Hypothalamic obesity sometimes occurs in children after therapy for brain tumors or acute lymphoblastic leukemia (ALL). However, its etiology and treatment remain obscure. In rats, damage to the ventromedial hypothalamus(VMH) causes hyperphagia, hyperinsulinism, and obesity; but is it true in humans, which pathology comes first, and can it be treated?

Insulin dynamics were assessed in 8 pts (4M, 4F; age 10-18) with marked obesity noted to start after therapy for ALL or brain tumors. Previous voluntary dietary restriction had no inhibitory effect on the rate of Δ Weight or Δ Body Mass Index (ΔBMI.). Patients' Δ Weight was+ 1.00 ± 0.12 kg/month and ΔBMI was +0.29 ± 0.04/month over the 6 months prior to study entry. Oral glucose tolerance testing (OGTT) showed normal fasting glucoses but mild biochemical glucose intolerance in 5/8 pts, with 2 hr glucoses of 131 ± 13 mg/dl. Fasting insulin levels (IRI) were minimally elevated (22.9 ± 4.9 μU/ml), but peak IRI to glucose were markedly exaggerated in 6/8 pts (mean peak 303.9 ± 50.5μU/ml).

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