Unveiling the Link: Obesity, Diet, Hypothalamic Inflammation, and Central Precocious Puberty - Recent Insights and Implications.

BACKGROUND

Childhood obesity is on the rise globally, raising concerns among the medical community. The phenomenon is closely linked to high-fat diets. Concurrently, the prevalence of central precocious puberty (CPP) is increasing. Recent evidence demonstrates that obesity and high-fat diets induce inflammation in the mediobasal hypothalamus in humans, a region housing both the primary appetite-regulating centers and the GnRH neurons. Early activation of GnRH neurons is implicated in CPP. The proximity of these hypothalamic sites, exposed to obesity-/diet-induced neuroinflammation, coupled with the positive association between CPP, obesity, and high-fat diets, prompts exploration into the potential involvement of hypothalamic inflammation (HI) in CPP occurrence.

SUMMARY: This article delves into the molecular mechanisms through which HI may contribute to CPP in obese and lean girls, based on existing literature. We present evidence suggesting that HI could activate the gonadotropic axis by influencing cytokines and prostaglandins production, BDNF, and potentially phoenixin.

KEY MESSAGES: HI emerges as a potential pathophysiological mechanism linking obesity, high-fat diets, and CPP. Further research is imperative to elucidate the relationship between HI and CPP, providing insights into the origins of CPP, often termed as idiopathic.