Abstract
One of the most striking examples of dysfunctional hypothalamic signaling of energy homeostasis is observed in patients with hypothalamic lesions leading to hypothalamic obesity (HO). This drastic condition is frequently seen in patients with craniopharyngioma (CP), an embryological tumor located in the hypothalamic and/or pituitary region, frequently causing not only hypopituitarism, but also leading to damage of medial hypothalamic nuclei due to the tumor and its treatment. HO syndrome in CP patients is characterized by fatigue, decreased physical activity, uncontrolled appetite, and morbid obesity, and is associated with insulin and leptin resistance. Mechanisms leading to the profoundly disturbed energy homeostasis are complex. This review summarizes different aspects of important clinical studies as well as data obtained in rodent studies. In addition a model is provided describing how medial hypothalamic lesion can interact simultaneously with several weight-regulating circuitries.
Highlights
Risk factors for developing obesity in CP patients include large hypothalamic lesions affecting several medial hypothalamic nuclei such as the arcuate nucleus (ARC), ventromedial nucleus (VMN), and the dorsomedial nucleus (DMN), and tumors that reach the floor of the third ventricle; hydrocephalus; transcranial surgery, which often causes greater damage to the hypothalamus compared to transnasal surgical tumor removal; aggressiveness of resection; reoperation for tumor recurrence; and hypothalamic irradiation (Muller et al, 2007; Gardner et al, 2008; Vinchon et al, 2009; Roth et al, 2011c; Figure 1)
The main mediators in the hypothalamic regulation of energy intake and EE appear to be proopiomelanocortin (POMC) and neuropeptide-Y/agouti-related peptide (NPY/AgRP) producing neurons, which are concentrated in the ARC and project mainly to the paraventricular nucleus (PVN) in the hypothalamus and to the VMN, lateral hypothalamus (LHA), as well as the DMN and the median preoptic area (Bai et al, 1985; Kerkerian and Pelletier, 1986; Schwartz et al, 2000; Schwartz and Gelling, 2002)
SUMMARY AND ETIOLOGICAL THEORIES Damage of medial hypothalamic nuclei due to the tumor and its treatment is frequently seen in patients with CP leading to hypothalamic obesity (HO) characterized by fatigue, decreased physical activity, uncontrolled appetite, and morbid obesity, and is associated with insulin and leptin resistance
Summary
Risk factors for developing obesity in CP patients include large hypothalamic lesions affecting several medial hypothalamic nuclei such as the arcuate nucleus (ARC), ventromedial nucleus (VMN), and the dorsomedial nucleus (DMN), and tumors that reach the floor of the third ventricle; hydrocephalus; transcranial surgery, which often causes greater damage to the hypothalamus compared to transnasal surgical tumor removal; aggressiveness of resection; reoperation for tumor recurrence; and hypothalamic irradiation (Muller et al, 2007; Gardner et al, 2008; Vinchon et al, 2009; Roth et al, 2011c; Figure 1).
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