INHIBITION OF MELATONIN PRODUCTION DURING NIGHT HOURS INCREASES THE IMPAIRMENT OF METABOLISM, ELEVATING THE RISK OF OBESITY, HYPERGLYCEMIA, AND DYSLIPIDEMIA DURING PREGNANCY. FRUCTOSE CONSUMPTION HAS DETRIMENTAL EFFECTS OVER METABOLISM AND THE CIRCADIAN SYSTEM. SEVERAL REPORTS SUGGEST THAT MELATONIN HAS A PROTECTOR ROLE DURING THE PREGNANCY BY THEIR ANTIOXIDANT/CHRONOBIOTIC PROPERTIES, AND FROM THE ABOVE, WE SPECULATES TO MELATONIN CAN BE REVERTING THE CHRONODISRUPTION AND ELEVATION OF MASTER REGULATORS OF LIPID METABOLISM IN THE NEWBORN. MEASURE IN THE LIVER OF NEWBORN THE MRNA EXPRESSION OF CLOCK-GENE BMAL-1, HMG-COA REDUCTASE, SREBP AND THE CLOCK-CONTROLLED GENE WEE-1 OF THE NEWBORN FROM MOTHER TREATED WITH FRUCTOSE AND MELATONIN.

HYPERTENSION CAN BE INDUCED BY THE DISRUPTION OF FACTORS IN BLOOD PRESSURE REGULATION. THIS INCLUDES SEVERAL SYSTEMS SUCH AS NEUROHUMORAL, RENIN-ANGIOTENSIN-ALDOSTERONE, THE CIRCADIAN CLOCK, AND MELATONIN PRODUCTION, WHICH CAN INDUCE ELEVATION AND NON-DIPPING BLOOD PRESSURE. MELATONIN HAS A SUPRAPHYSIOLOGICAL ROLE AS A CHRONOBIOTIC AGENT AND MODULATES VASCULAR SYSTEM PROCESSES VIA PRO/ANTIANGIOGENIC FACTORS, INFLAMMATION, THE IMMUNE SYSTEM, AND OXIDATIVE STRESS REGULATION. AN ELEVATION OF MELATONIN PRODUCTION IS OBSERVED DURING PREGNANCY, MODULATING THE PLACENTA AND FETUS S PHYSIOLOGICAL FUNCTIONS. THEIR IMPAIRMENT PRODUCTION CAN INDUCE TEMPORAL DESYNCHRONIZATION OF CELL PROLIFERATION, DIFFERENTIATION, OR INVASION FROM TROPHOBLAST CELLS RESULTS IN VASCULAR INSUFFICIENCIES, ELEVATING THE RISK OF POOR FETAL/PLACENTAL DEVELOPMENT. SEVERAL GENES ARE ASSOCIATED WITH VASCULAR DISEASE AND HYPERTENSION DURING PREGNANCY VIA IMPAIRED INFLAMMATORY RESPONSE, HYPOXIA, AND OXIDATIVE STRESS, SUCH AS CYTOKINES/CHEMOKINES IL-1?, IL-6, IL-8, AND IMPAIRMENT EXPRESSION IN ENDOTHELIAL CELLS/VSMCS OF HIF1? AND ENOS GENES. PATHOLOGICAL PLACENTAS SHOWED DIFFERENTIALLY EXPRESSED GENES (DEG), INCLUDING VASCULAR GENES AS CITED2, VEGF, PL-II, PIGF, SFLT-1, AND SENG, ONCOGENE JUNB, SCAFFOLDING PROTEIN CUL7, GPER1, AND THE PATHWAYS OF SIRT/AMPK AND MAPK/ERK. ADDITIONALLY, WE OBSERVED MODIFICATION OF SUBUNITS OF NADPH OXIDASE AND EXTRACELLULAR MATRIX ELEMENTS, I.E., GLYPICAN AND HEPARANASE AND KCA CHANNEL. MOTHERS WITH A LOW LEVEL OF MELATONIN SHOWED LOW PRODUCTION OF PROANGIOGENIC FACTOR VEGF, INCREASING THE RISK OF PREECLAMPSIA, PREMATURE BIRTH, AND ABORTION. IN CONTRAST, MELATONIN SUPPLEMENTATION CAN REDUCE SYSTOLIC PRESSURE, PREVENT OXIDATIVE STRESS, INDUCE THE ACTIVATION OF THE ANTIOXIDANTS SYSTEM, AND LESSEN PROTEINURIA AND SERUM LEVEL OF SFLT-1. MOREOVER, MELATONIN CAN REPAIR THE ENDOTHELIAL DAMAGE FROM PREECLAMPSIA AT THE PLACENTA LEVEL, INCREASING PIGF, NRF-2, HO-1 PRODUCTION AND REDUCIN