The hypothalamus plays an important role in the regulation of body weight and energy homeostasis. The disruptive mechanisms of regulation of various obesity-related and organ specific signals and their crosstalk may potentially differ in hypothalamic obesity (HO) and simple obesity (SO), because of the selective structural damage of the hypothalamus in HO. We evaluated various novel obesity-related signals in fat, brain and gut, such as spexin, total (T) and high molecular weight (HMW)- adiponectin, pro-uroguanylin (PUG) along with glucose and insulin and their potential crosstalk in children with brain tumors and HO compared to those with SO.
A total of 23 children (age: 6-18 yrs) in two groups, HO (n=6) and SO (n=17) were studied. Spexin, PUG, T- and HMW adiponectins and insulin were measured using specific enzyme linked immunoassays and glucose by GM9 Glucose Analyser.
In children with HO and SO, circulating fasting concentrations of spexin [median 0.43 ng/mL (0.27-1.29) in HO; median 0.37 ng/mL (0.22-0.85) in SO] and PUG [median 1.43 ng/mL (1.09-2.69) in HO; and [1.22 ng/mL (0.94-1.43) in SO] were comparable (p>0.05). While adiponectin (n=8 for SO) and insulin levels were not different between the two groups, fasting blood glucose was lower in HO (74 ±11 mg/dL vs. 86 ± 6 mg/dL; p=0.03). Spexin and PUG did not show correlations with BMI, glucose, insulin, T- or HMW-adiponectin (p>0.05 for all).
Circulating concentrations of PUG and spexin, potential regulators of energy homeostasis and satiety were similar in children with HO compared to those with SO in this pilot study. Despite the potential abnormal hypothalamic signaling in HO, the lack of difference in the concentration of these novel markers in HO and SO is intriguing. Further studies investigating other factors that may disrupt the normal homoeostatic mechanisms within the hypothalamus in both HO and SO are warranted.