Abdominal Obesity, Brain Glymphatic Function, and LH–dlHPC Appetite Regulation: Current Evidence, Potential Links, and Implications for Metabolic Health

Abdominal obesity is closely associated with adverse metabolic outcomes, but how visceral fat accumulation affects central feeding regulation remains incompletely understood. This narrative review integrates research on visceral adipose tissue (VAT), brain glymphatic processes, and lateral hypothalamus–dorsolateral hippocampus (LH–dlHPC) feeding regulation to examine potential links among peripheral metabolic signals, the brain microenvironment, and circuit function. Human imaging studies suggest associations of obesity-related phenotypes with changes in LH–dlHPC connectivity and glymphatic imaging markers; animal experiments provide mechanistic clues to adipose-derived signals affecting hippocampal synaptic plasticity. We propose that VAT-related inflammatory and extracellular vesicle signals may act on barrier and perivascular glial interfaces, contributing to feeding circuit changes through altered local transport and microenvironmental homeostasis. Current evidence supports parts of this model but has not established a causal relationship in which altered transport mediates dysfunction in specific feeding circuits. We also discuss the influences of sex, hormonal status, and sleep, and outline longitudinal and interventional approaches combining assessments of fat distribution, regional transport, circuit function, and feeding behavior to test these mechanisms and their implications for metabolic health.