Long-Term Effects of Early Overnutrition in the Heart of Male Adult Rats: Role of the Renin-Angiotensin System

Granado, Miriam; Fernández, Núria; Monge, Luis; Carreño‐Tarragona, Gonzalo; Figueras, Juan Carlos; Amor, Sara; Garcı́a-Villalón, Ángel Luis

doi:10.1371/journal.pone.0065172

Cited by 9 publications

(9 citation statements)

References 68 publications

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“…Five animals from each group were used for this assay. As previously described [ 21 , 22 ], hearts were removed from the mice under anesthesia with i.p. sodium pentobarbital (200 mg/kg) and following i.v.…”

Section: Methodsmentioning

confidence: 99%

Partial IGF-1 deficiency is sufficient to reduce heart contractibility, angiotensin II sensibility, and alter gene expression of structural and functional cardiac proteins

et al. 2017

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Circulating levels of IGF-1 may decrease under several circumstances like ageing, metabolic syndrome, and advanced cirrhosis. This reduction is associated with insulin resistance, dyslipidemia, progression to type 2 diabetes, and increased risk for cardiovascular diseases. However, underlying mechanisms between IGF-1 deficiency and cardiovascular disease remain elusive.The specific aim of the present work was to study whether the partial IGF-1 deficiency influences heart and/or coronary circulation, comparing vasoactive factors before and after of ischemia-reperfusion (I/R). In addition, histology of the heart was performed together with cardiac gene expression for proteins involved in structure and function (extracellular matrix, contractile proteins, active peptides); carried out using microarrays, followed by RT-qPCR confirmation of the three experimental groups. IGF-1 partial deficiency is associated to a reduction in contractility and angiotensin II sensitivity, interstitial fibrosis as well as altered expression pattern of genes involved in extracellular matrix proteins, calcium dynamics, and cardiac structure and function.Although this work is descriptive, it provides a clear insight of the impact that partial IGF-1 deficiency on the heart and establishes this experimental model as suitable for studying cardiac disease mechanisms and exploring therapeutic options for patients under IGF-1 deficiency conditions.

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Section: Methodsmentioning

confidence: 99%

Partial IGF-1 deficiency is sufficient to reduce heart contractibility, angiotensin II sensibility, and alter gene expression of structural and functional cardiac proteins

et al. 2017

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“…Associated with the improved cardiac output of the early phase of obesity an increased coronary flow and reserve could occur. Yet, all studies concerning this last parameter showed either an upholding [ 7 , 10 - 12 ] or a depression of the coronary reserve [ 13 - 18 ]. There is only one study performed on the isolated coronary arteriole [ 11 ] mentioning an obesity-related enhancement of the sensitivity of the coronary smooth muscle cells (SMCs) to nitric oxide (NO), which was however not associated with an improved endothelial-dependent vasodilatation (EDV).…”

Section: Introductionmentioning

confidence: 99%

Body adiposity dictates different mechanisms of increased coronary reactivity related to improved in vivo cardiac function

Mourmoura

Chaté

Couturier

et al. 2014

Cardiovasc Diabetol

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BackgroundSaturated fatty acid-rich high fat (HF) diets trigger abdominal adiposity, insulin resistance, type 2 diabetes and cardiac dysfunction. This study was aimed at evaluating the effects of nascent obesity on the cardiac function of animals fed a high-fat diet and at analyzing the mechanisms by which these alterations occurred at the level of coronary reserve.Materials and methodsRats were fed a control (C) or a HF diet containing high proportions of saturated fatty acids for 3 months. Thereafter, their cardiac function was evaluated in vivo using a pressure probe inserted into the cavity of the left ventricle. Their heart was isolated, perfused iso-volumetrically according to the Langendorff mode and the coronary reserve was evaluated by determining the endothelial-dependent (EDV) and endothelial-independent (EIV) vasodilatations in the absence and presence of endothelial nitric oxide synthase and cyclooxygenase inhibitors (L-NAME and indomethacin). The fatty acid composition of cardiac phospholipids was then evaluated.ResultsAlthough all the HF-fed rats increased their abdominal adiposity, some of them did not gain body weight (HF- group) compared to the C group whereas other ones had a higher body weight (HF+). All HF rats displayed a higher in vivo cardiac activity associated with an increased EDV. In the HF- group, the improved EDV was due to an increase in the endothelial cell vasodilatation activity whereas in the HF+ group, the enhanced EDV resulted from an improved sensitivity of coronary smooth muscle cells to nitric oxide. Furthermore, in the HF- group the main pathway implicated in the EDV was the NOS pathway while in the HF+ group the COX pathway.ConclusionsNascent obesity-induced improvement of cardiac function may be supported by an enhanced coronary reserve occurring via different mechanisms. These mechanisms implicate either the endothelial cells activity or the smooth muscle cells sensitivity depending on the body adiposity of the animals.

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“…Whole body composition analysis with magnetic resonance imaging (MRI) demonstrated that PNOF mice have more body fat mass and less lean mass [ 32 ]. Deeper analyses of fat location showed that PNOF rats have an increase in both subcutaneous and visceral fat (epididymal, retroperitoneal, perirenal, mesenteric) at weaning [ 20 ] and later [ 7 , 44 , 45 ], with an increased adipocyte surface [ 46 , 47 , 48 ]. The white adipose tissue of PNOF rodents also displays significant differences in the expression of proteins involved in insulin responsiveness, such as a downregulation of insulin receptor substrate-1, protein kinase B (Akt2) and glucose transporter 4 [ 49 ] and in the adipose glucocorticoid metabolism [ 46 , 47 , 50 , 51 ].…”

Section: Pnof Is Associated With Systemic and Cardiovascular Metabmentioning

confidence: 99%

“…Before the induction of ischemia in hearts isolated and perfused in basal conditions, some authors reported that hearts from PNOF rodents had a decreased cardiac contractility [ 37 ], while we never observed such initial alterations of left ventricular function neither in PNOF rats nor in mice [ 6 , 12 , 32 ]. After 30 min of ischemia, an impairment of myocardial contractility, characterized by a decrease in dP/dt and left ventricular developed pressure, was reported in overfed hearts [ 6 , 20 , 37 ] in comparison to their control littermates. Cardiac output recovery was also significantly lower in overfed animals and associated with the increased release of lactate dehydrogenase, a marker of cell injury [ 6 ].…”

Section: Pnof Affects Heart Structure Function and Adaptation Tomentioning

confidence: 99%

Programming of Cardiovascular Dysfunction by Postnatal Overfeeding in Rodents

Josse

Rigal

Rosenblatt‐Velin

et al. 2020

IJMS

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Nutritional environment in the perinatal period has a great influence on health and diseases in adulthood. In rodents, litter size reduction reproduces the effects of postnatal overnutrition in infants and reveals that postnatal overfeeding (PNOF) not only permanently increases body weight but also affects the cardiovascular function in the short- and long-term. In addition to increased adiposity, the metabolic status of PNOF rodents is altered, with increased plasma insulin and leptin levels, associated with resistance to these hormones, changed profiles and levels of circulating lipids. PNOF animals present elevated arterial blood pressure with altered vascular responsiveness to vasoactive substances. The hearts of overfed rodents exhibit hypertrophy and elevated collagen content. PNOF also induces a disturbance of cardiac mitochondrial respiration and produces an imbalance between oxidants and antioxidants. A modification of the expression of crucial genes and epigenetic alterations is reported in hearts of PNOF animals. In vivo, a decreased ventricular contractile function is observed during adulthood in PNOF hearts. All these alterations ultimately lead to an increased sensitivity to cardiac pathologic challenges such as ischemia-reperfusion injury. Nevertheless, caloric restriction and physical exercise were shown to improve PNOF-induced cardiac dysfunction and metabolic abnormalities, drawing a path to the potential therapeutic correction of early nutritional programming.

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Long-Term Effects of Early Overnutrition in the Heart of Male Adult Rats: Role of the Renin-Angiotensin System

Cited by 9 publications

References 68 publications

Partial IGF-1 deficiency is sufficient to reduce heart contractibility, angiotensin II sensibility, and alter gene expression of structural and functional cardiac proteins

Partial IGF-1 deficiency is sufficient to reduce heart contractibility, angiotensin II sensibility, and alter gene expression of structural and functional cardiac proteins

Body adiposity dictates different mechanisms of increased coronary reactivity related to improved in vivo cardiac function

Programming of Cardiovascular Dysfunction by Postnatal Overfeeding in Rodents

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