Advances in Understanding of the Role of Lipid Metabolism in Aging

During aging, body adiposity increases with changes in the metabolism of lipids and their metabolite levels. Considering lipid metabolism, excess adiposity with increased lipotoxicity leads to various age-related diseases, including cardiovascular disease, cancer, arthritis, type 2 diabetes, and Alzheimer’s disease. However, the multifaceted nature and complexities of lipid metabolism make it difficult to delineate its exact mechanism and role during aging. With advances in genetic engineering techniques, recent studies have demonstrated that changes in lipid metabolism are associated with aging and age-related diseases. Lipid accumulation and impaired fatty acid utilization in organs are associated with pathophysiological phenotypes of aging. Changes in adipokine levels contribute to aging by modulating changes in systemic metabolism and inflammation. Advances in lipidomic techniques have identified changes in lipid profiles that are associated with aging. Although it remains unclear how lipid metabolism is regulated during aging, or how lipid metabolites impact aging, evidence suggests a dynamic role for lipid metabolism and its metabolites as active participants of signaling pathways and regulators of gene expression. This review describes recent advances in our understanding of lipid metabolism in aging, including established findings and recent approaches.

Efficacy of Novavit in ameliorating the neurotoxicity of propionic acid

Oxidative stress, abnormal fatty acid metabolism, and impaired gut microbiota play a serious role in the pathology of autism. The use of dietary supplements to improve the core symptoms of autism is a common therapeutic strategy. The present study analyzed the effects of oral supplementation with Novavit, a multi-ingredient supplement, on ameliorating oxidative stress and impaired lipid metabolism in a propionic acid (PPA)-induced rodent model of autism. Male western albino rats were divided into three groups. The first group is the control, the second group was given an oral neurotoxic dose of PPA (250 mg/kg body weight/day) for 3 days and then received buffered saline until the end of the experiment. The third group received Novavit (70 mg/kg body weight/day for 30 days after the 3-day PPA treatment). Markers of oxidative stress and impaired fatty acid metabolism were measured in brain homogenates obtained from each group. Novavit modulation of the gut microbiota was also evaluated. While PPA induced significant increases in lipid peroxides and 5-lipoxygenase, together with significantly decreased glutathione, and cyclooxygenase 2, oral supplementation with Novavit ameliorated PPA-induced oxidative stress and impaired fatty acid metabolism. Our results showed that the presence of multivitamins, coenzyme Q10, minerals, and colostrum, the major components of Novavit, protects against PPA-induced neurotoxicity.