Hypothalamic damage from a tumor or cancer treatment can also result in hypothalamic obesity - unrelenting weight gain that does not respond to caloric restriction or exercise - attributable to ventromedial hypothalamus damage and abnormality in leptin, ghrelin and insulin feedback . In rodents, hypo-thalamic obesity can be suppressed by pancreatic vagotomy to prevent insulin hypersecretion. Recent studies in patients with cranial insult confirmed insulin hypersecretion as one of the major mechanisms for the development of hypothalamic obesity . In a study of 148 survivors of childhood brain tumors, the risk factors for hypothalamic obesity included age at diagnosis of cancer (<6 years), tumor location (hypothalamic or thalamic), tumor histology (craniopharyngioma, germinoma, optic glioma, prolactinoma or hypothalamic astrocytoma), hypothalamic irradiation (>51 Gy) and the presence of endo-crinopathy (deficiency of GH, sex hormones, ACTH or vasopressin) [27, 29]. No effects were noted on body mass index from V-P shunting, steroid use (<6 months) or chemotherapy. Thus, any form of hypothalamic damage, whether due to tumor, surgery or RT, is a regional-specific primary risk factor for the development of obesity.
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