P1-45 Maternal severe undernutrition during both late gestation and lactation period induce hypertension in male rat offspring

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    cardiac function in adult life, following catch up growth, and couldcontribute to the link between IUGR and heart disease at olderages.

    P1-44 Differential effects of maternal nutrient restrictionbetween early to mid gestation on cardiacacetyl CoA carboxylase (ACC) expression followingjuvenile obesity

    L.L.Y. Chan1, S. Sebert1, H. Budge1, T. Stephenson1,M.E. Symonds1 *, D.S. Gardner2. 1Centre for Reproduction andEarly Life, School of Human Development and 2Schools ofVeterinary Medicine and Science, University of Nottingham,United KingdomE-mail: michael.symonds@nottingham.ac.uk

    Aims: Obesity is associated with hypertension, leading topressure-overload left ventricular hypertrophy in conjunctionwith reduced energy production from fatty acid oxidation andmitochondrial dysfunction. The present study examined the extentto which maternal nutrient restriction, coincident with early heartdevelopment, may exacerbate the adverse cardiac effects of laterobesity.Study design: Welsh Mountain sheep (n = 21) were either nutrient-restricted (NR; i.e. fed 50% less than controls) between early-to-mid (30 80 days) gestation or fed a control diet throughoutpregnancy. From weaning to 12 months of age, offspring wereeither maintained out to pasture with unrestricted physical activity(Lean, L), or group-housed within a barn in order to restrict theiractivity and provided with ad libitum access to hay and concentratepellets (Obese, O; NR obese, NRO). At 12 months, the left ventriclewas sampled, snap frozen and mRNA subsequently extracted forreal-time PCR analysis.Results: Obesity resulted in pronounced left ventricular pressure-overload hypertrophy in conjunction with lower mRNA abundancefor both PGC-1a and AMPKa2 relative to lean sheep (p < 0.05). Incontrast, ACC mRNA abundance was only reduced in the O groupand was, thus, similar between L and ONR groups.Conclusions: Both AMPK and ACC are involved in the metabolicswitch in fatty acid oxidation. Thus, our results suggest that obesitydecreases capacity of mitochondrial oxidative energy metabolismin heart. Importantly, such an adaptation may be differentiallyrecruited in offspring born to nutrient restricted mothers, therebyaltering lipid accumulation in their hearts.Study supported by the British Heart Foundation

    P1-45 Maternal severe undernutrition during both lategestation and lactation period induce hypertension inmale rat offspring

    H. Takahashi *, T. Okawa, K. Fujimori, A. Sato. Department ofObstetrics and Gynecology Fukushima Medical University Schoolof Medicine, Fukushima, Japan

    Objective: Exposure to undernutrition during fetal life has beenproposed as an underlying cause of adult hypertension, butthe effect of undernutrition during lactation period is unclear.Our objective was to investigate the effects of either severeundernutrition during late gestation or lactation period on bloodpressure and the development of vascular function in male ratoffspring.Study design: We use normal pregnant Wistar rats (Group A),nutritionally restricted by feeding with 30% of the normal gestation-matched dietary intake from day 17 of gestation to delivery(Group B) and 30% restricted after delivery to the end of lactationperiod (Group C). The offspring was measured blood pressure at 12and 24 weeks by using indirect tail-cuff method.Rings of thoracic aorta with intact endothelium from the maleoffspring of A and B at 8 weeks, were equilibrated at 2 gpassive tension in organ chambers lled with Krebs-Henseleitsolution continuously bubbled with 5%CO2 in air (37C, pH 7.4) forisometric tension recording. Concentration response relationshipsto Norepinephrine (NE) and angiotensin II (AT II) were obtained in

    the absence or presence of N(omega)-nitro-L-arginine methyl ester(L-NAME) or a selective AT II type-1 receptor blocker (Valsartan).Responses to cumulative concentrations of sodium nitroprusside(SNP) and to 10 5M oxyhemoglobin (Hb, nitric oxide scavenger)were also determined. Contractions were expressed as a percent ofthe reference contraction induced by potassium chloride (60mM).Statically analysis was performed using one-way ANOVA.Results: Body weight was signicantly reduced in B offspringcompared to A and C in male offspring at day 1 (p < 0.01). At12 weeks the body weight of offspring of B was no differenceto catch up compared to A and C offspring. Systolic and Diastolicblood pressures were signicantly elevated at both 12 and 24 weeksin offspring of B >C >A. NE concentration-dependently stimulatedtension of aortic rings from in A and B offspring, which was notsignicantly (n = 6). Maximal contractions to NE were signicantlystimulated by L-NAME in A (p < 0.05), but not B offspring. Valsartansignicantly inhibited aortic contractions by NE in R (p < 0.05), butnot A offspring. There was no signicant difference on responses ofaortic rings by AT II, SNP and Hb in A and B offspring.Conclusions: Severe under nutrition during not only late gestationbut also lactation period induced hypertension in male rat offspringin adulthood. Fetal origin of adult hypertension might be vascularendothelial dysfunction.

    P1-46 Maternal regulation of high fat nourishment duringlactation period reduce a hypertension of maleoffspring

    H. Takahashi *, T. Okawa, K. Fujimori, A. Sato. Department ofObstetrics and Gynecology Fukushima Medical University Schoolof Medicine, Fukushima, Japan

    Objective: Exposure to undernutrition or high fat nourishmentduring fetal life has been proposed as an underlying cause ofadult hypertension, but the effect of maternal feeding regulationduring lactation period on blood pressure of offspring is unclear.Our objective was to investigate the effects of either high-fat diet(HFD) during gestation to lactation period or restrictive fed a HFDduring lactation period on blood pressure in male rat offspring.Study design: We use 3 types pregnant Wistar rats as fed withnormal nutrition (Group A), with a high fat diet (HFD) duringgestation to lactation period (Group B) and with HFD nutritionallyrestricted by feeding with 30% of the normal lactation-matcheddietary intake from the day of delivery to the end of lactationperiod (Group C). The male offspring was measured blood pressureat 12, 24 and 60 weeks by using indirect tail-cuff method. Staticallyanalysis was performed using one-way ANOVA.Results: Body weight was signicantly reduced in C offspringcompared to A and B in male offspring at day 28 after delivery(p < 0.01). At 12 weeks old, the body weight of C offspring was nodifference to catch up compared to A and B offspring. Systolic andDiastolic blood pressures were signicantly elevated at all 12, 24and 60 weeks in offspring of B >C >A (p < 0.01, vs. A).Conclusions: Under high-fat nutrition during gestation to lactationperiod induced hypertension in male rat offspring. Maternal highfat environment make a hypertensive offspring, but regulationof fat feeding during lactation period may reduce adulthoodhypertension.

    P1-47 Regulation of maternal feeding during lactation periodmay control adulthood hypertension

    H. Takahashi *, T. Okawa, K. Fujimori, A. Sato. Department ofObstetrics and Gynecology Fukushima Medical University Schoolof Medicine, Fukushima, Japan

    Objective: Exposure to undernutrition during fetal life has beenproposed as an underlying cause of adult hypertension, but theeffect of either high fat nourishment or undernutrition duringlactation period on blood pressure is unclear. Our objective was toinvestigate the most effective maternal nourishment and feedingperiod for offspring induced adulthood hypertension in using high-fat diet (HFD).

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