**Core Concept**
Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency is a disorder of mitochondrial beta-oxidation, leading to impaired breakdown of fatty acids for energy production. This results in an accumulation of toxic intermediates, including dicarboxylic acids, and a reliance on glucose for energy.

**Why the Correct Answer is Right**
In MCAD deficiency, the impaired breakdown of fatty acids leads to a decrease in the production of acetyl-CoA, which is the primary substrate for gluconeogenesis. However, gluconeogenesis also requires ATP to drive the conversion of pyruvate to glucose. The lack of ATP due to impaired fatty acid oxidation reduces the ability to support gluconeogenesis, leading to hypoglycemia. This is because the body's primary mechanism for maintaining blood glucose levels through gluconeogenesis is impaired.

**Why Each Wrong Option is Incorrect**
**Option A:** Increased dicarboxylic acid does not directly inhibit glycogenolysis; rather, it is a byproduct of impaired fatty acid oxidation.

**Option C:** Lack of acetyl-CoA to favour glycogenolysis is incorrect because impaired fatty acid oxidation leads to a decrease in acetyl-CoA production, but glycogenolysis is not directly favoured by acetyl-CoA.

**Option D:** Glycogen stores are inadequate in infants is not accurate as infants have sufficient glycogen stores to maintain blood glucose levels.

**Clinical Pearl / High-Yield Fact**
MCAD deficiency is a classic example of a disorder of fatty acid oxidation, which can lead to hypoglycemia, especially during periods of fasting or increased energy demand. This condition highlights the importance of adequate energy production through multiple pathways to maintain blood glucose levels.

**✓ Correct Answer:** B. Lack of ATP to support gluconeogenesis