Recent advancements in sensory research have brought to light the intricate relationship between taste perception and the oral microbiota, prompting investigations into their influence on human health, particularly in the context of dietary preferences and obesity. This review aims to update the current understanding of how oral microbiota influence taste perception and dietary choices, elucidating shared metabolic pathways between food processing and oral bacteria. Further, this review outlines the mechanisms underlying taste perception, emphasising the role of taste receptors and taste buds in shaping sensory experiences influenced by genetic and environmental factors. Notably, we explore the bidirectional relationship between oral microbiota and taste sensitivity, highlighting the potential impact of microbial composition on taste perception thresholds and implications for dietary habits and health outcomes, such as obesity and dental caries. However, significant research gaps remain, particularly in the understanding of the molecular mechanisms linking oral microbiota with taste sensitivity, as well as the long-term effects of microbiota-targeted interventions. Future research should focus on longitudinal studies and experimental interventions to explore these connections more deeply, offering insights into potential strategies for promoting healthier dietary behaviours and managing diet-related non-communicable diseases.

Thrombocytopenia is a common symptom and one of the warning signs of dengue virus (DENV) infection. Platelet depletion is critical as it may lead to other severe dengue symptoms. Understanding the molecular events of this condition during dengue infection is challenging because of the multifaceted factors involved in DENV infection and the dynamics of the disease progression. Platelet levels depend on the balance between platelet production and platelet consumption or clearance. Megakaryopoiesis and thrombopoiesis, two interdependent processes in platelet production, are hampered during dengue infection. Conversely, platelet elimination via platelet activation, apoptosis and clearance processes are elevated. Together, these anomalies contribute to thrombocytopenia in dengue patients. Targeting the molecular events of dengue-mediated thrombocytopenia shows great potential but still requires further investigation. Nonetheless, the application of new knowledge in this field, such as immature platelet fraction analysis, may facilitate physicians in monitoring the progression of the disease.

Complex tumour ecosystem comprising tumour cells and its associated tumour microenvironment (TME) constantly influence the tumoural behaviour and ultimately impact therapy failure, disease progression, recurrence and poor overall survival of patients. Crosstalk between tumour cells and TME amplifies the complexity by creating metabolic changes such as hypoxic environment and nutrient fluctuations. These changes in TME initiate stem cell-like programmes in cancer cells, contribute to tumoural heterogeneity and increase tumour robustness. Recent studies demonstrate the multifaceted role of autophagy in promoting fibroblast production, stemness, cancer cell survival during longer periods of dormancy, eventual growth of metastatic disease and disease resistance. Recent ongoing studies examine autophagy/mitophagy as a powerful survival strategy in response to environmental stress including nutrient deprivation, hypoxia and environmental stress in TME. It prevents irreversible senescence, promotes dormant stem-like state, induces epithelial–mesenchymal transition and increases migratory and invasive potential of tumour cells. The present review discusses various theories and mechanisms behind the autophagy-dependent induction of cancer stem cell (CSC) phenotype. Given the role of autophagic functions in CSC aggressiveness and therapeutic resistance, various mechanisms and studies based on suppressing cellular plasticity by blocking autophagy as a powerful therapeutic strategy to kill tumour cells are discussed.

This article aims to study the different dietary fat types associated with obesity and coronary indices. A sample of 491 healthy adults was included in a cross-sectional manner. Dietary fats intake, obesity indices (conicity index (CI), body adiposity index (BAI), abdominal volume index (AVI), body roundness index (BRI), and weight-adjusted-waist index (WWI)), and cardiovascular indices (cardiometabolic index (CMI), lipid accumulation product (LAP), and atherogenic index of plasma (AIP)) were calculated and studied. Participants with an acceptable intake of omega-3 had a higher BRI score (1⋅90 ± 0⋅06 v. 1⋅70 ± 0⋅06). Participants with an unacceptable intake of cholesterol had a higher CI (1⋅31 ± 0⋅11 v. 1⋅28 ± 0⋅12; P = 0⋅011), AVI (20⋅24 ± 5⋅8 v. 18⋅33 ± 6⋅0; P < 0⋅001), BRI (2⋅00 ± 1⋅01 v. 1⋅70 ± 1⋅00; P = 0⋅003), WWI (11⋅00 ± 0⋅91 v. 10⋅80 ± 0⋅97; P = 0⋅032), and lower AIP (0⋅46 ± 0⋅33 v. 0⋅53 ± 0⋅33; P = 0⋅024). Total fat, saturated fat (SFA), and polyunsaturated fat (PUFA) intake had a significant moderate correlation with AVI and BRI. The monounsaturated fat (MUFA) intake had a significantly weak correlation with CI, AVI, BRI, WWI, and AIP. Cholesterol and omega-6 had weak correlations with all indices. Similar correlations were seen among male and female participants. The different types of fat intake significantly affected obesity and coronary indices, especially SFA and PUFA, as well as omega-3 and cholesterol. Gender and the dietary type of fat intake have a relationship to influence the indicators of both obesity and coronary indices.

A12-week experiment was conducted to evaluate the influences of thiamine ongrowth performance, and intestinal mitochondrial biogenesis and function of Megalobramaamblycephala fed a high-carbohydrate (HC) diet. Fish (24·73 (sem 0·45) g) were randomly assigned to one of four diets: two carbohydrate (CHO) levels (30 and 45 %) and two thiamine levels (0 and 1·5 mg/kg). HC diets significantly decreased DGC, GRMBW, FIMBW, intestinal activities of amylase, lipase, Na+, K+-ATPase, CK, complexes I, III and IV, intestinal ML, number of mitochondrial per field, ΔΨm, the P-AMPK: T-AMPK ratio, PGC-1β protein expression as well as the transcriptions of AMPKα1, AMPKα2, PGC-1β, mitochondrial transcription factor A, Opa-1, ND-1 and COX-1 and 2, while the opposite was true for ATP, AMP and reactive oxygen species, and the transcriptions of dynamin-related protein-1, fission-1 and mitochondrial fission factor. Dietarythiamine concentrations significantly increased DGC, GRMBW, intestinal activities of amylase, Na+, K+-ATPase, CK, complexes I and IV, intestinal ML, number of mitochondrial per field, ΔΨm, the P-AMPK:T-AMPK ratio, PGC-1β protein expression as well as the transcriptions of AMPKα1, AMPKα2, PGC-1β, Opa-1, ND-1, COX-1 and 2, SGLT-1 and GLUT-2. Furthermore, a significant interaction between dietary CHO and thiamine was observed in DGC, GRMBW, intestinal activities of amylase, CK, complexes I and IV, ΔΨm, the AMP:ATP ratio, the P-AMPK:T-AMPK ratio, PGC-1β protein expression as well as the transcriptions of AMPKα1, AMPKα2, PGC-1β, Opa-1, COX-1 and 2, SGLT-1 and GLUT-2. Overall, thiamine supplementation improved growth performance, and intestinal mitochondrial biogenesis and function of M. amblycephala fed HC diets.