Concurrent with the epidemic of childhood obesity (17% of adolescents), an unprecedented world-wide increase in the prevalence of several adiposity-related complications (including fatty liver disease (hepatic steatosis), type 2 diabetes and early cardiovascular disorders) in this age group, has emerged. Two principle environmental variables play an essential role in the development and maintenance of obesity and in disturbing glucose homeostasis: a lack of physical exercise and overnutrition, i.e., high carbohydrate and high fat diets (HFD). It was our laboratory's intention to develop a rodent model to examine whether the metabolic instability observed in human pubertal children is also present in maturing rats and whether a HFD during this maturational period enhances adipose-related complications with or without an increase in body weight. We hypothesized that maturing Sprague-Dawley rats would reveal a profile of metabolic disturbances and that a disruption of the hyperbolic arrangement between insulin sensitivity and insulin release would be evident (statistically significant changes in fasting hyperinsulinemia, insulin resistance, and insulin release) indicating a high risk environment for future cardiometabolic diseases. It was observed that pubertal rats are metabolically impaired and that a HFD substantially enhances metabolic deficits with marked disturbance in insulin sensitivity (hyperinsulinemia). Additionally, substantial lipogenesis was observed in visceral and liver tissue, potentially as a result of hyperinsulinemia. Both phenotypes of maturing rats exposed to a HFD (obesity prone and obesity resistant) demonstrated "metabolic obesity" regardless of physical phenotype. These outcomes have relevance in the context of public health, particularly if lipocentricity is viewed as an essential element in the challenge of preventing and/or treating perturbations to the metabolic health of pubertal children.