title: Is metabolic syndrome X a disorder of the brain with the initiation of low-grade systemic inflammatory events during the perinatal period?
abstract: An imbalance between pro- and anti-inflammatory molecules occurs in metabolic syndrome X. High-energy diet, saturated fats and trans-fats during perinatal period could suppress Delta(6) and Delta(5) desaturases both in the maternal and fetal tissues, resulting in a decrease in the concentrations of long-chain polyunsaturated fatty acids (LCPUFAs): arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) that have a negative feedback control on inflammation. EPA, DHA and AA augment endothelial nitric oxide synthesis, potentiate insulin action both in the peripheral tissues and brain and alter leptin production. LCPUFAs are essential for brain growth and development and synaptogenesis and modulate the action of several neurotransmitters and hypothalamic peptides. This suggests that metabolic syndrome X could be a disorder of the brain due to suboptimal LCPUFAs during perinatal period that triggers low-grade systemic inflammation, implying that perinatal strategies are needed to prevent its development.
authors.affiliation: Department of Molecular and Clinical Medicine, Care Hospital, The Institute of Medical Sciences, Banjara Hills, Hyderabad-500 034, India; UND Life Sciences, Shaker Heights, OH 44120, USA.
authors.forename: Undurti N
authors.initials: UN
authors.lastname: Das
mesh_terms: D000818:Animals; D001069:Appetite Regulation / Q000502:physiology; D016718:Arachidonic Acid / Q000502:physiology; D001921:Brain / Q000254:growth & development / Q000503:physiopathology*; D003924:Diabetes Mellitus, Type 2 / Q000150:complications; D004281:Docosahexaenoic Acids / Q000494:pharmacology; D004298:Dopamine / Q000502:physiology; D015118:Eicosapentaenoic Acid / Q000502:physiology; D005228:Fatty Acids, Essential / Q000172:deficiency; D005231:Fatty Acids, Unsaturated / Q000494:pharmacology; D006801:Humans; D007033:Hypothalamus, Middle / Q000503:physiopathology; D007231:Infant, Newborn; D007249:Inflammation / Q000503:physiopathology*; D007328:Insulin / Q000502:physiology; D020738:Leptin / Q000502:physiology; D024821:Metabolic Syndrome / Q000503:physiopathology*; D016202:N-Methylaspartate / Q000502:physiology; D009474:Neurons / Q000502:physiology; D050765:Qa-SNARE Proteins / Q000502:physiology; D011972:Receptor, Insulin / Q000502:physiology; D018168:Receptors, Retinoic Acid / Q000502:physiology; D012701:Serotonin / Q000502:physiology; D013569:Synapses / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000502:physiology
chemical_list: D005228:Fatty Acids, Essential; D005231:Fatty Acids, Unsaturated; D007328:Insulin; D020738:Leptin; D050765:Qa-SNARE Proteins; D018168:Receptors, Retinoic Acid; D004281:Docosahexaenoic Acids; D016718:Arachidonic Acid; D012701:Serotonin; D005680:gamma-Aminobutyric Acid; D016202:N-Methylaspartate; D015118:Eicosapentaenoic Acid; D011972:Receptor, Insulin; D004298:Dopamine