Metabolic and hormonal indices in rats with a prolonged model of the metabolic syndrome induced by a high-carbohydrate and high-fat diet

2017 ◽  
Vol 7 (2) ◽  
pp. 130-136
Author(s):  
K. V. Derkach ◽  
V. M. Bondareva ◽  
A. P. Trashkov ◽  
O. V. Chistyakova ◽  
N. A. Verlov ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
High Fat Diet ◽  
High Fat ◽  
High Carbohydrate ◽  
The Metabolic Syndrome

scholarly journals Comparison of purple carrot juice and β-carotene in a high-carbohydrate, high-fat diet-fed rat model of the metabolic syndrome

2010 ◽  
Vol 104 (9) ◽  
pp. 1322-1332 ◽  
Author(s):  
Hemant Poudyal ◽  
Sunil Panchal ◽  
Lindsay Brown
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
High Fat Diet ◽  
Structure And Function ◽  
Carrot Juice ◽  
High Fat ◽  
High Carbohydrate ◽  
The Metabolic Syndrome ◽  
And Function ◽  
Β Carotene

Anthocyanins, phenolic acids and carotenoids are the predominant phytochemicals present in purple carrots. These phytochemicals could be useful in treatment of the metabolic syndrome since anthocyanins improve dyslipidaemia, glucose tolerance, hypertension and insulin resistance; the phenolic acids may also protect against CVD and β-carotene may protect against oxidative processes. In the present study, we have compared the ability of purple carrot juice and β-carotene to reverse the structural and functional changes in rats fed a high-carbohydrate, high-fat diet as a model of the metabolic syndrome induced by diet. Cardiac structure and function were defined by histology, echocardiography and in isolated hearts and blood vessels; liver structure and function, oxidative stress and inflammation were defined by histology and plasma markers. High-carbohydrate, high-fat diet-fed rats developed hypertension, cardiac fibrosis, increased cardiac stiffness, endothelial dysfunction, impaired glucose tolerance, increased abdominal fat deposition, altered plasma lipid profile, liver fibrosis and increased plasma liver enzymes together with increased plasma markers of oxidative stress and inflammation as well as increased inflammatory cell infiltration. Purple carrot juice attenuated or reversed all changes while β-carotene did not reduce oxidative stress, cardiac stiffness or hepatic fat deposition. As the juice itself contained low concentrations of carotenoids, it is likely that the anthocyanins are responsible for the antioxidant and anti-inflammatory properties of purple carrot juice to improve glucose tolerance as well as cardiovascular and hepatic structure and function.

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

Effects of ALA, EPA and DHA in high-carbohydrate, high-fat diet-induced metabolic syndrome in rats

2013 ◽  
Vol 24 (6) ◽  
pp. 1041-1052 ◽  
Author(s):  
Hemant Poudyal ◽  
Sunil K. Panchal ◽  
Leigh C. Ward ◽  
Lindsay Brown
Keyword(s):  
Metabolic Syndrome ◽  
High Fat Diet ◽  
High Fat ◽  
High Carbohydrate ◽  
Epa And Dha

The effects of palm tocotrienol on metabolic syndrome and bone loss in male rats induced by high-carbohydrate high-fat diet

2018 ◽  
Vol 44 ◽  
pp. 246-254 ◽  
Author(s):  
Sok Kuan Wong ◽  
Kok-Yong Chin ◽  
Farihah Hj Suhaimi ◽  
Fairus Ahmad ◽  
Soelaiman Ima-Nirwana
Keyword(s):  
Metabolic Syndrome ◽  
Bone Loss ◽  
High Fat Diet ◽  
Male Rats ◽  
High Fat ◽  
High Carbohydrate

Osteoporosis is associated with metabolic syndrome induced by high-carbohydrate high-fat diet in a rat model

2018 ◽  
Vol 98 ◽  
pp. 191-200 ◽  
Author(s):  
Sok Kuan Wong ◽  
Kok-Yong Chin ◽  
Farihah Hj Suhaimi ◽  
Fairus Ahmad ◽  
Nor Aini Jamil ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Rat Model ◽  
High Fat Diet ◽  
High Fat ◽  
High Carbohydrate

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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