**Core Concept**
Glucose-6-phosphatase is a crucial enzyme involved in the final step of gluconeogenesis and glycogenolysis, converting glucose-6-phosphate to glucose in the liver and kidneys. Deficiencies in this enzyme lead to an inability to convert glucose-6-phosphate to glucose, resulting in the accumulation of glucose-6-phosphate and its subsequent metabolites.

**Why the Correct Answer is Right**
The deficiency of glucose-6-phosphatase leads to an accumulation of glucose-6-phosphate, which is then shunted towards the pentose phosphate pathway, resulting in the overproduction of ribulose-5-phosphate. This, in turn, causes an increase in the levels of lactate, pyruvate, and uric acid, ultimately leading to the development of hypoglycemia, lactic acidosis, and hyperuricemia. The enzyme deficiency also results in the accumulation of glycogen, leading to hepatomegaly and potentially, glycogen storage disease type I (GSD I).

**Why Each Wrong Option is Incorrect**
**Option A:** This option is incorrect as it does not directly relate to the deficiency of glucose-6-phosphatase. While lactate levels may increase, it is not the primary issue caused by the enzyme deficiency.
**Option B:** This option is incorrect as it is unrelated to the deficiency of glucose-6-phosphatase. The accumulation of glucose-6-phosphate does not directly lead to hyperkalemia.
**Option C:** This option is incorrect as it is a consequence of other metabolic disorders, not the deficiency of glucose-6-phosphatase.

**Clinical Pearl / High-Yield Fact**
Glucose-6-phosphatase deficiency leading to GSD I is characterized by hypoglycemia, lactic acidosis, and hyperuricemia, and is often associated with hepatomegaly and an increased risk of infections due to impaired gluconeogenesis and glycogenolysis.

**Correct Answer: C. Lactic acidosis and hyperuricemia.**