The Link Between Salivary Amylase Activity, Overweight, and Glucose Homeostasis

This doctoral Thesis explores the role of salivary amylase activity (SAA) as a potential non-invasive biomarker of metabolic health by examining its associations with overweight status, visceral fat, and markers of glucose homeostasis, emphasising that current evidence is largely correlational and requires further investigation to establish causality. In a well-characterised cohort of overweight women of reproductive age, the crosssectional study, integrated as a foundational component of the interventional study, analysed associations between salivary amylase activity, visceral fat, and the triglyceride glucose index to establish baseline metabolic relationships, while the subsequent 12-week dietary intervention, stratified by salivary amylase activity levels, evaluated differential metabolic responses including changes in insulin sensitivity, GLP1 secretion, adipokines, and glucose homeostasis under calorie restricted and low starch diets, highlighting the potential of personalised nutrition in optimising metabolic health. The findings of this investigation were reported through three thematically aligned peerreviewed original research articles as well as two comprehensive review articles. A robust inverse relationship was observed between SAA and visceral adiposity, independent of total body fat, suggesting that higher SAA may be indicative of a metabolically healthier fat distribution phenotype. While visceral fat was positively correlated with the triglycerideglucose (TyG) index, a surrogate marker of insulin resistance, SAA exhibited no direct association with the TyG index. These findings support the hypothesis that SAA may influence glucose regulation indirectly, potentially through its modulation of fat accumulation and cephalic-phase insulin dynamics patterns rather than directly. While variability in SAA activity, largely driven by AMY1 gene copy number variation (CNV), also has been regulated by adrenergic activity, which can be partially modulated through lifestyle interventions. This is particularly relevant, as impaired autonomic regulation is commonly observed in individuals with obesity and metabolic syndrome and may be improved through targeted lifestyle changes. This potential responsiveness further supports its relevance as a candidate biomarker for metabolic plasticity. This Thesis proposes that SAA, as a non-invasive and easily measurable biomarker, could play a valuable role in the early identification of individuals at metabolic risk and in guiding personalised lifestyle interventions for the prevention of insulin resistance and obesity related complications.