Overnourishment during lactation induces metabolic and haemodynamic heart impairment during adulthood

Vieira, Anatalia Kutianski Gonzalez; Soares, Vivian M.; Bernardo, Amélia Faustino; Neves, Fabiana Alves; Mattos, Ana Barbosa Marcondes de; Guedes, Rui Miguel Sá Maia; Cortez, Erika; Andrade, Daniela Caldas de; Miranda, Glauciane L.; Garcia-Souza, Érica Patrícia; Moura, Aníbal Sanchez

doi:10.1016/j.numecd.2015.07.009

Cited by 14 publications

(13 citation statements)

References 28 publications

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“…The lactational period has been shown to be a critical time window for programming of hypertension. 47 , 58 Using the same mouse model as in this study, Samuelsson et al have showed that maternal obesity results in maternal hyperleptinaemia and programmes hypertension of sympathetic origin in the offspring due to leptin-induced over-activation of the central melanocortin system in lactating mice. 47 Indeed, mice with a specific deletion of melanocortin-4 receptors in the paraventricular nucleus of the hypothalamus were protected from sympathetic over-activation by maternal leptin and consequently hypertension.…”

Section: Discussionmentioning

confidence: 82%

Maternal diet-induced obesity programmes cardiac dysfunction in male mice independently of post-weaning diet

Loche

Blackmore

Carpenter

et al. 2018

Cardiovascular Research

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AimsObesity during pregnancy increases risk of cardiovascular disease (CVD) in the offspring and individuals exposed to over-nutrition during fetal life are likely to be exposed to a calorie-rich environment postnatally. Here, we established the consequences of combined exposure to a maternal and post-weaning obesogenic diet on offspring cardiac structure and function using an established mouse model of maternal diet-induced obesity.Methods and resultsThe impact of the maternal and postnatal environment on the offspring metabolic profile, arterial blood pressure, cardiac structure, and function was assessed in 8-week-old C57BL/6 male mice. Measurement of cardiomyocyte cell area, the transcriptional re-activation of cardiac fetal genes as well as genes involved in the regulation of contractile function and matrix remodelling in the adult heart were determined as potential mediators of effects on cardiac function. In the adult offspring: a post-weaning obesogenic diet coupled with exposure to maternal obesity increased serum insulin (P < 0.0001) and leptin levels (P < 0.0001); maternal obesity (P = 0.001) and a post-weaning obesogenic diet (P = 0.002) increased absolute heart weight; maternal obesity (P = 0.01) and offspring obesity (P = 0.01) caused cardiac dysfunction but effects were not additive; cardiac dysfunction resulting from maternal obesity was associated with re-expression of cardiac fetal genes (Myh7: Myh6 ratio; P = 0.0004), however, these genes were not affected by offspring diet; maternal obesity (P = 0.02); and offspring obesity (P = 0.05) caused hypertension and effects were additive.ConclusionsMaternal diet-induced obesity and offspring obesity independently promote cardiac dysfunction and hypertension in adult male progeny. Exposure to maternal obesity alone programmed cardiac dysfunction, associated with hallmarks of pathological left ventricular hypertrophy, including increased cardiomyocyte area, upregulation of fetal genes, and remodelling of cardiac structure. These data highlight that the perinatal period is just as important as adult-onset obesity in predicting CVD risk. Therefore, early developmental periods are key intervention windows to reduce the prevalence of CVD.

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Section: Discussionmentioning

confidence: 82%

Maternal diet-induced obesity programmes cardiac dysfunction in male mice independently of post-weaning diet

Loche

Blackmore

Carpenter

et al. 2018

Cardiovascular Research

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“…These results revealed that hearts from adult SL mice were more prone to ischemia-reperfusion injury with a markedly greater area of infarct, which is consistent with our previous studies 10 . A recent study showed that adult SL mice had significant alterations in heart metabolism proteins and a reduction in their efficiency after ischemia-reperfusion 43 . We also confirmed increased levels of oxidative stress in adult SL myocardial tissue, which is specifically reduced by CR in these mice.…”

Section: Discussionmentioning

confidence: 99%

Short-term moderate diet restriction in adulthood can reverse oxidative, cardiovascular and metabolic alterations induced by postnatal overfeeding in mice

Guenancia

Rigal

et al. 2016

Sci Rep

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We aimed to determine whether moderate diet restriction could restore cardiac, oxidative and metabolic alterations induced by postnatal overfeeding (PNOF). Litters of C57BL/6 male mice were either maintained at 9 (normal litter, NL), or reduced to 3 (small litter, SL) in order to induce PNOF. At 6 months, half of the NL and SL mice were subjected to 20% calorie-restriction (CR: NLCR, SLCR) for one month, while the other half continued to eat ad libitum (AL: NLAL, SLAL). Six-month old SL mice presented overweight, fat accumulation, hyperleptinemia, glucose intolerance, insulin resistance, increased cardiac ROS production and decreased left ventricular ejection fraction (LVEF). After CR, SL mice body weight was normalized; however, their fat mass and leptinemia were not decreased, glucose metabolism was improved and LVEF was increased. In SL mice, CR increased the cardiac mitochondrial respiratory rate and decreased cardiac ROS production. Hearts from SLCR mice showed better recovery and smaller postischemic infarct size. Intriguingly, no difference was observed between NLAL and NLCR mice for most of the parameters investigated. Short-term moderate CR not only normalized body weight in SL mice but also improved metabolic programming and reversed oxidative and cardiac dysfunction induced by PNOF.

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“…The cardiovascular system is particularly sensitive to nutritional imbalances during lactation [18]. Studies on overfed pups in rodents have shown that overnutrition during lactation results in left ventricular cardiac hypertrophy and increased susceptibility to ischemia-reperfusion injury [20], impaired insulin signalling [21]* and leptin signalling [22], and leads to dysregulation of gene expression of cardiac structural proteins [23].…”

Section: Early Post-natal Life: Nutrition and Growthmentioning

confidence: 99%

Early nutrition, epigenetics, and cardiovascular disease

Loche

Ozanne²

2016

Current Opinion in Lipidology

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The burden of obesity and associated cardiometabolic diseases is believed to arise through interaction between an individual's genetics and the environment. Moreover, the risk of developing poor cardiometabolic health in adulthood is defined by early life exposure to pathological cues and can be inherited by future generations, initiating a vicious cycle of transmission of disease. Elucidating the molecular triggers of such a process will help tackle and prevent the uncontrolled rise in obesity and cardiometabolic disease.

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Overnourishment during lactation induces metabolic and haemodynamic heart impairment during adulthood

Cited by 14 publications

References 28 publications

Maternal diet-induced obesity programmes cardiac dysfunction in male mice independently of post-weaning diet

Maternal diet-induced obesity programmes cardiac dysfunction in male mice independently of post-weaning diet

Short-term moderate diet restriction in adulthood can reverse oxidative, cardiovascular and metabolic alterations induced by postnatal overfeeding in mice

Early nutrition, epigenetics, and cardiovascular disease

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