Abstract
Metabolic syndrome X is an inflammatory condition. Increased consumption of high-energy diet, saturated and trans-fats by pregnant women and lactating mothers suppresses the activities of enzymes Δ6 and Δ5 desaturases in maternal and fetal tissues resulting in a decrease in the concentrations of long-chain polyunsaturated fatty acids (LCPUFAs) such as arachidonic acid (AA), eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA). These LCPUFAs have a regulatory role on inflammation. EPA, DHA, and AA augment eNO synthesis, augment insulin action both in the peripheral tissues and brain, and are critical for brain growth and development, synaptogenesis, and modulate the action of neurotransmitters and hypothalamic peptides. These evidences suggest that sub-optimal LCPUFAs during perinatal period could initiate low-grade systemic inflammation and development of metabolic syndrome X in these children if they continue to consume energy dense diet. This implies that perinatal supplementation of LCPUFAs could aid to prevent, arrest or postpone the development of metabolic syndrome X.
Keywords: manganese superoxide dismutase, tumor necrosis factor alpha, coronary heart disease, C-reactive protein, noradrenaline
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