Hartnup's disease involves a defect in what process?

Hartnup's disease is primarily associated with a defect in the transport of neutral amino acids, particularly in the renal tubules and intestinal mucosa. The underlying issue is a mutation in the SLC6A19 gene, which encodes a transporter responsible for the reabsorption of neutral amino acids (like tryptophan) from the renal filtrate back into the bloodstream and their absorption in the intestines.

Because neutral amino acids are essential for various physiological functions, a deficiency due to impaired absorption can lead to clinical manifestations such as aminoaciduria, which may contribute to symptoms like skin rashes, neurological issues, and growth problems. Notably, tryptophan plays a critical role in the synthesis of niacin (vitamin B3), so its deficiency can lead to secondary pellagra-like symptoms.

In the context of the other options, while fat absorption, glucose utilization, and lipid metabolism are important processes, they are not directly related to the defect seen in Hartnup's disease. The condition is specifically linked to amino acid transport, making the absorption of neutral amino acids the correct answer.