UC Irvine

Storage of adipose tissue is a trait belonging to all humans, historically borne from the necessity to survive extended periods of famine. Yet, there is clear inter-individual variability in our propensity to accumulate excess fat. In addition, this variability is present as early as infancy and persists into adulthood. In adults, the regulation of energy homeostasis (balance) by the brain is evident not only through signaling provided by peripheral systems to the hypothalamus, such as fat (leptin) and the stomach (ghrelin), but also by the downstream cognition required to decide what, when and how much to eat. Magnetic Resonance Imaging has been instrumental in identifying the brain regions and circuitry involved in food-related behaviors as well as the identification of brain differences between obese and normal weight adults. It is, however, unclear whether the observed differences in brain regions and circuitry in obese relative to normal weight individuals are a cause, consequence, or both, of the obese state. Moreover, relatively little is known about the developmental ontogeny of these food-related brain regions and circuitry, particularly during the period of intrauterine development (when the postnatal obesogenic environment could not yet have affected this circuitry), and its prospective role in shaping propensity for childhood obesity. Knowledge of early life brain structure and function in the context of energy imbalance would contribute to an improved understanding of propensity for obesity, early identification of at-risk individuals, and intervention targets for primary prevention. This thesis has addressed this fundamental knowledge gap by using an imaging based approach to: 1) quantify and describe early life patterns of fat deposition, 2) shed new insights on perinatal brain development, and 3) identify prospective associations between interoceptive, reward, and gustatory properties of the newborn brain and subsequent early life fat gain.