Журнал метаболического синдрома

Trimethylamine-N-oxide (TMAO) is the gut microbiome derived metabolite synthesized from a volatile amine-containing organic compound called Trimethylamine (TMA) by the action of the hepatic Flavin Monooxygenase enzyme (FMO) isoform 1 and 3. TMA is largely synthesized from choline, betaine and L-carnitine by gut microbial enzymes. TMAO has been speculated to be independently associated with various cardiometabolic and chronic diseases in humans such as atherosclerosis, type 2 diabetes mellitus, cancers, Chronic Kidney Disease (CKD), heart failure and dyslipidemia. In marine animals, TMAO has been purported to be useful in counteracting the effect of osmotic stress and hydrostatic pressure emanating from their surrounding environment. In this review, the potential benefits and comparable deleterious effect of TMAO in animals and human has been elucidated. The interventions targeting TMAO in mitigating diseases have also been reviewed and concluded that based on the current stance of available literature on the effect of TMAO, the development of a validated non-lethal antagonist would confer protection and extend the life of patients with cardiometabolic and other chronic diseases.

Oxidative stress plays a significant role in the development and progression of various diseases, including cardiovascular disorders, neurodegenerative conditions and cancer. This article provides an in-depth understanding of oxidative stress, its causes, effects on health and strategies to mitigate its harmful impact. The biology of oxidative stress is explored, highlighting the generation and function of ROS. Environmental factors, diet and lifestyle choices, mitochondrial dysfunction and inflammation are identified as key contributors to oxidative stress. The effects of oxidative stress on cardiovascular health, neurodegenerative disorders, cancer and aging are discussed. Moreover, the role of antioxidants in combating oxidative stress is emphasized, encompassing enzymatic and non-enzymatic antioxidants and their synergistic effects. Diagnostic tools to assess oxidative stress levels are examined, including biomarkers, advanced oxidation protein products and total antioxidant capacity assays.

Lipotoxicity is a condition characterized by the harmful effects of excessive lipids on cellular health. It plays a significant role in the development of metabolic disorders such as obesity, type 2 diabetes, Non-Alcoholic Fatty Liver Disease (NAFLD), and cardiovascular complications. The accumulation of lipids, particularly Free Fatty Acids (FFAs), disrupts cellular function through mechanisms such as impaired insulin signalling, Endoplasmic Reticulum (ER) stress, oxidative stress, and mitochondrial dysfunction. This article provides an in-depth exploration of lipotoxicity, including its mechanisms, consequences, interventions, and future directions. Understanding lipotoxicity is crucial for developing effective strategies to prevent and manage its detrimental effects on human health.

Adipokines, a group of bioactive molecules secreted by adipose tissue, have emerged as key regulators of metabolism, inflammation, and overall health. Once considered solely as energy storage depots, adipose tissue is now recognized as a dynamic endocrine organ that communicates with various organs throughout the body via the secretion of adipokines. This article provides a comprehensive overview of adipokines, including their classification, physiological roles, and implications in metabolic disorders and chronic diseases. Adipokines are classified into several groups, such as adiponectins, leptin, pro-inflammatory cytokines, anti-inflammatory cytokines, chemokines, and growth factors. Adiponectins exhibit insulinsensitizing and anti-inflammatory properties, while leptin regulates energy balance and neuroendocrine function. Pro-inflammatory cytokines contribute to chronic low-grade inflammation, and anti-inflammatory cytokines counteract their effects.