 ATP per carbon atom. Recall that the ratio for glucose is 5.2 ATP per carbon atom.

Under severe starvation conditions, people develop "acetone breath". Explain.

There is an excess of acetyl-CoA (from the B-oxidation of FA's) and very low reserves of glucose, so ketone bodies are formed to be metabolized for energy. When the concentration of acetoacetate is high, it decarboxylates to form acetone, which may be detected in the breath.

Bile salts form mixed micelles which are then taken up into enterocytes (intestinal wall cells) and reconverted to TG's.

These TG's are combined with cholesterol, phospholipids, and protein to form *chylomicrons* and are transported out to the lymph and then into the bloodstream for distribution to cells.

fatty acids synthesized in the liver are carried through the body as triacylglycerols by

VLDL's. (very low density lipoproteins)

During periods of stress or fasting, blood glucose levels fall. In response, fatty acids are released by adipocytes. Explain how the drop in blood glucose triggers fatty acid release.

When glucagon levels are high, which occurs when blood glucose levels are low, glucagon triggers increased FA oxidation.

B-oxidation

degrades FA's to form acetyl-CoA within the mitochondria. also occurs in peroxisomes.

Lipolysis

degrades TG's to fatty acids and glycerol when energy is low.

Fats that enter the small intestine from the stomach are insoluble, so they must be..

emulsified by bile acids (i.e. glyycocholate)

Bile Salts: Made in the liver, stored in the gall bladder, secreted into the small intestine.

emulsify (solubilize) fats in the lumen of the small intestine b/c they are amphipathic w/ detergent like properties.

Fatty acyl-CoA synthetase: "priming reaction"

enzyme that catalyzes FFA's in cytosol into fatty acyl-CoA using energy from ATP and PPi hydrolysis. (low energy charge = FA oxidation in mitochondria. high energy charge = synthesize TG's or membrane lipids)

Ketogenesis

excess acetyl-CoA molecules are converted to acetoacetate, B-hydroxybutyrate, and acetone. This group is known as *ketone bodies*

Products of lipolysis:

fatty acids and glycerol (both are released into the blood)

Lipoprotein lipase converts TGs in chylomicrons (and VLDLs) to ..

fatty acids and glycerol. Glycerol must be transported back to the liver to be metabolized.

During fasting, many tissues use ______ or _______ for energy.

fatty acids, ketone bodies.

Examples of FA metabolism in real life?

foods labeled "non-fat", even though they contain high calorie count from carbs. Ex. Olestra; a fat substitute composed of sucrose molecules with sever FA's attached.

What is the function of Fatty acid-binding proteins?

transporting FA's once they have entered a cell (mitochondria, endoplasmic reticulum, etc.)

Lipases:

water soluble enzymes in the small intestine that hydrolyze the acyl-ester bonds in TG's to release FFA's, which then pass through the membrane on the luminal side of intestinal epithelial cells.

When are fatty acids synthesized?

when an organism has met its energy needs and nutrient levels are high.

What is lipolysis and when does it occur? (degradation/catabolism)

when energy reserves are low and energy (ATP) is needed. happens with fasting, exercise, stress response. Hormones bind to specific adipocyte receptors that elevate cytoplasmic cAMP levels, which activates hormone-sensitive triacylglycerol lipase. Both products of lipolysis are released into the blood.