Dietary fat perception influences food preference, satiety, and metabolic regulation but remains incompletely understood. This review examines current knowledge regarding receptor-mediated fat sensing, neural integration, adaptive plasticity, and their clinical implications. Evidence was collected from major biomedical databases through June 2026. Human and experimental studies addressing molecular receptors, psychophysical testing, electrophysiology, neuroimaging, genetics, and metabolic physiology were critically synthesized. CD36 and GPR120 function as principal lipid sensors alongside FFAR1, GPR84, FFAR2, and TGR5. Oral lipid detection is integrated with retronasal olfactory processing, trigeminal signaling, endocrine responses, and cortical reward networks. Fat perception demonstrates remarkable adaptability through receptor regulation, inflammatory remodeling, epigenetic modification, and dietary exposure. Methodological heterogeneity remains a major limitation across psychophysical and molecular investigations. Evidence supports a distributed, adaptive, and metabolically regulated system of dietary fat perception rather than an isolated sensory pathway. Improved methodological standardization and multidisciplinary approaches will accelerate translation into personalized dietary interventions and metabolic therapeutics.
Maintaining temporal coordination of physiological function is essential for good health. To determine how the endothelin axis regulates the timing of blood pressure (BP) and key physiological rhythms, we monitored circadian rhythmicity of BP and other variables by telemetry in male and female Sprague Dawley rats with or without chronic ET B receptor blockade (A-192621). Rats were maintained under constant dark conditions to ensure a free-running status of the circadian clock. Rats were divided into groups being fed either normal salt (NS) or high salt (HS) diets starting the day of release into constant darkness. After 1 week, a subset of rats was given A-192621 in the food for 2 weeks. HS diet exacerbated amplitude of mean arterial pressure (MAP) in ET B antagonist-treated rats. ET B antagonism was sufficient to delay MAP rhythms in either diet. There were no changes in amplitude of heart rate (HR) or body temperature resulting in desynchrony between the phases with MAP. Rats fed an HS diet without an antagonist also displayed desynchrony among all peripheral rhythms. Together, these data support the notion of the endothelial system regulating BP rhythms and maintaining synchrony with peripheral physiological rhythms.
Acute cervical spinal cord injury (cSCI) disrupts supraspinal autonomic cardiovascular control. Heart rate variability (HRV), assessed using linear and nonlinear methods, provides a sensitive index of cardiovascular autonomic regulation. To evaluate linear and nonlinear HRV parameters associated with autonomic cardiovascular dysregulation in acute cSCI. This monocentric prospective study included 500 patients with traumatic or non-traumatic acute cSCI and 200 age- and sex-matched healthy controls. All participants underwent 24 h Holter ECG monitoring. Time- and frequency-domain indices and nonlinear metrics, including Poincaré plot analysis, entropy, detrended fluctuation analysis, and recurrence quantification analysis, were calculated. Predictive modeling used logistic regression, random forest, gradient boosting, and support vector machine algorithms with cross-validation. Both cSCI groups showed significantly reduced HRV amplitude and altered autonomic cardiovascular regulation. Nonlinear indices demonstrated reduced entropy, altered fractal scaling, and decreased recurrence dynamics. Female patients showed relatively preserved nonlinear HRV parameters. Models combining linear and nonlinear features discriminated autonomic dysfunction better than models using conventional HRV metrics alone. Combined linear and nonlinear HRV analysis provides complementary characterization of autonomic cardiovascular dysregulation following acute cSCI.
