Diosmetin attenuates the metabolic syndrome and left ventricular alterations via suppression of angiotensin II/AT1 receptor/ gp91phox /p-NF-κB protein expression in high-fat diet fed rats

2021 ◽  
Author(s):  
Sariya Meephat ◽  
Patoomporn Prasatthong ◽  
Siwayu Rattanakanokchai ◽  
Sarawoot Bunbupha ◽  
Putcharawipa Maneesai ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Angiotensin Ii ◽  
Protein Expression ◽  
High Fat Diet ◽  
Left Ventricular ◽  
Biological Role ◽  
Citrus Fruits ◽  
High Fat ◽  
The Metabolic Syndrome

Diosmetin, a monomethoxyflavone, is isolated from citrus fruits. The objective of this research was to test the biological role of diosmetin on parameters of the metabolic syndrome (MS) and left...

scholarly journals 7-Hydroxymatairesinol improves body weight, fat and sugar metabolism in C57BJ/6 mice on a high-fat diet

2018 ◽  
Vol 120 (7) ◽  
pp. 751-762 ◽  
Author(s):  
Giorgio Biasiotto ◽  
Isabella Zanella ◽  
Federica Predolini ◽  
Ivonne Archetti ◽  
Moris Cadei ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Body Weight ◽  
High Fat Diet ◽  
Sugar Metabolism ◽  
Lipid Uptake ◽  
High Fat ◽  
Total Extract ◽  
The Metabolic Syndrome ◽  
Metabolic Genes

Abstract7-Hydroxymatairesinol (7-HMR) is a plant lignan abundant in various concentrations in plant foods. The objective of this study was to test HMRLignan™, a purified form of 7-HMR, and the correspondingPicea abiesextract (total extractP. abies; TEP) as dietary supplements on a background of a high-fat diet (HFD)-induced metabolic syndrome in mice and in the 3T3-L1 adipogenesis model. Mice, 3 weeks old, were fed a HFD for 60 d. Subgroups were treated with 3 mg/kg body weight 7-HMR (HMRLignan™) or 10 mg/kg body weight TEP by oral administration. 7-HMR and TEP limited the increase in body weight (−11 and −13 %) and fat mass (−11 and −18 %) in the HFD-fed mice. Epididymal adipocytes were 19 and −12 % smaller and the liver was less steatotic (−62 and −65 %). Serum lipids decreased in TEP-treated mice (−11 % cholesterol, −23 % LDL and −15 % TAG) and sugar metabolism was ameliorated by both lignan preparations, as shown by a more than 70 % decrease in insulin secretion and insulin resistance. The expression of several metabolic genes was modulated by the HFD with an effect that was reversed by lignan. In 3T3-L1 cells, the 7-HMR metabolites enterolactone (ENL) and enterodiol (END) showed a 40 % inhibition of cell differentiation accompanied by the inhibited expression of the adipogenic genesPPARγ,C/EBPαandaP2. Furthermore, END and ENL caused a 10 % reduction in TAG uptake in HEPA 1–6 hepatoma cells. In conclusion, 7-HMR and TEP reduce metabolic imbalances typical of the metabolic syndrome and obesity in male mice, whereas their metabolites inhibit adipogenesis and lipid uptakein vitro.

Monounsaturated Fatty Acids in a High‐Fat Diet and Niacin Protect from White Fat Dysfunction in the Metabolic Syndrome

2019 ◽  
Vol 63 (19) ◽  
pp. 1900425 ◽  
Author(s):  
Sergio Montserrat‐de la Paz ◽  
Maria C. Naranjo ◽  
Maria C. Millan‐Linares ◽  
Sergio Lopez ◽  
Rocio Abia ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Fatty Acids ◽  
High Fat Diet ◽  
Monounsaturated Fatty Acids ◽  
High Fat ◽  
The Metabolic Syndrome ◽  
White Fat

Hepatic accumulation of S-adenosylmethionine in hamsters with non-alcoholic fatty liver disease associated with metabolic syndrome under selenium and vitamin E deficiency

2019 ◽  
Vol 133 (3) ◽  
pp. 409-423 ◽  
Author(s):  
Josep Maria del Bas ◽  
Benjamín Rodríguez ◽  
Francesc Puiggròs ◽  
Silvia Mariné ◽  
Miguel Angel Rodríguez ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Metabolic Syndrome ◽  
Vitamin E ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Cell Cycle Control ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

AbstractProgression of non-alcoholic fatty liver disease (NAFLD) in the context of metabolic syndrome (MetS) is only partially explored due to the lack of preclinical models. In order to study the alterations in hepatic metabolism that accompany this condition, we developed a model of MetS accompanied by the onset of steatohepatitis (NASH) by challenging golden hamsters with a high-fat diet low in vitamin E and selenium (HFD), since combined deficiency results in hepatic necroinflammation in rodents. Metabolomics and transcriptomics integrated analyses of livers revealed an unexpected accumulation of hepatic S-Adenosylmethionine (SAM) when compared with healthy livers likely due to diminished methylation reactions and repression of GNMT. SAM plays a key role in the maintenance of cellular homeostasis and cell cycle control. In agreement, analysis of over-represented transcription factors revealed a central role of c-myc and c-Jun pathways accompanied by negative correlations between SAM concentration, MYC expression and AMPK phosphorylation. These findings point to a drift of cell cycle control toward senescence in livers of HFD animals, which could explain the onset of NASH in this model. In contrast, hamsters with NAFLD induced by a conventional high-fat diet did not show SAM accumulation, suggesting a key role of selenium and vitamin E in SAM homeostasis. In conclusion, our results suggest that progression of NAFLD in the context of MetS can take place even in a situation of hepatic SAM excess and that selenium and vitamin E status might be considered in current therapies against NASH based on SAM supplementation.

scholarly journals A Preclinical Rat Model of Heart Failure With Preserved Ejection Fraction With Multiple Comorbidities

2022 ◽  
Vol 8 ◽  
Author(s):  
Géraldine Hubesch ◽  
Aliénor Hanthazi ◽  
Angela Acheampong ◽  
Laura Chomette ◽  
Hélène Lasolle ◽  
...  
Keyword(s):  
Heart Failure ◽  
Metabolic Syndrome ◽  
Ejection Fraction ◽  
Diastolic Dysfunction ◽  
High Fat Diet ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Sequencing Analysis ◽  
Preserved Ejection Fraction ◽  
High Fat

Heart failure with preserved ejection fraction (HFpEF) is a common complex clinical syndrome for which there are currently few evidence-based therapies. As patients with HFpEF very often present with comorbidities comprising the metabolic syndrome, we hypothesized, that metabolic syndrome could lead over time to the development of diastolic dysfunction and HFpEF. Obesity-prone rats were exposed to high-fat diet and compared to obesity-resistant rats fed with standard chow. Phenotyping of metabolic syndrome, associated with echocardiographic and cardiac hemodynamic measurements, was performed after 4 and 12 months. Blood and myocardial tissue sampling were performed for pathobiological evaluation. High-fat diet in obesity-prone rats elicited metabolic syndrome, characterized by increased body and abdominal fat weights, glucose intolerance and hyperlipidemia, as well as increased left ventricular (LV) systolic pressure (after 12 months). This was associated with LV diastolic dysfunction (assessed by increased LV end-diastolic pressure) and pulmonary hypertension (assessed by increased right ventricular systolic pressure). Echocardiography revealed significant concentric LV hypertrophy, while LV ejection fraction was preserved. LV remodeling was associated with cardiomyocyte hypertrophy, as well as myocardial and perivascular fibrosis. Circulating levels of soluble ST2 (the interleukin-1 receptor-like) markedly increased in rats with HFpEF, while plasma NT-proBNP levels decreased. RNA-sequencing analysis identified clusters of genes implicated in fatty acid metabolism and calcium-dependent contraction as upregulated pathways in the myocardium of rats with HFpEF. High-fat diet during 12 months in obesity-prone rats led to the development of a relevant preclinical model of HFpEF with multiple comorbidities, suitable for investigating novel therapeutic interventions.

The role of high fat diet in the regulation of MAP kinases activity in left ventricular fibrosis

2019 ◽  
Vol 121 (3) ◽  
pp. 303-310 ◽  
Author(s):  
Katarzyna Czarzasta ◽  
Lukasz Koperski ◽  
Agnieszka Segiet ◽  
Maciej Janiszewski ◽  
Marek Kuch ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Map Kinases ◽  
Left Ventricular ◽  
High Fat ◽  
Ventricular Fibrosis

scholarly journals Circadian mutant mice with obesity and metabolic syndrome are resilient to cardiovascular disease

2020 ◽  
Vol 319 (5) ◽  
pp. H1097-H1111
Author(s):  
Cristine J. Reitz ◽  
Faisal J. Alibhai ◽  
Bruna Gazzi de Lima-Seolin ◽  
Ashley Nemec-Bakk ◽  
Neelam Khaper ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Cardiac Dysfunction ◽  
High Fat Diet ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Metabolic Dysfunction ◽  
Wild Type ◽  
High Fat

We examined whether obesity and metabolic syndrome underlie the development of cardiac dysfunction in circadian mutant ClockΔ19/Δ19 mice. Surprisingly, we demonstrate that although ClockΔ19/Δ19 mice develop metabolic dysfunction, they are protected from cardiac hypertrophy, left ventricular remodeling, and diastolic dysfunction, in contrast to wild-type controls, even when challenged with a chronic high-fat diet. These findings shed new light on the circadian regulation of oxidative stress pathways that can mediate resilience to cardiovascular disease.

scholarly journals Fetal origins of insulin resistance and obesity

2005 ◽  
Vol 64 (2) ◽  
pp. 143-151 ◽  
Author(s):  
Claire J. Stocker ◽  
Jonathan R. S. Arch ◽  
Michael A. Cawthorne
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
G Protein ◽  
High Fat Diet ◽  
High Fat ◽  
Fetal Origins ◽  
Thrifty Phenotype ◽  
The Metabolic Syndrome ◽  
Increased Susceptibility

A number of epidemiological studies worldwide have demonstrated a relationship between poor early growth and an increased susceptibility to insulin resistance, visceral obesity, type 2 diabetes and other features of the metabolic syndrome in adulthood. However, the mechanistic basis of this relationship and the relative roles of genes and the environment remain a subject of debate. The ‘thrifty phenotype’ hypothesis proposes that poor fetal nutrition leads to programming of metabolism and an adult phenotype that is adapted to poor but not plentiful nutrition. The maternal reduced-protein rat model has been used to examine the importance of the maternal environment in determining susceptibility to adult disease. Pregnant and lactating rat dams are fed a diet containing 80 g protein/kg as compared with 200 g protein/kg, which leads to growth restriction in utero. Offspring of low-protein dams have increased susceptibility to diabetes, insulin resistance and hypertension when fed a palatable high-fat diet that promotes obesity. Administration of leptin during pregnancy and lactation to these protein-restricted dams produces offspring that have increased metabolic rate and do not become obese or insulin resistant when fed on a high-fat diet. Increased glucocorticoid exposure, particularly during late gestation, has been linked with insulin resistance in adulthood. High levels of fetal glucocorticoids may result from a decreased activity of placental 11β-hydroxysteroid dehydrogenase (11β-HSD) type 2, which normally protects the fetus from high maternal glucocorticoid levels. Leptin administration to protein-restricted dams inhibits the suppression of 11β-HSD-2 and may be one mechanism by which the metabolic syndrome is prevented.

scholarly journals Inulin oligofructose attenuates metabolic syndrome in high-carbohydrate, high-fat diet-fed rats

2016 ◽  
Vol 116 (9) ◽  
pp. 1502-1511 ◽  
Author(s):  
Senthil A. Kumar ◽  
Leigh C. Ward ◽  
Lindsay Brown
Keyword(s):  
Metabolic Syndrome ◽  
Corn Starch ◽  
Body Weight Gain ◽  
Fasting Blood Glucose ◽  
Plasma Concentrations ◽  
Left Ventricular ◽  
High Fat ◽  
Soluble Fibre ◽  
High Carbohydrate ◽  
The Metabolic Syndrome

AbstractPrebiotics alter bacterial content in the colon, and therefore could be useful for obesity management. We investigated the changes following addition of inulin oligofructose (IO) in the food of rats fed either a corn starch (C) diet or a high-carbohydrate, high-fat (H) diet as a model of diet-induced metabolic syndrome. IO did not affect food intake, but reduced body weight gain by 5·3 and 12·3 % in corn starch+inulin oligofructose (CIO) and high-carbohydrate, high-fat with inulin oligofructose (HIO) rats, respectively. IO reduced plasma concentrations of free fatty acids by 26·2 % and TAG by 75·8 % in HIO rats. IO increased faecal output by 93·2 %, faecal lipid excretion by 37·9 % and weight of caecum by 23·4 % and colon by 41·5 % in HIO rats. IO improved ileal morphology by reducing inflammation and improving the density of crypt cells in HIO rats. IO attenuated H diet-induced increases in abdominal fat pads (C 275 (sem 19), CIO 264 (sem 40), H 688 (sem 55), HIO 419 (sem 32) mg/mm tibial length), fasting blood glucose concentrations (C 4·5 (sem 0·1), CIO 4·2 (sem 0·1), H 5·2 (sem 0·1), HIO 4·3 (sem 0·1) mmol/l), systolic blood pressure (C 124 (sem 2), CIO 118 (sem 2), H 152 (sem 2), HIO 123 (sem 3) mmHg), left ventricular diastolic stiffness (C 22·9 (sem 0·6), CIO 22·9 (sem 0·5), H 27·8 (sem 0·5), HIO 22·6 (sem 1·2)) and plasma alanine transaminase (C 29·6 (sem 2·8), CIO 32·1 (sem 3·0), H 43·9 (sem 2·6), HIO 33·6 (sem 2·0) U/l). IO attenuated H-induced increases in inflammatory cell infiltration in the heart and liver, lipid droplets in the liver and plasma lipids as well as impaired glucose and insulin tolerance. These results suggest that increasing soluble fibre intake with IO improves signs of the metabolic syndrome by decreasing gastrointestinal carbohydrate and lipid uptake.

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