Dietary Betaine and Polyunsaturated Fatty Acids Influence Circulating Fatty Acids and Alpha-Tocopherol in Cats

Objectives Evaluate the interaction of dietary betaine and two different sources of dietary polyunsaturated fatty acids (PUFA): alpha-linolenate (ALA) and combined eicosapentaenoate (EPA) and docosahexaenoate (DHA) on subsequent circulating single carbon metabolism and metabolomics. Methods This study was a complete factorial with or without added betaine and 3 levels of PUFA. Forty eight domestic short hair cats with an average age of 5.8 years (range 1–12) were used in this study. All cats were assigned to a pre-feed period (14 days) and then assigned to one of the six treatment foods: control, control plus 0.35% ALA (flaxseed used to increase ALA), control plus 0.27% EPA&DHA combined (added fish oil as a source), control plus 0.5% betaine, control plus ALA and 0.5% betaine or control plus EPA&DHA and 0.5% betaine. All treatment foods were fed for sixty days. Blood analysis (CBC, chem screens, fatty acid profiles, and metabolome) was completed at the beginning and at the end of the study. Statistical analysis used PUFA source or intake, betaine and interaction with p ≤ 0.05 used as significant. Results Dietary betaine increased circulating betaine, dimethyl glycine, sarcosine and methionine while adding ALA increased circulating ALA, and EPA&DHA increased their respective circulating concentrations. Betaine increased circulating arachidonic acid when added alone or with ALA with no change when betaine and EPA&DHA were added together. Dietary betaine increased the slope of the linear relationship between circulating EPA (or DHA) to dietary EPA (or DHA). Dietary betaine resulted in an increased concentration of alpha-tocopherol. Similar results were observed with circulating beta- and gamma-tocopherol (combined). Conclusions Dietary betaine influences the circulating concentration of polyunsaturated fatty acids and the methyl donor pathway. It also increases circulating tocopherols. Funding Sources This study was funded by Hill's Pet Nutrition, Inc.

Perinatal Dietary Polyunsaturated Fatty Acids in Brain Development, Role in Neurodevelopmental Disorders

n-3 and n-6 polyunsaturated fatty acids (PUFAs) are essential fatty acids that are provided by dietary intake. Growing evidence suggests that n-3 and n-6 PUFAs are paramount for brain functions. They constitute crucial elements of cellular membranes, especially in the brain. They are the precursors of several metabolites with different effects on inflammation and neuron outgrowth. Overall, long-chain PUFAs accumulate in the offspring brain during the embryonic and post-natal periods. In this review, we discuss how they accumulate in the developing brain, considering the maternal dietary supply, the polymorphisms of genes involved in their metabolism, and the differences linked to gender. We also report the mechanisms linking their bioavailability in the developing brain, their transfer from the mother to the embryo through the placenta, and their role in brain development. In addition, data on the potential role of altered bioavailability of long-chain n-3 PUFAs in the etiologies of neurodevelopmental diseases, such as autism, attention deficit and hyperactivity disorder, and schizophrenia, are reviewed.

Worms, Fat, and Death: Caenorhabditis elegans Lipid Metabolites Regulate Cell Death

Caenorhabditis elegans is well-known as the model organism used to elucidate the genetic pathways underlying the first described form of regulated cell death, apoptosis. Since then, C. elegans investigations have contributed to the further understanding of lipids in apoptosis, especially the roles of phosphatidylserines and phosphatidylinositols. More recently, studies in C. elegans have shown that dietary polyunsaturated fatty acids can induce the non-apoptotic, iron-dependent form of cell death, ferroptosis. In this review, we examine the roles of various lipids in specific aspects of regulated cell death, emphasizing recent work in C. elegans.