Regulation of Fatty Acid Synthesis

Acetyl CoA carboxylase deficiency drastically alters the ability of the patient to synthesize fatty acids. The fact that the infant was born at all is due to the body’s ability to utilize fatty acids provided to it. However, all processes dependent  upon  de  novo  fatty  acid  biosynthesis  are  affected.  The  lungs,  in  particular,  require  surfactant,  a lipoprotein substance secreted by alveolar type II cells, to function properly. Surfactant lowers alveolar surface tension, facilitating gas exchange. It contains significant amounts of dipalmitoyl phosphatidylcholine. Palmitate is the major end product of de novo fatty acid synthesis. Acetyl CoA carboxylase formation of malonyl CoA is the first step of fatty acid synthesis. Biotin deficiency cannot be the problem because pyruvate carboxylase in gluconeogenesis is not affected. None of the other answers listed would result in all of the symptoms given.

Citrate

Ans. is ‘a’ i.e., Cytosol

This question is slightly different from previous one.

The major acetyl CoA carboxylase which is involved in lipogenesis is acetyl CoA Carboxylase-1 (ACC-1). It is a cytosolic enzyme. In general acetyl CoA carboxylase refers to ACC-1.

There is one more isoform of acetyl CoA carboxylase, i.e. ACC-2. Which is present in muscle, allowing muscle to regulate β-oxidation. ACC-2 is present in mitochondria.