Adolescence is a brief developmental window during which limited energy reserves are redistributed from linear somatic growth toward reproductive maturation. Rising rates of childhood obesity and earlier puberty raise the possibility that modern, energy-dense diets may alter these evolved allocation rules. The present preprint tests whether exposure to an obesogenic diet during the sexual maturation window shifts energy investment toward reproduction at the cost of skeletal and metabolic health.
The investigators exposed male and female mice of two genotypes — wild-type (WT) and leptin receptor deficient (Db/Db) — to either a high fat diet (HFD) or normal chow. Animals were followed longitudinally through the sexual maturation window in mice, from 4 to 10 weeks of age. The report is a preprint posted to bioRxiv and has not been peer reviewed.
From 4–10 weeks, the researchers assessed multiple domains relevant to energy allocation: systemic metabolic state (including adiposity and glucose tolerance), skeletal morphology (with attention to growth plates and joint structure), gonadal maturation (testes in males, ovaries in females), endocrine markers, and distribution of insulin receptor expression across tissues. These measures were intended to capture trade-offs between growth and reproduction during the adolescent period.
In WT males fed a high fat diet, the study observed increased adiposity and impaired glucose tolerance. Concomitant with systemic metabolic disruption, HFD exposure produced selective remodeling of joint morphology and measurable advancement of gonadal maturation. The authors also report a shift in insulin receptor expression away from growth plates and toward the testes in WT males on HFD. Together, these male-specific changes were interpreted as evidence that energy use was being rebalanced toward reproductive development at the expense of skeletal integrity and metabolic homeostasis.
WT females displayed more subtle systemic metabolic disruption on HFD compared with males, according to the reported findings. Nevertheless, females showed clear diet-responsive alteration in growth plate characteristics and accelerated ovarian maturation. The pattern described suggests that although systemic metabolic markers were less pronounced than in males, reproductive and skeletal endpoints in females remained sensitive to diet during the adolescent window.
A notable endocrine-related observation in the report is the apparent redistribution of insulin receptor expression in HFD-exposed WT males — specifically, a shift from growth plates toward the testes. This change is presented alongside accelerated gonadal maturation and suggests a mechanism by which an energy-dense diet could preferentially support reproductive readiness over somatic growth during adolescence.
The authors frame their results in terms of evolutionary trade-offs: under obesogenic conditions during adolescence, evolved allocation rules may be redirected to favor early reproductive capability even when that reallocation compromises bone development and metabolic health. They highlight sex-dependent outcomes, with males showing pronounced metabolic disturbance and joint remodeling alongside reproductive advancement, and females showing diet-sensitive changes in growth plate and ovarian maturation. The authors suggest these mouse data have potential implications for understanding trends in human precocious puberty and bone health in the context of increasing childhood obesity.
This article is a preprint on bioRxiv and has not been certified by peer review. The provided source excerpt does not report full methodological details such as sample sizes, specific statistical outcomes, or procedural nuances; those details were not available in the excerpt. The authors declared no competing interests and acknowledged funding from a Harvard Dean’s Competitive Award.
In this mouse model, exposure to an energy-dense high fat diet during the adolescent 4–10 week window shifted physiological allocation of resources toward reproductive maturation and away from skeletal robustness in a sex-dependent manner. The pattern supports the hypothesis that obesogenic diets can distort evolved energy allocation rules during adolescence, with possible relevance to rising rates of early puberty and future bone health concerns in humans. As a preprint, these findings should be interpreted cautiously until peer review and full methodological reporting are available.