International Hellenic University

Phenolic acids commonly co-exist in foods with polysaccharides, and play a significant part in structuring the food matrix.Although their sensory and functional effects are well-documented, the physicochem. basis of their interactions with the other food structural components, especially during their oral mixing with saliva, is largely unexplored.This is a preliminary examination of the mol. and colloidal-level interactions between an in vitro oral model system containing guar gum, gallic acid, and mucin and an ex vivo model containing guar gum, green tea, and human saliva.In the in vitro model, data from light scattering and spectrophotometry revealed an increase in turbidity and particle sizes upon transitioning from a binary guar gum-gallic acid to a ternary system with mucin.At pH 7, their z-average diameter ranges from 1400 nm (binary) to 1800 nm (ternary) and further to 3300 nm at pH3, indicating aggregation and phase separationThis phenomenon is also reflected in their relaxation time which drops from 30ms for the guar gum-mucin system to 10-20ms upon gallic acid addition at oral conditions.Moving to ex-vivo, human saliva particle size drops dramatically from 10 μm to 594 nm with the addition of gallic acid, indicating aggregation.The particle size increases with the addition of guar gum (740 nm), followed by the decrease of saliva′s relaxation time from 15 to 7ms with the addition of tea/guar gum system.The above findings provide some insights into the structure-function aspects of polysaccharide-phenolic acid complex systems, highlighting mucin′s role in modulating the food matrix′s phase behavior in the presence of phenolic acids, and point to potential implications on flow and structural changes during oral processing from a physicochem. aspect.

In recent years, the terms "metabolic associated fatty liver disease-MAFLD" and "metabolic dysfunction-associated steatotic liver disease-MASLD" were introduced to improve the encapsulation of metabolic dysregulation in this patient population, as well as to avoid the negative/stigmatizing terms "non-alcoholic" and "fatty".

There is evidence suggesting links between MASLD and coronary heart disease (CHD), heart failure (HF), atrial fibrillation (AF), stroke, peripheral artery disease (PAD) and chronic kidney disease (CKD), although the data for HF, AF, stroke and PAD are scarcer. Physicians should consider the associations between MASLD and CV diseases in their daily practice. Based on this knowledge and current guidelines, they should also assess and manage CV risk/co-morbidities in such patients. It is important to further investigate the impact of MASLD on CV outcomes, a knowledge that will help to elucidate the clinical implications of this "novel" liver entity.

Chronic bacterial infections exert profound systemic effects beyond their primary infection sites, influencing a range of inflammatory, metabolic, and neurodegenerative diseases. Helicobacter pylori (Hp) and Porphyromonas gingivalis (Pg) are two highly prevalent pathogens that, despite occupying distinct niches, share remarkable pathogenic similarities. Both bacteria, connected with metabolic syndrome, employ immune evasion strategies, induce chronic inflammation, and contribute to systemic diseases such as metabolic-associated steatotic liver disease, cardiovascular disease, and neurodegeneration, such as Alzheimer's disease. A key unifying factor in their pathogenicity is the role of gingipains-cysteine proteases produced by Pg-which facilitate bacterial invasion, immune modulation, and tissue destruction. Emerging evidence suggests that Hp possesses analogous proteolytic enzymes, further supporting their potential synergistic impact on host health. Moreover, both pathogens have been implicated in metabolic syndrome-related blood-brain barrier disruption, chronic (smoldering) systemic inflammation, and lipid metabolism dysregulation, contributing to progressive neurodegenerative and cardiovascular disorders. The role of galectins, particularly galectin-3, in modulating microglial activation and inflammatory pathways further highlights their involvement in neuroinflammatory diseases. Targeting gingipains presents a promising therapeutic avenue, with bismuth compounds and novel inhibitors showing potential in disrupting these proteases and mitigating their systemic effects. Understanding the interactions between Hp and metabolic syndrome-related Pg is crucial for developing comprehensive treatment strategies, integrating gastroenterology, periodontology, and neurology. Addressing these infections at both local and systemic levels may improve long-term health outcomes and reduce the burden of chronic inflammatory diseases linked to microbial persistence.