Fatty Acid Synthesis Quiz

<p>It binds and transfers acyl groups (A)</p> Signup and view all the answers

<p>Malate undergoes decarboxylation and oxidation (D)</p> Signup and view all the answers

<p>Liver (B)</p> Signup and view all the answers

<p>Catalyzes the carboxylation of acetyl CoA to malonyl CoA (D)</p> Signup and view all the answers

<p>Inhibits isocitrate production (C)</p> Signup and view all the answers

<p>Low energy charge in the cell (A)</p> Signup and view all the answers

<p>Malonyl CoA (C)</p> Signup and view all the answers

<p>Acting as a cofactor for carboxylation reactions (B)</p> Signup and view all the answers

<p>Both allosteric and covalent regulation (C)</p> Signup and view all the answers

<p>Fatty acid synthesis requires ATP and NADPH. (B)</p> Signup and view all the answers

<p>Malonyl CoA (A)</p> Signup and view all the answers

<p>Long chain unsaturated (D)</p> Signup and view all the answers

<p>Converted to glucose (C)</p> Signup and view all the answers

<p>Facilitates fatty acid transport into mitochondria (A)</p> Signup and view all the answers

<p>It inhibits CPT-1, reducing fatty acid oxidation. (C)</p> Signup and view all the answers

<p>Accumulation of toxic FFAs in cells (B)</p> Signup and view all the answers

<p>Acyl-CoA synthetase (A)</p> Signup and view all the answers

<p>Mitochondrial matrix (B)</p> Signup and view all the answers

<p>Impaired glucose synthesis during fasting (B)</p> Signup and view all the answers

<p>Muscle weakness with myoglobinemia (C)</p> Signup and view all the answers

<p>Acetyl-CoA (C)</p> Signup and view all the answers

<p>It inhibits CPT-1 function (A)</p> Signup and view all the answers

<p>β-hydroxyacyl-CoA dehydrogenase (A)</p> Signup and view all the answers

<p>Isomerase and reductase (C)</p> Signup and view all the answers

<p>β-oxidation in mitochondria or conversion to TAGs and PLs (B)</p> Signup and view all the answers

<p>15 (A)</p> Signup and view all the answers

The process of building fatty acids from acetyl CoA units using the enzyme fatty acid synthase. It occurs primarily in the liver, lactating mammary glands, and adipose tissue. Requires ATP and NADPH.

The carboxylation of acetyl CoA to form malonyl CoA, catalyzed by acetyl CoA carboxylase (ACC). This step is regulated by both allosteric and covalent mechanisms.

High cellular energy charge (abundant ATP) inhibits isocitrate dehydrogenase, leading to the buildup of citrate. Citrate can readily exit the mitochondria and serve as a precursor for acetyl CoA in the cytosol, facilitating FA synthesis.

ACC is activated by citrate and inhibited by long-chain fatty acyl-CoA, which are indicators of energy status and FA levels.

AMP-activated protein kinase (AMPK), which is activated by low energy levels, phosphorylates ACC, making it less active. This helps to conserve energy and prevent FA synthesis when needed.

Insulin upregulates the synthesis of ACC, leading to increased fatty acid synthesis. This is particularly important after a meal rich in carbohydrates.

Biotin acts as a prosthetic group for ACC, essential for its carboxylase activity during the conversion of acetyl CoA to malonyl CoA.

Fatty acid synthase is a multi-enzyme complex responsible for elongating the fatty acid chain by successively adding 2-carbon units from malonyl CoA to the growing fatty acid.

The primary source of reductant (electrons) for fatty acid synthesis is NADPH. NADPH is generated mainly through the pentose phosphate pathway (PPP) and the cytosolic conversion of malate to pyruvate by malic enzyme.

After each 2-carbon unit is added, the growing fatty acyl chain undergoes two reduction reactions that require NADPH. These reductions essentially convert a double bond to a single bond, making the fatty acid chain saturated.

Palmitate (16 carbons) is the primary end product of fatty acid synthase. This fully saturated long-chain fatty acid can be further elongated by the addition of 2-carbon units in the smooth endoplasmic reticulum (ER).

Fatty acid synthase is composed of two identical subunits. Each subunit contains 7 catalytic activities and an acyl carrier protein (ACP) segment containing a phosphopantetheine residue, derived from pantothenic acid (vitamin B5).

A genetic disorder affecting the liver's ability to use long-chain fatty acids (LCFA) for fuel, leading to impaired glucose synthesis during fasting.

Severe hypoglycemia (low blood sugar), coma, and potentially death due to the liver's inability to generate glucose during fasting.

A genetic disorder mainly affecting skeletal and cardiac muscle, leading to problems with using LCFA for energy.

Symptoms include cardiomyopathy (heart muscle disease), muscle weakness, and myoglobinemia (excess muscle protein in the blood) after prolonged exercise.

The primary metabolic pathway for breaking down fatty acids, generating acetyl-CoA, NADH, and FADH2 as energy sources.

Malonyl-CoA, a key intermediate in fatty acid synthesis, inhibits CPT-1, preventing the futile cycle of simultaneous fatty acid synthesis and breakdown.

Beta-oxidation is regulated by controlling the entry of fatty acids into mitochondria and by feedback mechanisms involving NADH and acetyl-CoA.

Genetic defects in enzymes involved in fatty acid metabolism can cause a variety of inherited diseases.

A 2-carbon donor molecule involved in fatty acid synthesis. It is a key regulator of fatty acid metabolism, inhibiting the breakdown of fatty acids when energy stores are high.

An electron-carrying molecule used in fatty acid synthesis. It provides the reducing power needed to add carbon units to the growing fatty acid chain.

Very Long Chain Fatty Acids – Fatty acids with more than 22 carbon atoms, required for specific lipids in the brain.

Enzymes in the Smooth Endoplasmic Reticulum (SER) that introduce double bonds into fatty acid chains.

A transport system that shuttles long-chain fatty acids from the cytosol to the mitochondria, where they are degraded for energy production.

Carnitine Palmitoyl Transferase 1 – The enzyme that controls the movement of long-chain fatty acids into the mitochondria.

Malonyl CoA, a molecule involved in fatty acid SYNTHESIS, inhibits the enzyme CPT-1, preventing long-chain fatty acids from being transported into the mitochondria for BREAKDOWN. This ensures that the energy is used for building fat when there is enough energy available, preventing the unnecessary breakdown of fat stores.

Carnitine, a molecule crucial for fatty acid transport, can be obtained from the diet (meat) or synthesized in the liver and kidneys.

A lack of carnitine can lead to decreased ability to use fatty acids as fuel and accumulation of toxic fatty acids and branched-chain acyl groups in cells.