A 22-year-old man experiences muscle weakness and arrhythmias due to a fatty acid oxidation disorder. Which genetic factor is most likely implicated?

In this scenario, the patient presents with muscle weakness and arrhythmias, which are characteristic symptoms associated with disorders of fatty acid metabolism. The most likely genetic factor implicated is a defect in carnitine transport.

Carnitine plays a crucial role in the transport of long-chain fatty acids into the mitochondria, where they undergo beta-oxidation to produce energy. A defect in carnitine transport prevents fatty acids from entering the mitochondria, resulting in insufficient energy production from fat metabolism. This leads to muscle weakness, as muscles rely heavily on fatty acids for energy, especially during prolonged exercise or fasting. Additionally, the resulting accumulation of fatty acids and their derivatives can lead to arrhythmias, as the heart also requires a steady source of energy, predominantly from fatty acids.

The other options, while related to metabolic processes, do not specifically address the primary defect observed in this patient. Inability to beta-oxidize fatty acids refers to a problem occurring downstream of carnitine transport and would lead to a similar clinical picture, but the initial defect indicates a transport issue. Impaired glucose uptake and alteration of lipoprotein metabolism do not directly explain the presentation relating to fatty acid oxidation disorders in this context.