FATTY ACID SYNTHESIS WORKSHEET 9

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27 Terms

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Hypercaloric state

A condition where there is an excess of calories consumed.

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What happens to carbs and proteins eaten in excess?

They are converted into fatty acids and incorporated into triglycerides.

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Organ for lipid conversion

The liver.

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Mechanism of transport for lipids out of the liver?

They are packed into VLDL in the liver.

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Destination for transported lipids from the liver?

Adipocytes.

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Barrier protein for stored energy

Perilipins.

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Circumstances for fatty acid oxidation

Occurs under low glucose conditions or increased activity.

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Circumstances for fatty acid synthesis

Occurs under high glucose or caloric excess.

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Main substrate for fatty acid oxidation

Fatty acids.

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Main substrate for fatty acid synthesis

MalonylCoA.

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Location of fatty acid oxidation

Mitochondria.

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Location of fatty acid synthesis

Cytosol.

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Mitochondrial transport mechanism for oxidation

Carnitine shuttle.

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Rate limiting enzyme for oxidation

CAT I.

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Mitochondrial transport mechanism for synthesis

Citrate shuttle.

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Rate limiting enzyme for synthesis

AcetylCoA carboxylase (ACC).

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Hormones controlling fatty acid/glucose metabolism

Main ones are glucagon, epinephrine and insulin.

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Regulatory enzymes in fatty acid metabolism

CAT I, AcetylCoA Carboxylase (ACC), Hormone sensitive lipase (HSL).

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What hormone is released in a high carbohydrate/energy rich environment?

Insulin

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Effect of insulin in high carbohydrate environment

Activates ACC and inhibits HSL.

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End result of ACC activation in a high carb environment?

Increases the conversion of AcetylCoA to MalonylCoA.

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Effect of MalonylCoA on CAT I in a high carb environment?

Increased levels of MalonylCoA inhibit CAT I which prevents fatty acids from entering the mitochondria for oxidation.

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Effect of HSL inhibition in a high carb environment?

Prevents stored lipids from being released from the adipocytes.

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Hormones released in low carbohydrate environment

Glucagon and epinephrine.

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Effect of glucagon on regulatory enzymes (ACC and HSL)?

Inactivates ACC but activates HSL.

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End result of ACC inactivation in a low carb environment?

Malonyl-CoA falls, allowing fatty acids to enter the mitochondria and become the major fuel.

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Effect of glucagon on HSL in a low carb environment?

Triggers HSL and the mobilization of fatty acids from the adipose tissue.