scholarly journals Cardiac Remodeling During Pregnancy With Metabolic Syndrome

Circulation ◽  
2021 ◽  
Vol 143 (7) ◽  
pp. 699-712
Author(s):  
Yijun Yang ◽  
Justin Kurian ◽  
Giana Schena ◽  
Jaslyn Johnson ◽  
Hajime Kubo ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Cardiac Remodeling ◽  
Control Diet ◽  
Western Diet ◽  
Pregnant Female ◽  
Female Mice ◽  
Child Bearing ◽  
Pathological Hypertrophy ◽  
Phenylephrine Infusion ◽  
Physiological Hypertrophy

Background: The heart undergoes physiological hypertrophy during pregnancy in healthy individuals. Metabolic syndrome (MetS) is now prevalent in women of child-bearing age and might add risks of adverse cardiovascular events during pregnancy. The present study asks if cardiac remodeling during pregnancy in obese individuals with MetS is abnormal and whether this predisposes them to a higher risk for cardiovascular disorders. Methods: The idea that MetS induces pathological cardiac remodeling during pregnancy was studied in a long-term (15 weeks) Western diet–feeding animal model that recapitulated features of human MetS. Pregnant female mice with Western diet (45% kcal fat)–induced MetS were compared with pregnant and nonpregnant females fed a control diet (10% kcal fat). Results: Pregnant mice fed a Western diet had increased heart mass and exhibited key features of pathological hypertrophy, including fibrosis and upregulation of fetal genes associated with pathological hypertrophy. Hearts from pregnant animals with WD-induced MetS had a distinct gene expression profile that could underlie their pathological remodeling. Concurrently, pregnant female mice with MetS showed more severe cardiac hypertrophy and exacerbated cardiac dysfunction when challenged with angiotensin II/phenylephrine infusion after delivery. Conclusions: These results suggest that preexisting MetS could disrupt physiological hypertrophy during pregnancy to produce pathological cardiac remodeling that could predispose the heart to chronic disorders.

The effects of two types of Western diet on the induction of metabolic syndrome and cardiac remodeling in obese rats

2021 ◽  
Vol 92 ◽  
pp. 108625
Author(s):  
Danielle Fernandes Vileigas ◽  
Sérgio Luiz Borges de Souza ◽  
Camila Renata Corrêa ◽  
Carol Cristina Vágula de Almeida Silva ◽  
Dijon Henrique Salomé de Campos ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Cardiac Remodeling ◽  
Western Diet ◽  
Obese Rats

scholarly journals Consuming a Western diet for two weeks suppresses fetal genes in mouse hearts

2014 ◽  
Vol 306 (8) ◽  
pp. R519-R526 ◽  
Author(s):  
Heidi M. Medford ◽  
Emily J. Cox ◽  
Lindsey E. Miller ◽  
Susan A. Marsh
Keyword(s):  
Transcription Factor ◽  
Control Diet ◽  
Saturated Fat ◽  
Western Diet ◽  
Hypertrophic Response ◽  
Protein Levels ◽  
Pathological Hypertrophy ◽  
Cardiac Gene ◽  
Glcnac Transferase ◽  
Transcription Factor Complex

Diets high in sugar and saturated fat (Western diet) contribute to obesity and pathophysiology of metabolic syndrome. A common physiological response to obesity is hypertension, which induces cardiac remodeling and hypertrophy. Hypertrophy is regulated at the level of chromatin by repressor element 1-silencing transcription factor (REST), and pathological hypertrophy is associated with reexpression of a fetal cardiac gene program. Reactivation of fetal genes is commonly observed in hypertension-induced hypertrophy; however, this response is blunted in diabetic hearts, partially due to upregulation of the posttranslational modification O-linked-β- N-acetylglucosamine ( O-GlcNAc) to proteins by O-GlcNAc transferase (OGT). OGT and O-GlcNAc are found in chromatin-modifying complexes, but it is unknown whether they play a role in Western diet-induced hypertrophic remodeling. Therefore, we investigated the interactions between O-GlcNAc, OGT, and the fetal gene-regulating transcription factor complex REST/mammalian switch-independent 3A/histone deacetylase (HDAC). Five-week-old male C57BL/6 mice were fed a Western ( n = 12) or control diet ( n = 12) for 2 wk to examine the early hypertrophic response. Western diet-fed mice exhibited fasting hyperglycemia and increased body weight ( P < 0.05). As expected for this short duration of feeding, cardiac hypertrophy was not yet evident. We found that REST is O-GlcNAcylated and physically interacts with OGT in mouse hearts. Western blot analysis showed that HDAC protein levels were not different between groups; however, relative to controls, Western diet hearts showed increased REST and decreased ANP and skeletal α-actin. Transcript levels of HDAC2 and cardiac α-actin were decreased in Western diet hearts. These data suggest that REST coordinates regulation of diet-induced hypertrophy at the level of chromatin.

scholarly journals Endothelial Estrogen Receptor-α Does Not Protect Against Vascular Stiffness Induced by Western Diet in Female Mice

Endocrinology ◽  
2016 ◽  
Vol 157 (4) ◽  
pp. 1590-1600 ◽  
Author(s):  
Camila Manrique ◽  
Guido Lastra ◽  
Francisco I. Ramirez-Perez ◽  
Dominic Haertling ◽  
Vincent G. DeMarco ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Estrogen Receptor ◽  
Vascular Reactivity ◽  
Control Diet ◽  
Western Diet ◽  
Vascular Stiffness ◽  
Whole Body ◽  
Chow Diet ◽  
Female Mice ◽  
Vascular Stiffening

Abstract Consumption of a diet high in fat and refined carbohydrates (Western diet [WD]) is associated with obesity and insulin resistance, both major risk factors for cardiovascular disease (CVD). In women, obesity and insulin resistance abrogate the protection against CVD likely afforded by estrogen signaling through estrogen receptor (ER)α. Indeed, WD in females results in increased vascular stiffness, which is independently associated with CVD. We tested the hypothesis that loss of ERα signaling in the endothelium exacerbates WD-induced vascular stiffening in female mice. We used a novel model of endothelial cell (EC)-specific ERα knockout (EC-ERαKO), obtained after sequential crossing of the ERα double floxed mice and VE-Cadherin Cre-recombinase mice. Ten-week-old females, EC-ERαKO and aged-matched genopairs were fed either a regular chow diet (control diet) or WD for 8 weeks. Vascular stiffness was measured in vivo by pulse wave velocity and ex vivo in aortic explants by atomic force microscopy. In addition, vascular reactivity was assessed in isolated aortic rings. Initial characterization of the model fed a control diet did not reveal changes in whole-body insulin sensitivity, aortic vasoreactivity, or vascular stiffness in the EC-ERαKO mice. Interestingly, ablation of ERα in ECs reduced WD-induced vascular stiffness and improved endothelial-dependent dilation. In the setting of a WD, endothelial ERα signaling contributes to vascular stiffening in females. The precise mechanisms underlying the detrimental effects of endothelial ERα in the setting of a WD remain to be elucidated.

scholarly journals Temporal Measures in Cardiac Structure and Function During the Development of Obesity Induced by Different Types of Western Diet in a Rat Model

Nutrients ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 68 ◽  
Author(s):  
Danielle Fernandes Vileigas ◽  
Cecília Lume de Carvalho Marciano ◽  
Gustavo Augusto Ferreira Mota ◽  
Sérgio Luiz Borges de Souza ◽  
Paula Grippa Sant’Ana ◽  
...  
Keyword(s):  
Cardiac Remodeling ◽  
Systolic Function ◽  
Control Diet ◽  
Structure And Function ◽  
Western Diet ◽  
Cardiac Structure ◽  
Different Types ◽  
Cardiac Structure And Function ◽  
And Function

Obesity is recognized worldwide as a complex metabolic disorder that has reached epidemic proportions and is often associated with a high incidence of cardiovascular diseases. To study this pathology and evaluate cardiac function, several models of diet-induced obesity (DIO) have been developed. The Western diet (WD) is one of the most widely used models; however, variations in diet composition and time period of the experimental protocol make comparisons challenging. Thus, this study aimed to evaluate the effects of two different types of Western diet on cardiac remodeling in obese rats with sequential analyses during a long-term follow-up. Male Wistar rats were distributed into three groups fed with control diet (CD), Western diet fat (WDF), and Western diet sugar (WDS) for 41 weeks. The animal nutritional profile and cardiac histology were assessed at the 41st week. Cardiac structure and function were evaluated by echocardiogram at four different moments: 17, 25, 33, and 41 weeks. A noninvasive method was performed to assess systolic blood pressure at the 33rd and 41st week. The animals fed with WD (WDF and WDS) developed pronounced obesity with an average increase of 86.5% in adiposity index at the end of the experiment. WDF and WDS groups also presented hypertension. The echocardiographic data showed no structural differences among the three groups, but WDF animals presented decreased endocardial fractional shortening and ejection fraction at the 33rd and 41st week, suggesting altered systolic function. Moreover, WDF and WFS animals did not present hypertrophy and interstitial collagen accumulation in the left ventricle. In conclusion, both WD were effective in triggering severe obesity in rats; however, only the WDF induced mild cardiac dysfunction after long-term diet exposure. Further studies are needed to search for an appropriate DIO model with relevant cardiac remodeling.

scholarly journals Association between Cardiac Remodeling and Metabolic Alteration in an Experimental Model of Obesity Induced by Western Diet

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1675 ◽  
Author(s):  
Artur Ferron ◽  
Fabiane Francisqueti ◽  
Igor Minatel ◽  
Carol Silva ◽  
Silméia Bazan ◽  
...  
Keyword(s):  
Lipid Profile ◽  
Cardiac Remodeling ◽  
Control Diet ◽  
Caloric Intake ◽  
Density Lipoprotein ◽  
Western Diet ◽  
Control Group ◽  
Glucose Levels ◽  
Diet Control ◽  
Deceleration Time

The high consumption of fat and sugar contributes to the development of obesity and co-morbidities, such as dyslipidemia, hypertension, and cardiovascular disease. The aim of this study was to evaluate the association between dyslipidemia and cardiac dysfunction induced by western diet consumption. Wistar rats were randomly divided into two experimental groups and fed ad libitum for 20 weeks with a control diet (Control, n = 12) or a high-sugar and high-fat diet (HSF, n = 12). The HSF group also received water + sucrose (25%). Evaluations included feed and caloric intake; body weight; plasma glucose; insulin; uric acid; HOMA-IR; lipid profile: [total cholesterol (T-chol), high-density lipoprotein (HDL), non-HDL Chol, triglycerides (TG)]; systolic blood pressure, and Doppler echocardiographic. Compared to the control group, animals that consumed the HSF diet presented higher weight gain, caloric intake, feed efficiency, insulin, HOMA-IR, and glucose levels, and lipid profile impairment (higher TG, T-chol, non-HDL chol and lower HDL). HSF diet was also associated with atrial-ventricular structural impairment and systolic-diastolic dysfunction. Positive correlation was also found among the following parameters: insulin versus estimated LV mass (r = 0.90, p = 0.001); non-HDL versus deceleration time (r = 0.46, p = 0.02); TG versus deceleration time (r = 0.50, p = 0.01). In summary, our results suggest cardiac remodeling lead by western diet is associated with metabolic parameters.

scholarly journals Long-term effects of western diet consumption in male and female mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yu Hasegawa ◽  
Shin-Yu Chen ◽  
Lili Sheng ◽  
Prasant Kumar Jena ◽  
Karen M. Kalanetra ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Western Diet ◽  
Long Term Effects ◽  
Alcoholic Fatty Liver ◽  
Male And Female ◽  
Sexual Dimorphisms ◽  
Female Mice ◽  
Males And Females ◽  
The Impact

Abstract Long-term consumption of a diet with excessive fat and sucrose (Western diet, WD) leads to an elevated risk of obesity and metabolic syndrome in both males and females. However, there are sexual dimorphisms in metabolism which are apparent when considering the prevalence of complications of metabolic syndrome, such as non-alcoholic fatty liver disease. This study aimed to elucidate the impact of a WD on the metabolome and the gut microbiota of male and female mice at 5, 10, and 15 months to capture the dynamic and comprehensive changes brought about by diet at different stages of life. Here we show that there are important considerations of age and sex that should be considered when assessing the impact of diet on the gut microbiome and health.

scholarly journals Metabolic Effects of the Sweet Protein MNEI as a Sweetener in Drinking Water. A Pilot Study of a High Fat Dietary Regimen in a Rodent Model

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2643
Author(s):  
Rosa Cancelliere ◽  
Serena Leone ◽  
Cristina Gatto ◽  
Arianna Mazzoli ◽  
Carmine Ercole ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Profile ◽  
Western Diet ◽  
Metabolic Effects ◽  
High Fat ◽  
Metabolic Derangement ◽  
Dietary Regimen ◽  
Sweet Proteins ◽  
Sweet Protein ◽  
Typical Western Diet

Sweeteners have become integrating components of the typical western diet, in response to the spreading of sugar-related pathologies (diabetes, obesity and metabolic syndrome) that have stemmed from the adoption of unbalanced dietary habits. Sweet proteins are a relatively unstudied class of sweet compounds that could serve as innovative sweeteners, but their introduction on the food market has been delayed by some factors, among which is the lack of thorough metabolic and toxicological studies. We have tried to shed light on the potential of a sweet protein, MNEI, as a fructose substitute in beverages in a typical western diet, by studying the metabolic consequences of its consumption on a Wistar rat model of high fat diet-induced obesity. In particular, we investigated the lipid profile, insulin sensitivity and other indicators of metabolic syndrome. We also evaluated systemic inflammation and potential colon damage. MNEI consumption rescued the metabolic derangement elicited by the intake of fructose, namely insulin resistance, altered plasma lipid profile, colon inflammation and translocation of lipopolysaccharides from the gut lumen into the circulatory system. We concluded that MNEI could represent a valid alternative to fructose, particularly when concomitant metabolic disorders such as diabetes and/or glucose intolerance are present.

scholarly journals Exercise prevents Western diet-associated erectile dysfunction and coronary artery endothelial dysfunction: response to acute apocynin and sepiapterin treatment

2013 ◽  
Vol 305 (4) ◽  
pp. R423-R434 ◽  
Author(s):  
Justin D. La Favor ◽  
Ethan J. Anderson ◽  
Jillian T. Dawkins ◽  
Robert C. Hickner ◽  
Christopher J. Wingard
Keyword(s):  
Erectile Dysfunction ◽  
Coronary Artery ◽  
Exercise Training ◽  
Erectile Function ◽  
Dietary Intervention ◽  
Ex Vivo ◽  
Control Diet ◽  
Western Diet ◽  
Treadmill Running ◽  
Aerobic Exercise Training

The aim of this study was to investigate aerobic exercise training as a means to prevent erectile dysfunction (ED) and coronary artery disease (CAD) development associated with inactivity and diet-induced obesity. Male Sprague-Dawley rats were fed a Western diet (WD) or a control diet (CD) for 12 wk. Subgroups within each diet remained sedentary (Sed) or participated in aerobic interval treadmill running throughout the dietary intervention. Erectile function was evaluated under anesthesia by measuring the mean arterial pressure and intracavernosal pressure in response to electrical field stimulation of the cavernosal nerve, in the absence or presence of either apocynin, an NADPH oxidase inhibitor, or sepiapterin, a tetrahydrobiopterin precursor. Coronary artery endothelial function (CAEF) was evaluated ex vivo with cumulative doses of ACh applied to preconstricted segments of the left anterior descending coronary artery. CAEF was assessed in the absence or presence of apocynin or sepiapterin. Erectile function ( P < 0.0001) and CAEF ( P < 0.001) were attenuated in WD-Sed. Exercise preserved erectile function ( P < 0.0001) and CAEF ( P < 0.05) within the WD. Erectile function ( P < 0.01) and CAEF ( P < 0.05) were augmented by apocynin only in WD-Sed, while sepiapterin ( P < 0.05) only augmented erectile function in WD-Sed. These data demonstrate that a chronic WD induces impairment in erectile function and CAEF that are commonly partially reversible by apocynin, whereas sepiapterin treatment exerted differential functional effects between the two vascular beds. Furthermore, exercise training may be a practical means of preventing diet-induced ED and CAD development.

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