RESUMEN
High-fat diet consumption for an extended period causes obesity, systemic metabolic disturbance, and brain insulin resistance, resulting in neuroinflammation. Although the beneficial effect of Cyclosorus terminans extract on obesity-related insulin resistance has been demonstrated, little is known about how it affects neuroinflammation and brain insulin resistance in obese rats. Male Wistar rats were given either a normal diet (ND, n = 6) or a high-fat diet (HFD, n = 24) for a total of 14 weeks. At the beginning of the week, 13 rats in the ND group were given vehicle orally for 2 weeks, while rats on HFD diets were randomized to one of four groups and given either vehicle, 100 mg/kg/day of Cyclosorus terminans extract, 200 mg/kg/day of Cyclosorus terminans extract, or 20 mg/kg/day of pioglitazone orally for 2 weeks. After the experimental period, blood and brain samples were taken to assess metabolic and brain parameters. HFD-fed rats had obesity, systemic and brain insulin resistance, brain inflammation, microglial and astrocyte hyperactivity, and brain necroptosis. Treatment with 200 mg/kg/day of Cyclosorus terminans extract and pioglitazone equally attenuated obesity, insulin resistance, brain insulin dysfunction, and neuroinflammation in insulin resistant rats. Our findings suggest that Cyclosorus terminans extract may hold promise as a therapeutic agent for insulin resistance and neuroinflammation in obese conditions.
RESUMEN
Alzheimer's disease is associated with multiple risk factors and is the most common type of dementia. Trimethylamine-N-oxide (TMAO), a gut microbiota metabolite derived from dietary choline and carnitine, has recently been identified as a potential risk factor of Alzheimer's disease. It has been demonstrated that TMAO is associated with Alzheimer's disease through various pathophysiological pathways. As a result of molecular crowding effects, TMAO causes the aggregation of the two proteins, amyloid-beta peptide and tau protein. The aggregation of these proteins is the main pathology associated with Alzheimer's disease. In addition, it has been found that TMAO can activate astrocytes, and inflammatory response. Besides molecular investigation, animal and human studies have also supported the existence of a functional relationship between TMAO and cognitive decline. This article comprehensively summarizes the relationship between TMAO and Alzheimer's disease including emerging evidence from in vitro, in vivo, and clinical studies. We hope that this knowledge will improve the prevention and treatment of Alzheimer's disease in the near future.
