In the US, the number of children with obesity has reached a staggering 13.7 million. Though there are diets to assist weight loss, recent research suggests a neurobiological basis of obesity specifically related to the mediobasal hypothalamus (MBH), a critical brain structure involved in energy homeostasis, metabolism, and appetite. However, proliferation of hypothalamic gliosis, a cellular inflammatory response, disrupts the function and is shown, in rodents, as a key component in diet-induced obesity. Further conclusions reveal that highly caloric and high-fat diets, in rodents, can cause MBH gliosis. This project seeks to investigate the relationship between diet and hypothalamic gliosis in children, the latter assessed by magnetic resonance imaging (MRI). We expect children with an unhealthy diet to have an increased BMI z-score and greater evidence of MBH gliosis. Participants (N=192) were recruited as part of the longitudinal NIH Adolescent Brain Cognitive Development study. Anthropometric and demographic data were collected along with brain MRI T2-weighted images at the baseline visit. MBH gliosis was measured by using the signal ratio for T2 intensity of the mean bilateral MBH/Amygdala signal ratio; Putamen/Amygdala was used as control ratio. At the one year follow-up, the child’s habitual diet in the past year was assessed using a parent-report food frequency questionnaire. Higher total points represented a healthier overall diet. Additionally, follow-up anthropometric data was obtained to determine the child’s adiposity change over time. At baseline, mean age was 9.9±0.6 and 49% were males. Mean BMI z-score was 0.76±1.05, 19% were overweight and 23% with obesity. Preliminary results in a subset of participants (N=60) revealed a trend for an association between an unhealthy diet and evidence of MBH gliosis (t=1.59, P=0.117). By emphasizing the neurobiological basis of obesity, potential insights can inform targeted diet-related treatments of childhood obesity; thus, furthering the understanding of child obesity pathogenesis.

Children have more exposure to screen media today than any other generation. In the U.S., rates of obesity in children have also tripled in 4 decades. A disruption in the brain called gliosis has been described to participate in obesity pathophysiology if it occurs in a brain region important for energy balance, called the mediobasal hypothalamus (MBH). The objective of this study is to explore possible relationships between MBH gliosis and parents’ reports on screen time their child engages in. This study will also look into variables that may mediate these relationships, such as body adiposity and impulsivity. I hypothesize that there will be a positive correlation between screen media use and MBH gliosis with obesity and the level of impulsivity being positively correlated to both gliosis and screen time. The methodology consists of data from participants (N = 192) in the NIH Adolescent Brain Cognitive Development study. The NIH Toolbox Flanker Inhibitory Control and Attention Test was used to measure child’s impulsivity, and the parents were given the Screen time report to measure the average daily screen media time of each child. Along with these measures, participant’s age, sex, race, BMI z-score, waist/height ratio, and T2-weighted MRI will be included. MBH gliosis will be measured by T2 MRI signal intensity (brightness) of the mean bilateral MBH/Amygdala signal ratio; Putamen/Amygdala will be used as control ratio. Participants were 51% female with an average age of 9.9±0.63 years. Within our sample, 57.3%, 19.3%, and 23.4% of subjects were considered healthy weight, overweight, and with obesity, respectively. Anthropometric and behavioral data recorded on average 11.2 months after the initial tests will be included to calculate changes over time. This research will help to further illuminate the relationships between screen time and obesity, and will potentially be helpful in proposing new treatments for children with obesity.