scholarly journals Goat Milk Kefir Supplemented with Porang Glucomannan Improves Lipid Profile and Haematological Parameter in Rat Fed High Fat and High Fructose Diet

2018 ◽  
Vol 25 (1) ◽  
pp. 11-21
Author(s):  
◽  
Eni Harmayani ◽  
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Profile ◽  
Total Cholesterol ◽  
Goat Milk ◽  
Normal Diet ◽  
Haematological Parameter ◽  
High Fat ◽  
The Metabolic Syndrome ◽  
High Fructose

AbstractBackground and Aims: Diet with a high fat and high sugar is associated with an increased incindence of the metabolic syndrome. Kefir has been known as a natural probiotic, while glucomannan from porang (Amorphophallus oncophyllus) tuber was demonstrated as prebiotic in vivo. Probiotics and prebiotics can be used adjuvant nutritional therapy for metabolic syndrome. The aim of this study was to evaluate the effect of goat milk kefir supplemented with porang glucomannan on the lipid profile and haematological parameters in rats fed with a high-fat/high-fructose (HFHF) diet.Materials and methods: Rats were divided into 5 groups: normal diet; HFHF; HFHF + kefir; HFHF + kefir + glucomannan; and HFHF + simvastatin.Results: There were significant differences before and after treatment in triglycerides and total cholesterol in HFHF + kefir+glucomannan group. The HFHF rats administered kefir with or without glucomannan had higher levels of lymphocytes and lower neutrophils compared to HFHF group (p<0.05). Only goat milk kefir without glucomannan proved to reduce platelets number.Conclusion: Goat milk kefir supplemented with porang glucomannan could improve the health of rats fed high-fat/high-fructose, by decreasing plasma triglycerides, total cholesterol, and their immunomodulatory effect by decreasing number of neutrophils and increasing the lymphocytes. Especially for goat milk kefir had antithrombotic activity which important to prevent cardiovascular diseases.

scholarly journals Effects of Unfiltered Coffee and Bioactive Coffee Compounds on the Development of Metabolic Syndrome Components in a High‐Fat/High‐Fructose-Fed Rat Model

2018 ◽  
Author(s):  
Pedram Shokouh ◽  
Per Bendix Jeppesen ◽  
Kjeld Hermansen ◽  
Christoffer Laustsen ◽  
Hans Stødkilde-Jørgensen ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Drinking Water ◽  
Liver Steatosis ◽  
Coffee Consumption ◽  
Metabolic Effects ◽  
Oral Glucose ◽  
Sprague Dawley ◽  
High Fat ◽  
The Metabolic Syndrome

Literature is inconsistent as to how coffee affects the features of the metabolic syndrome (MetS), and which bioactive compounds are responsible for its metabolic effects. We aimed to compare the in-vivo effects of unfiltered coffee with a selected mixture of its compounds on diet-induced MetS. 24 male Sprague-Dawley rats were fed a high-fat (35% W/W) food plus 20% W/W fructose in drinking water for 14 weeks, and were randomized into three groups: control, coffee, or nutraceuticals (5-O-caffeoylquinic acid, caffeic acid, and trigonelline). Coffee or nutraceuticals were provided in drinking water in a dosage equal to 4 cups/day in a human. Compared to the controls, only coffee supplementation decreased total food intake, weight gain, and estimated average plasma glucose. Surrogate measures of insulin resistance (fasting insulin, HOMA-IR, and oral glucose tolerance) were improved at endpoint in the coffee group. Circulating triglyceride levels were also reduced by coffee. Histopathological and quantitative measurements indicated lower grades of liver steatosis after long-term coffee consumption. In conclusion, a combination of phenolic acids and trigonelline was not as effective as coffee per se in improving the components of the MetS. This points to the role of other coffee chemicals and a potential synergism between compounds.

scholarly journals Etlingera elatior (Jack) R.M, Sm Containing Diet Normalizes some Metabolic Syndrome Markers due to High-Fat High-Fructose Diet in Wistar Rats

2020 ◽  
Vol 16 ◽  
Author(s):  
Nur Islami Dini Hanifah ◽  
Retno Murwani ◽  
Achmad Zulfa Juniarto
Keyword(s):  
Metabolic Syndrome ◽  
Body Weight ◽  
Total Cholesterol ◽  
Wistar Rats ◽  
Density Lipoprotein ◽  
Standard Diet ◽  
High Fat ◽  
High Fructose Diet ◽  
High Fructose ◽  
Etlingera Elatior

Background: Etlingera elatior (Ee) contains phytochemical compounds that are rich in antioxidants, which may reduce several biochemical markers of metabolic syndrome (MetS). Objective: We aimed to study the effect of fresh Etlingera elatior (FEe) and steamed Etlingera elatior (SEe) as a part of rat diet on the body weight, serum lipid, and malondialdehyde (MDA) level in Wistar rats with MetS induced by a highfat, high-fructose diet. Method: Our research was a true experimental randomized control group design with pre- and post-test. A total of 24 male Wistar rats were divided randomly into the following four groups: 1) Control, fed standard rat diet during the whole duration of the study, 2) HFFr-Sd, fed high-fat high-fructose (HFFr) diet for 29 days, followed by 29 days of the standard diet, 3) HFFr-FEe, fed HFFr diet for 29 days, followed by 29 days of a standard diet containing 33.3% FEe, and 4) HFFrSEe, fed HFFr diet for 29 days, followed by 29 days of a standard diet containing 33.3% SEe. The HFFr diet was given at 15 g/day along with fructose drink (20% pure fructose) at 100 ml/day. The diets in each group after the MetS induction period is referred to as intervention diets. Data at the end of HFFr (pre) and intervention diets (post) were analyzed by paired t-test. The data among groups were analyzed by one-way analysis of variance followed by post hoc test. Results: HFFr diet for 29 days induced MetS in Wistar rats fulfilling the criteria of obesity (Lee Index), hypertriglyceridemia, and decreased high-density lipoprotein cholesterol (HDL-C). Also, there was a significant increase in serum total cholesterol, low-density lipoprotein cholesterol (LDL-C), and MDA level (p < 0.05). Feeding a diet contaning FEe or SEe can significantly reduce body weight, serum triglyceride, total cholesterol, LDL-C, and MDA, and increase HDL-C levels (p < 0.05). The effect of FEe was more pronounced in ameliorating body weight and lipid profile than SEe. Conclusion: Fresh Ee and Steamed Ee can ameliorate obesity, dyslipidemia, and oxidative stress in MetS Wistar rats induced by a high-fat high-fructose diet. It suggests that dietary Ee accounting for one-third of daily standard diet can assist in normalizing some MetS markers in rats.

Dietary Switch from High Fat Diet to Normal Diet During Early Adulthood Does Not Restore Sperm Quality But Prevents Onset of the Metabolic Syndrome

2019 ◽  
Author(s):  
Lu&iacute;s Cris&oacute;stomo ◽  
Lu&iacute;s Rato ◽  
Ivana Jarak ◽  
Branca M. Silva ◽  
Jo&atilde;o F. Raposo ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
High Fat Diet ◽  
Sperm Quality ◽  
Early Adulthood ◽  
Normal Diet ◽  
High Fat ◽  
The Metabolic Syndrome ◽  
Dietary Switch

scholarly journals Lactobacillus plantarum ATG-K2 and ATG-K6 Ameliorates High-Fat with High-Fructose Induced Intestinal Inflammation

2021 ◽  
Vol 22 (9) ◽  
pp. 4444
Author(s):  
Miey Park ◽  
Eun-Jung Park ◽  
So-Hyeun Kim ◽  
Hae-Jeung Lee
Keyword(s):  
Small Intestine ◽  
Cell Injury ◽  
Intestinal Inflammation ◽  
Liver Weight ◽  
Diet Group ◽  
Normal Diet ◽  
Control Group ◽  
High Fat ◽  
Inflammatory Reactions ◽  
High Fructose

Obesity has become a worldwide health problem, and many significant inflammatory markers have been associated with the risk of side effects of obesity and obesity-related diseases. After a normal diet or high-fat diet with high-fructose water (HFHF) for 8 weeks, male Wistar rats were divided randomly into four experimental groups according to body weight. Next, for 8 weeks, a normal diet, HFHF diet, and HFHF diet with L. plantarum strains ATG-K2 or ATG-K6 were administered orally. Compared to the control group, the HFHF diet group showed significantly increased visceral fat, epididymal fat, and liver weight. The mRNA and protein expression levels of FAS and SREBP-1c were higher in the HFHF diet group than in the HFHF diet with L. plantarum strains ATG-K2 and ATG-K6. The HFHF diet with L. plantarum strain ATG-K2 showed significantly decreased inflammatory cytokine expression in the serum and small intestine compared to the HFHF diet group. Furthermore, histological morphology showed minor cell injury, less severe infiltration, and longer villi height in the small intestine ileum of the HFHF diet with L. plantarum strains groups than in the HFHF diet group. These results suggest that L. plantarum strains K2 and K6 may help reduce intestinal inflammation and could be used as treatment alternatives for intestinal inflammatory reactions and obesity.

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 Glucose Transporter 8 (GLUT8) Regulates Enterocyte Fructose Transport and Global Mammalian Fructose Utilization

Endocrinology ◽  
2012 ◽  
Vol 153 (9) ◽  
pp. 4181-4191 ◽  
Author(s):  
Brian J. DeBosch ◽  
Maggie Chi ◽  
Kelle H. Moley
Keyword(s):  
Glucose Transporter ◽  
Serum Insulin ◽  
Density Lipoprotein ◽  
Wild Type ◽  
In Vivo Models ◽  
The Metabolic Syndrome ◽  
High Fructose

Enterocyte fructose absorption is a tightly regulated process that precedes the deleterious effects of excess dietary fructose in mammals. Glucose transporter (GLUT)8 is a glucose/fructose transporter previously shown to be expressed in murine intestine. The in vivo function of GLUT8, however, remains unclear. Here, we demonstrate enhanced fructose-induced fructose transport in both in vitro and in vivo models of enterocyte GLUT8 deficiency. Fructose exposure stimulated [14C]-fructose uptake and decreased GLUT8 protein abundance in Caco2 colonocytes, whereas direct short hairpin RNA-mediated GLUT8 knockdown also stimulated fructose uptake. To assess GLUT8 function in vivo, we generated GLUT8-deficient (GLUT8KO) mice. GLUT8KO mice exhibited significantly greater jejunal fructose uptake at baseline and after high-fructose diet (HFrD) feeding vs. wild-type mice. Strikingly, long-term HFrD feeding in GLUT8KO mice exacerbated fructose-induced increases in blood pressure, serum insulin, low-density lipoprotein and total cholesterol vs. wild-type controls. Enhanced fructose uptake paralleled with increased abundance of the fructose and glucose transporter, GLUT12, in HFrD-fed GLUT8KO mouse enterocytes and in Caco2 cultures exposed to high-fructose medium. We conclude that GLUT8 regulates enterocyte fructose transport by regulating GLUT12, and that disrupted GLUT8 function has deleterious long-term metabolic sequelae. GLUT8 may thus represent a modifiable target in the prevention and treatment of malnutrition or the metabolic syndrome.

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.

scholarly journals Enhanced phosphorylation of Na+–Cl− co-transporter in experimental metabolic syndrome: role of insulin

2012 ◽  
Vol 123 (11) ◽  
pp. 635-647 ◽  
Author(s):  
Radko Komers ◽  
Shaunessy Rogers ◽  
Terry T. Oyama ◽  
Bei Xu ◽  
Chao-Ling Yang ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Time Course ◽  
Kinase Inhibitor ◽  
Endogenous Expression ◽  
The Metabolic Syndrome ◽  
Mammalian Cell Lines ◽  
Phosphoinositide 3 Kinase

In the present study, we investigated the activity of the thiazide-sensitive NCC (Na+–Cl− co-transporter) in experimental metabolic syndrome and the role of insulin in NCC activation. Renal responses to the NCC inhibitor HCTZ (hydrochlorothiazide), as a measure of NCC activity in vivo, were studied in 12-week-old ZO (Zucker obese) rats, a model of the metabolic syndrome, and in ZL (Zucker lean) control animals, together with renal NCC expression and molecular markers of NCC activity, such as localization and phosphorylation. Effects of insulin were studied further in mammalian cell lines with inducible and endogenous expression of this molecule. ZO rats displayed marked hyperinsulinaemia, but no differences in plasma aldosterone, compared with ZL rats. In ZO rats, natriuretic and diuretic responses to NCC inhibition with HCTZ were enhanced compared with ZL rats, and were associated with a decrease in BP (blood pressure). ZO rats displayed enhanced Thr53 NCC phosphorylation and predominant membrane localization of both total and phosphorylated NCC, together with a different profile in expression of SPAK (Ste20-related proline/alanine-rich kinase) isoforms, and lower expression of WNK4. In vitro, insulin induced NCC phosphorylation, which was blocked by a PI3K (phosphoinositide 3-kinase) inhibitor. Insulin-induced reduction in WNK4 expression was also observed, but delayed compared with the time course of NCC phosphorylation. In summary, we report increased NCC activity in hyperinsulinaemic rodents in conjunction with the SPAK expression profile consistent with NCC activation and reduced WNK4, as well as an ability of insulin to induce NCC stimulatory phosphorylation in vitro. Together, these findings indicate that hyperinsulinaemia is an important driving force of NCC activity in the metabolic syndrome with possible consequences for BP regulation.

Components of the Metabolic Syndrome Are Not Affected Differently by Regular Consumption of Sucrose or High Fructose Corn Syrup.

2010 ◽  
pp. P2-523-P2-523
Author(s):  
J Lowndes ◽  
D Kawieki ◽  
TJ Angelopoulos ◽  
K Melanson ◽  
JM Rippe
Keyword(s):  
Metabolic Syndrome ◽  
High Fructose Corn Syrup ◽  
Corn Syrup ◽  
The Metabolic Syndrome ◽  
Regular Consumption ◽  
High Fructose
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