A 22-year-old boy presents with weakness, vomiting, and coma after reduced food intake. Intravenous glucose leads to increased serum B-hydroxybutyrate after feeding medium-chain triglycerides. What is the likely disorder?

The clinical scenario describes a young patient showing symptoms of weakness, vomiting, and coma after a period of reduced food intake, indicating a potential metabolic disorder related to fatty acid oxidation. The key points to focus on are the administration of intravenous glucose leading to an increase in serum B-hydroxybutyrate and the response to medium-chain triglycerides.

In the case of carnitine-acylcarnitine translocase deficiency, the body is unable to transport long-chain fatty acids into the mitochondria for beta-oxidation due to a defect in this specific transport protein. This leads to a build-up of fatty acids outside the mitochondria and a subsequent increased production of ketone bodies, including B-hydroxybutyrate, when glucose levels rise. The fact that feeding medium-chain triglycerides resulted in an increase in serum B-hydroxybutyrate further supports this condition. Medium-chain fatty acids do not require the transport mechanism that is deficient in this disorder, allowing their oxidation and leading to ketone production amidst the body's stress response to low food intake.

Overall, this combination of symptoms and test result uniquely points to carnitine-acylcarnitine translocase deficiency as the underlying metabolic disorder.