title: Pathophysiology of metabolic syndrome X and its links to the perinatal period.
abstract: It is proposed that metabolic syndrome X is initiated in the perinatal period as a low-grade systemic inflammatory condition. Increased consumption of energy-dense diets by pregnant women and lactating mothers suppresses the activities of Delta-6 and Delta-5 desaturases not only in maternal tissues but also in fetal liver and the placenta, resulting in decreased plasma and tissue concentrations of long-chain polyunsaturated fatty acids omega-6 arachidonic acid (AA), omega-3 eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). EPA, DHA, and AA have negative feedback control on tumor necrosis factor-alpha and IL-6 synthesis. Hence, EPA, DHA, and AA deficiencies induced by an energy-dense diet increase generation of tumor necrosis factor-alpha and interleukin-6, markers of inflammation that in turn decrease production of endothelial nitric oxide and adiponectin to induce insulin resistance in maternal and fetal tissues. Increased concentrations of tumor necrosis factor-alpha and interleukin-6 enhance expression and activity of 11beta-hydroxysteroid dehydrogenase type 1 enzyme, which produces abdominal obesity, insulin resistance, hyperlipidemia, hyperphagia, and hyperleptinemia, characteristic features of metabolic syndrome X. Continued consumption of an energy-dense diet in childhood aggravates these molecular events. This implies that supplementation of long-chain polyunsaturated fatty acids (especially AA, EPA, and DHA in appropriate ratios) from the perinatal period through adulthood could prevent, arrest, or postpone development of metabolic syndrome X.
authors.affiliation: UND Life Sciences, Walpole, Massachusetts, USA. undurti@hotmail.com
authors.forename: Undurti N
authors.initials: UN
authors.lastname: Das
mesh_terms: D005260:Female; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D039382:Maternal Nutritional Physiological Phenomena; D024821:Metabolic Syndrome / Q000209:etiology* / Q000378:metabolism*; D009765:Obesity / Q000150:complications / Q000378:metabolism*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects