Developmental Origins of Cardiometabolic Diseases: Role of the Maternal Diet

Costa‐Silva, João Henrique; Simões‐Alves, Aiany C.; Fernandes, Mariana P.

doi:10.3389/fphys.2016.00504

Cited by 24 publications

(12 citation statements)

References 127 publications

(151 reference statements)

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“…Maternal pre-pregnancy obesity, diabetes and excessive gestational weight gain, whose inflammatory pathways are activated (Burton, Fowden, & Thornburg, 2016) together with macrophage accumulation and inflammation in the placenta (Challier, et al, 2008), are considered important risk factors for the development of cardiovascular and metabolic diseases in early postnatal life and adulthood. This topic has been extensively reviewed in several recent publications (Aceti, et al, 2012;Costa-Silva, Simoes-Alves, & Fernandes, 2016;Ma, Tutino, Lillycrop, Hanson, & Tam, 2015;Roberts, Frias, & Grove, 2015).…”

Section: Maternal Cold Inflammation and Pie-programed Cvdsmentioning

confidence: 99%

Prenatal inflammation exposure-programmed cardiovascular diseases and potential prevention

Deng

Song

Nie

et al. 2018

Pharmacology & Therapeutics

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In recent years, the rapid development of medical and pharmacological interventions has led to a steady decline in certain noncommunicable chronic diseases (NCDs), such as cancer. However, the overall incidence of cardiovascular diseases (CVDs) has not seemed to decline. CVDs have become even more prevalent in many countries and represent a global health threat and financial burden. An increasing number of epidemiological and experimental studies have demonstrated that maternal insults not only can result in birth defects but also can cause developmental functional defects that contribute to adult NCDs. In the current review, we provide an overview of evidence from both epidemiological investigations and experimental animal studies supporting the concept of developmental reprogramming of adult CVDs in offspring that have experienced prenatal inflammation exposure (PIE) during fetal development (PIE-programmed CVDs), a disease-causing event that has not been effectively controlled. This review describes the epidemiological observations, data from animal models, and related mechanisms for the pathogenesis of PIE-programmed CVDs. In addition, the potential therapeutic interventions of PIE-programmed CVDs are discussed. Finally, we also deliberate the need for future mechanistic studies and biomarker screenings in this important field, which creates a great opportunity to combat the global increase in CVDs by managing the adverse effects of inflammation for prepregnant and pregnant individuals who are at risk for PIE-programmed CVDs.

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Section: Maternal Cold Inflammation and Pie-programed Cvdsmentioning

confidence: 99%

Prenatal inflammation exposure-programmed cardiovascular diseases and potential prevention

Deng

Song

Nie

et al. 2018

Pharmacology & Therapeutics

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“…The excessive consumption of fat and sugar, usually described as the westernised lifestyle, has contributed to the growing incidence of metabolic disorders such as dyslipidaemia and type 2 diabetes (3) . It has been established that metabolic disorders, especially during pregnancy and early life, enhance susceptibility to the development of cardiometabolic diseases (4)(5)(6)(7) . For example, offspring from dams exposed to a high-fat diet during pregnancy exhibit hypertension and metabolic alterations in adult life (8,9) .…”

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confidence: 99%

Effect of maternal dyslipidaemia on the cardiorespiratory physiology and biochemical parameters in male rat offspring

et al. 2017

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The present study evaluated the effects of maternal dyslipidaemia on blood pressure (BP), cardiorespiratory physiology and biochemical parameters in male offspring. Wistar rat dams were fed either a control (CTL) or a dyslipidaemic (DLP) diet during pregnancy and lactation. After weaning, both CTL and DLP offspring received standard diet. On the 30th and 90th day of life, blood samples were collected for metabolic analyses. Direct measurements of BP, respiratory frequency (RF), tidal volume (VT) and ventilation (VE) under baseline condition, as well as during hypercapnia (7 % CO2) and hypoxia (KCN, 0·04 %), were recorded from awake 90-d-old male offspring. DLP dams exhibited raised serum levels of total cholesterol (TC) (4·0-fold), TAG (2·0-fold), VLDL+LDL (7·7-fold) and reduced HDL-cholesterol (2·4-fold), insulin resistance and hepatic steatosis at the end of lactation. At 30 d of age, the DLP offspring showed an increase in the serum levels of TC (P<0·05) and VLDL+LDL (P<0·05) in comparison with CTL offspring. At 90 d of age, DLP offspring exhibited higher mean arterial pressure (MAP, approximately 34 %). In the spectral analysis, the DLP group showed augmented low-frequency (LF) power and LF:high-frequency (HF) ratio when compared with CTL offspring. In addition, the DLP animals showed a larger delta variation in arterial pressure after administration of the ganglionic blocker (P=0·0003). We also found that cardiorespiratory response to hypercapnia and hypoxia was augmented in DLP offspring. In conclusion, the present data show that maternal dyslipidaemia alters cardiorespiratory physiology and may be a predisposing factor for hypertension at adulthood.

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“…Clinical and experimental data involving hypertension models have demonstrated that increased sympathetic activity plays a key role in the development of hypertension. 9,11,30,[47][48][49][50] Towards an understanding of the important role of the autonomic nervous system (parasympathetic and sympathetic branches) under the condition of hypertension, it is essential to identify possible dysfunctions within the brain areas, such as the hypothalamus or medulla, and the influence of peripheral sensors, notably that performed by the arterial baroreceptors (mechanical information), chemoreceptors (information about the level of oxygen and carbon dioxide in the blood) and the renal system. 51,52 Our laboratory demonstrated that hypertension evidenced in rat adult offspring (90 days old) from dams exposed to protein restriction during pregnancy and lactation is associated with augmented sympathetic tone.…”

Section: Maternal Protein Restriction and The Development Of Hypertmentioning

confidence: 99%

Maternal protein malnutrition induced‐hypertension: New evidence about the autonomic and respiratory dysfunctions and epigenetic mechanisms

Alves

Costa‐Silva

2017

Clin Exp Pharma Physio

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SummaryMaternal protein malnutrition during the critical stages of development (pregnancy, lactation and first infancy) can lead to adult hypertension. Studies have shown that renal and cardiovascular dysfunctions can be associated to the development of hypertension in humans and rats exposed to maternal protein malnutrition. The etiology of hypertension, however, includes a complex network involved in central and peripheral blood pressure control. Recently, the hyperactivity of the sympathetic nervous system in protein-restricted rats has been reported. Studies have shown that protein malnutrition during pregnancy and/or lactation alters blood pressure control through mechanisms that include central sympathetic-respiratory dysfunctions and epigenetic modifications, which may contribute to adult hypertension. Thus, this review will discuss the historical context, new evidences of neurogenic disruption in respiratorysympathetic activities and possible epigenetic mechanisms involved in maternal protein malnutrition induced-hypertension. K E Y W O R D Shypertension, malnutrition, phenotypic plasticity, sympathetic activity, ventilation | INTRODUCTIONArterial hypertension (AH) affects more than 1 billion people around the world and is a major risk factor for cardiovascular dysfunction, recognized as the main cause of morbidity and mortality. Because of the interaction between the sympathetic and respiratory nervous systems, growing evidence supports the notion that an increase in sympathetic and respiratory activities plays an important role in the development of hypertension. [8][9][10] This observation has prompted the development of several studies evaluating sympathetic and respiratory activities and sensitivity of peripheral and central chemoreceptors in various hypertension models. For example, in chronic intermittent hypoxia 8,11 in spontaneously hypertensive rats (SHR) 4 and in renovascular hypertension, 12 augmented sympathetic-respiratory activities and higher peripheral chemosensitivity were seen to be associated to hypertension.

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Developmental Origins of Cardiometabolic Diseases: Role of the Maternal Diet

Cited by 24 publications

References 127 publications

Prenatal inflammation exposure-programmed cardiovascular diseases and potential prevention

Prenatal inflammation exposure-programmed cardiovascular diseases and potential prevention

Effect of maternal dyslipidaemia on the cardiorespiratory physiology and biochemical parameters in male rat offspring

Maternal protein malnutrition induced‐hypertension: New evidence about the autonomic and respiratory dysfunctions and epigenetic mechanisms

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