Postnatal early overfeeding induces cardiovascular dysfunction by oxidative stress in adult male Wistar rats

Ferreira-Junior, Marcos Divino; Cavalcante, Keilah Valéria Naves; Ferreira, Lucas Araújo; Lopes, Paulo Ricardo; Pontes, Carolina Nobre Ribeiro; Bessa, Amanda de Sá Martins de; Neves, Ângela Ribeiro; Francisco, Flávio Andrade; Pedrino, Gustavo Rodrigues; Xavier, Carlos Henrique; Mathias, Paulo Cézar de Freitas; Castro, Carlos H.; Gomes, Rodrigo Mello

doi:10.1016/j.lfs.2019.04.018

Cited by 13 publications

(11 citation statements)

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“…Thus, puberty is a critical period for cardiovascular programming, and nutritional disturbances in this period lead to permanent changes in the cardiovascular system. As observed in our previous study, the SL group presented increased body weight and food intake than their counterparts (28) . However, high Na intake lowered weight gain in both NLHS and SLHS throughout HS exposure, due to reduced food intake in this period, as previously reported by Moreira et al (16) .…”

Section: Discussionsupporting

confidence: 86%

“…Our main interest was to detect how BP would behave in the presence of both factors, obesity and high Na consumption. For this, a minimum variation of 10 % in mean BP was estimated, based on the previous studies of our group as effect of those interventions (16,28) . For a power of 80 % and a significance level of 5 %, this allows detection of a difference of 14 % between the groups, with a minimum sample size of eight rats/group.…”

Section: Discussionmentioning

confidence: 99%

“…Animal models also develop left ventricular hypertrophy due to metabolic programming. It is well established that PO induces cardiac remodelling due to increased oxidative stress and modified gene expression in the heart (28,(40)(41)(42) .…”

Section: Discussionmentioning

confidence: 99%

“…Here, the SL, NLHS and SLHS groups had cardiac hypertrophy and greater cardiomyocyte diameter. It has been demonstrated that the hearts from obese animal models have increased fibrosis around the coronary vessels, as well as deposit of collagen in the interstitial area (28,44) . Further, cardiac fibrosis is another important factor to diastolic dysfunction (45) .…”

Section: Discussionmentioning

confidence: 99%

“…Left ventricle samples (n 4 animals from different litters to each group) were processed as previously described (28) . Briefly, samples were griound in ice-cold lysis buffer, the lysates were centrifuged and the supernatants collected.…”

Section: Western Blotmentioning

confidence: 99%

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High salt intake during puberty leads to cardiac remodelling and baroreflex impairment in lean and obese male Wistar rats

et al. 2019

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Modern lifestyle increases the prevalence of obesity and its co-morbidities in the young population. High-salt (HS) diets are associated with hypertension and cardiac remodelling. The present study evaluated the potential effects of cardiometabolic programming induced by HS intake during puberty in lean and obese rats. Additionally, we investigated whether HS could exacerbate the impairment of cardiovascular parameters in adult life due to postnatal early overnutrition (PO). At postnatal day 3 (PN3), twenty-four litters of Wistar rats were divided into two groups: normal litter (NL, nine pups/dam) and small litter (SL, three pups/dam) throughout the lactation period; weaning was at PN21. At PN30, the pups were subdivided into two more groups: NL plus HS (NLHS) and SL plus HS (SLHS). HS intake was from PN30 until PN60. Cardiovascular parameters were evaluated at PN120. SL rats became overweight at adulthood due to persistent hyperphagia; however, HS exposure during puberty reduced the weight gain and food intake of NLHS and SLHS. Both HS and obesity raised the blood pressure, impaired baro- and chemoreflex sensitivity and induced cardiac remodelling but no worsening was observed in the association of these factors, except a little reduction in the angiotensin type-2 receptor in the hearts from SLHS animals. Our results suggest that the response of newborn offspring to PO and juveniles to a HS diet leads to significant changes in cardiovascular parameters in adult rats. This damage may be accompanied by impairment of both angiotensin signalling and antioxidant defence in the heart.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Western Blotmentioning

confidence: 99%

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High salt intake during puberty leads to cardiac remodelling and baroreflex impairment in lean and obese male Wistar rats

et al. 2019

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Short‐Term Postnatal Overfeeding Induces Long‐Lasting Cardiometabolic Syndrome in Mature and Old Mice Associated with Increased Sensitivity to Myocardial Infarction

Rigal,

Josse,

Greco

et al. 2024

Molecular Nutrition Food Res

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ScopePerinatal nutritional disturbances may “program” an increased cardio‐metabolic risk in adulthood; however, few experimental studies have explored their effects on mature and/or old animal. This study aims to investigate the influence of postnatal overfeeding (PNOF) on cardiac function, sensitivity to ischemia‐reperfusion (I‐R) injury in vivo, glucose metabolism, and metabolic profile of pericardial adipose tissue (PAT) in young (4 months), adult (6 months), old (12 months), and very old (18 months) male mice.Methods and resultsTwo days after birth, PNOF is induced by adjusting the litter size of C57BL/6 male mice to three pups/mother, while the normally fed (NF) control group is normalized to nine pups/mother. After weaning, all mice have free access to standard diet. Glucose/insulin tests and in vivo myocardial I‐R injury are conducted on mice aged from 2 to 12 months, while echocardiography is performed at all ages up to 18 months. PNOF mice exhibit an early and persistent 10–20% increase in body weight and a 10% decrease in left ventricular ejection fraction throughout their lifespan. In PNOF mice aged 4, 6, and 12 months, glucose intolerance and insulin resistance are observed, as well as a 27–34% increase in infarct size. This is accompanied by a higher PAT mass with increased inflammatory status.ConclusionShort‐term PNOF results in nutritional programming, inducing long‐lasting alterations in glucose metabolism and cardiac vulnerability in male mice, lasting up to 12 months.

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Ethanol exposure in prenatal and early postnatal induced cardiac injury in rats: involvement of oxidative stress, Hsp70, ERK 1/2, JNK, and apoptosis in a 3-month follow-up study

Shirpoor

Gaderi

Naderi

2019

Cell Stress and Chaperones

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Alcohol exposure during pregnancy induces a wide range of structural and functional abnormalities in the fetal heart. However, the underlying mechanism of this phenomenon is not well known. This study was undertaken to elucidate probable mechanisms of myocardial damage induced by prenatal and early postnatal ethanol treatment. Pregnant Wistar rats received ethanol 4.5 g/kg BW once per day from the seventh day of gestation (GD7) throughout lactation. The oxidative stress injury of the myocardium in pups was evaluated by measuring levels of oxidative stress biomarkers. Histopathological examinations and Western blot were performed to evaluate histological features, apoptosis, and molecular alterations in the myocardial tissue of male pups on the postnatal day 21 (PN-21) and postnatal day 90 (PN-90). The results showed that maternal ethanol consumption caused oxidative stress (impaired total antioxidant capacity and malondialdehyde), histological changes, and apoptosis of the myocardium in the pups on PN-21 and PN-90. At the molecular levels, Western blot analysis revealed that ethanol modulated the protein expression of p-ERK1/2, p-JNK, and Hsp70 in the myocardial tissue of the pups after 21 and 90 days of birth compared with the controls. These findings revealed that maternal ethanol intake induced cardiac toxicity in part, mediated by oxidative stress and apoptosis in the pups. A further mechanism study revealed that ethanol enhanced ERK1/2 and JNK phosphorylation and Hsp70 protein expression.

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Postnatal early overfeeding induces cardiovascular dysfunction by oxidative stress in adult male Wistar rats

Cited by 13 publications

References 50 publications

High salt intake during puberty leads to cardiac remodelling and baroreflex impairment in lean and obese male Wistar rats

High salt intake during puberty leads to cardiac remodelling and baroreflex impairment in lean and obese male Wistar rats

Short‐Term Postnatal Overfeeding Induces Long‐Lasting Cardiometabolic Syndrome in Mature and Old Mice Associated with Increased Sensitivity to Myocardial Infarction

Ethanol exposure in prenatal and early postnatal induced cardiac injury in rats: involvement of oxidative stress, Hsp70, ERK 1/2, JNK, and apoptosis in a 3-month follow-up study

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