Abstract
Abstract Type 2 Diabetes conditions are associated with hyperglycemia and hyperlipidemia; however, the role of Saturated Fatty Acids (SFA) vs. Unsaturated Fatty Acids (UFA) and high glucose on human T lymphocytes (T cells) is not known. We investigated the salutary effect of the UFA ω-3 fatty acid, α- linolenic acid, on glucose and SFA, palmitic acid, induced activation on T cells as a cause of the inflammatory process with high glucose and SFA foods. These cells in the presence of palmitic acid and/or high glucose but not linolenic acid exhibited a concentration and time-dependent emergence of insulin receptors (INSR), expression, generation of ROS, lipid peroxidation, cytokines and NF-kB p65 translocation to the nucleus. Whereas, activation of the cells by elevated levels of glucose and palmitic acid were additive, addition of linolenic acid in a dose-related manner inhibited activation of cells by glucose and palmitic acid and reduced markers of oxidative stress, lipid peroxidation and cytokines. We propose that UFAs such as α-linolenic acid may serve as a protective mechanism against the deleterious effects of hyperglycemia and hyperlipidemia of high sugar and SFA foods as in diabetes.
Highlights
65% of patients with T2DM die as a result of cardiovascular disease with hyperglycemia and hyperlipidemia being important risk factors for cardiovascular diseases [1]
Previous investigations demonstrated the ability of high glucose concentrations and the saturated fatty acid (SFA) palmitate to induce T cell activation, insulin receptor emergence, cytokine and reactive oxygen species (ROS) production and lipid peroxidation
Studies have shown that the Saturated Fatty Acids (SFA) can bind to the Toll-like receptors (TLR) and induce the inflammatory response through NF-kB [18, 19], whereas Unsaturated Fatty Acids (UFA) do not bind to the TLR
Summary
65% of patients with T2DM die as a result of cardiovascular disease with hyperglycemia and hyperlipidemia being important risk factors for cardiovascular diseases [1]. Both Type 2 diabetes (T2DM) and atherosclerosis are considered to be inflammatory processes [2]. T cells are unique in that in their naive state they have no insulin receptors [3] but become activated in presence of phytohemagglutinin (PHA) in vitro [3,4], as well as, in vitro hyperglycemia [5] and in situ hyperglycemic conditions such as diabetic ketoacidosis [6] These activated T cells can metabolize glucose in response to insulin with emergence of insulin receptors [7,8] and develop growth factor receptors such as IGF-1, IL2 [9]. We have previously shown that T-cells in the presence of
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