Nature and Science 2010;8(4) http://www.sciencepub.net/nature naturesciencej@gmail.com 33 Biochemical and neurological effects of obesity on primary school girls Hanaa H. Ahmed 1 ; Abla G. Khalifa 2 ; Emad F. Eskander 1 ; Alaa H. Sayed 1 and Ismail M. Abdel-Nabi 3 1 Hormones Dept., National Research Centre, Dokki, Giza, Egypt 2 Child Health Dept., National Research Centre, Dokki, Giza, Egypt 3 Zoology Dept., Fac. Of Science, Suez Canal University, Ismailia, Egypt alaasc@yahoo.com The prevalence of childhood obesity has increased considerably worldwide. As with adults, obesity in childhood is strongly related to hypertension, dyslipidemia, type II diabetes, and insulin resistance. Also, obese children are at increased risk of becoming obese adults. Therefore, obese children tend to develop serious medical and psychosocial complications, and have a greater risk of adult morbidity and mortality. The principal goal of this study was to investigate the effects of obesity on the levels of some biomarkers and their relation to the cognitive function in elementary school obese girls. The current study was conducted on 45 obese girls (mean age 10.53 ± 1.29 years; mean BMI 28.43 ± 4.62 kg/m 2 ) and 45 normal age-matched girls (mean age 10.36 ± 1.53 years; mean BMI 19.07 ± 3.47 kg/m 2 ). Estimation of serum adrenomedullin (AM) and substance P (SP), and plasma noradrenaline (NA) and acetylcholine (ACh) were carried out. Cognitive function tests (auditory vigilance, digit span, coding and visual memory) were done for all subjects. The levels of serum AM and SP as well as plasma NA were highly significantly increased (P<0.01) in the obese group as compared with the control group. The total right response of auditory vigilance (TR) showed insignificant decrease while the total wrong response to auditory vigilance test (TW) showed a significant increase (P<0.05) in the obese group as compared with the control group. Digit span and visual memory classification showed a highly significant decrease (P<0.01) while coding showed a significant increase (P<0.05). Our study showed that obesity affected the measured biomarkers and, to some extent, has an adverse effect on cognitive function in primary school girls. [Nature and Science 2010;8(4):33-43]. (ISSN: 1545-0740)] Key words: obesity- adrenomedullin -substance P - noradrenaline - acetylcholine – cognition – girls Introduction Obesity is well-known to result from the disturbance of the homeostasis between food intake and energy expenditure (Gura, 2003). It is a major risk factor for the development of type II diabetes and its complications such as the metabolic syndrome, coronary heart disease and peripheral neuropathy (Lazar, 2005). It also increases the risk for insulin resistance (Formiguera and Canton, 2004), high blood pressure, and other medical problems (Sothern et al., 2000). Obesity may also disturb cognition, as deficits in learning, memory, and executive functioning were reported in obese when compared to non-obese subjects (Waldstein and Katzel, 2006). A recent study suggested that obesity and its consequences, including midlife hypertension, diabetes, and cerebrovascular disease, contribute significantly to cognitive decline and accelerate the development of dementia (Qiu et al., 2007). Adrenomedullin (AM) belongs to the family of adipokines (Nambu et al., 2005). This 52-amino acid peptide was first isolated from phaeochromocytoma tissue as a vasoactive and cardioprotective factor (Shimosawa et al., 2002). AM has been also found in the hypothalamus-pituitary- adrenal axis (Letizia et al., 2003) and produced largely by mature adipocytes and stromal vascular cells (Fukai et al., 2005). AM has local paracrine or autocrine effects on the tissue so that it can trigger many physiologic events by remaining in the plasma like the circulating hormone (Letizia et al., 2005). AM elicits a long-lasting vasodilatation and diuresis. Its action is mainly mediated by the intracellular adenylate cyclase coupled with cyclic adenosine monophosphate (cAMP) and nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) pathway through its specific receptor (Eto, 2001).