Sodium metavanadate treatment improves glycogen levels in multiple tissues in a model of metabolic syndrome caused by chronic cadmium exposure in Wistar rats

BioMetals ◽  
2021 ◽  
Author(s):  
Victor Enrique Sarmiento-Ortega ◽  
Diana Moroni-González ◽  
Alfonso Díaz ◽  
Carolina Morán ◽  
Eduardo Brambila ◽  
...  
2012 ◽  
Vol 6 (2) ◽  
Author(s):  
Sudiarto . ◽  
Sri Hidayati Suprihatin

Obesity, one of the degenerative diseases, is a risk factor for chronical disease and an ultimate cause of metabolic syndrome which ismarked by the raising level of leptin on blood (hyperleptinemia). Metabolic syndrome is marked by the size of the waist is more than 40 inchfor man or 35 inch for woman, hypertension, hyperglycemia, high level of triglyceride, and the level of HDL (high-density lipoprotein) is low.This research is aimed to know the giving of quercetin (which has high anti oxide activities) on the declining level of leptin to the giving of DIO(Diet Induced Obesity). An experimental study using Post Test Control Group was done to the experimental wistar rats. Samples werechosen by using randomized complete block design. Rats were treated for 8 weeks. The dose of given quercetin were 2 mg/kgBB/day, 10mg/kgBB/day, and 50 mg/kgBB/day during the last 8 weeks of research. The variable measured in this research is the level of leptin onblood. Based on the experiment, quercetin is proven that gives influence to the level of leptin on obesity wistar rats’ serum compare to the givenlevel of leptin on controlled rats. There is different average on the level of leptin on wistar rats’ serum which being obesity on each grouptreatment. The giving of quercetin have significant correlation (p<0.05) with the level of leptin on wistar rats’ serum which being obesity (r = -0.704, p = 0.001). The conclusion from this research is the giving of quercetin to obesity rats for 8 weeks can decline the level of leptin onblood.Keywords: quercetin, leptin, high fat diet


Author(s):  
RAKESH V. MISHRA ◽  
SHASHIKANT N. DHOLE

Objective: The present research aims to design and optimize gastroretentive floating pellets of anagliptin (a dipeptidyl peptidase-4 inhibitor), so as to reduce P-Glycoprotein (PGP)–mediated efflux in the intestine hence to improve oral bioavailability. Methods: The drug-containing core pellets were prepared by extrusion and spheronization process followed by subsequent coating with three successive layers i.e. Eudragit RS 100, sodium bicarbonate (NaHCO3): hydroxypropyl methylcellulose E5LV (HPMC E5LV) and Eudragit RL 100 using fluidized bed processor. A 3 level 3 factor box-behnken design was adopted to investigate the effect of Eudragit RS 100, NaHCO3: HPMC E5LVand Eudragit RL 100 on floating lag time and drug release at 10 h. Desirability function under numerical optimization technique was used to identify the optimum formulation. Results: The study reveals the significant effect of the amount of NaHCO3 and coating level of polymers on floating lag time and drug release. The optimum system could float within 4 min and exhibited more than 85% drug release in 10 h. The pharmacokinetic study conducted in male Wistar rats indicated 2.51 fold increase in relative bioavailability of optimized formulation compare to anagliptin drug. Formulated anagliptin pellets were evaluated in cafeteria diet-induced metabolic syndrome model in male Wistar rats. Anagliptin floating pellets treatment compared to cafeteria diet group significantly inhibited increase in body weight (238.79±2.52 g vs. 277.98±3.69 g, P<0.001), calorie intake (2283.99 kcal vs. 3086.05 kcal, P<0.05) and serum levels of total cholesterol (95.19±0.61 mg/dl vs. 110.04±1.31 mg/dl, P<0.01), triglycerides (96.12±1.25 mg/dl vs. 105.99±1.29 mg/dl, P<0.01) while high-density lipoproteins levels were improved (42.15±0.92 mg/dl vs. 30.92±0.77 mg/dl, P<0.01) indicated its hypophagic and anti-hyperlipidemic effects. Conclusion: The gastroretentive floating pellets of anagliptin was obtained and could be a promising technique to deliver anagliptin with improved bioavailability in the management of the metabolic syndrome.


2016 ◽  
Vol 259 ◽  
pp. S162
Author(s):  
S. Treviño ◽  
A. Diaz ◽  
P. Aguilar-Alonso ◽  
J.A. Flores-Hernández ◽  
E. Brambila

2015 ◽  
Vol 12 (9) ◽  
pp. 11396-11409 ◽  
Author(s):  
Seung Han ◽  
Kyoung Ha ◽  
Ja Jeon ◽  
Hae Kim ◽  
Kwan Lee ◽  
...  

2008 ◽  
Vol 101 (8) ◽  
pp. 1178-1184 ◽  
Author(s):  
Rodrigo Ferreira de Moura ◽  
Carla Ribeiro ◽  
Juliana Aparecida de Oliveira ◽  
Eliane Stevanato ◽  
Maria Alice Rostom de Mello

In search of an adequate model for the human metabolic syndrome, the metabolic characteristics of Wistar rats were analysed after being submitted to different protocols of high fructose ingestion. First, two adult rat groups (aged 90 d) were studied: a control group (C1;n6) received regular rodent chow (Labina, Purina) and a fructose group (F1;n6) was fed on regular rodent chow. Fructose was administered as a 10 % solution in drinking water. Second, two adult rat groups (aged 90 d) were evaluated: a control group (C2;n6) was fed on a balanced diet (AIN-93G) and a fructose group (F2;n6) was fed on a purified 60 % fructose diet. Finally, two young rat groups (aged 28 d) were analysed: a control group (C3;n6) was fed on the AIN-93G diet and a fructose group (F3;n6) was fed on a 60 % fructose diet. After 4–8 weeks, the animals were evaluated. Glucose tolerance, peripheral insulin sensitivity, blood lipid profile and body fat were analysed. In the fructose groups F2 and F3 glucose tolerance and insulin sensitivity were lower, while triacylglycerolaemia was higher than the respective controls C2 and C3 (P < 0·05). Blood total cholesterol, HDL and LDL as well as body fat showed change only in the second protocol. In conclusion, high fructose intake is more effective at producing the signs of the metabolic syndrome in adult than in young Wistar rats. Additionally, diet seems to be a more effective way of fructose administration than drinking water.


2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Norshalizah Mamikutty ◽  
Zar Chi Thent ◽  
Farihah Haji Suhaimi

Background.Nonalcoholic fatty liver disease (NAFLD) is one of the complications of the metabolic syndrome. It encompasses a wide range of disease spectrum from simple steatosis to liver cirrhosis. Structural alteration of hepatic mitochondria might be involved in the pathogenesis of NAFLD.Aims.In the present study, we used a newly established model of fructose-induced metabolic syndrome in male Wistar rats in order to investigate the ultrastructural changes in hepatic mitochondria that occur with fructose consumption and their association with NAFLD pathogenesis.Methods.The concentration of fructose-drinking water (FDW) used in this study was 20%. Six male Wistar rats were supplemented with FDW 20% for eight weeks. Body composition and metabolic parameters were measured before and after 8 weeks of FDW 20%. Histomorphology of the liver was evaluated and ultrastructural changes of mitochondria were assessed with transmission electron micrograph.Results.After 8 weeks of fructose consumption, the animals developed several features of the metabolic syndrome. Moreover, fructose consumption led to the development of macrovesicular hepatic steatosis and mitochondrial ultrastructural changes, such as increase in mitochondrial size, disruption of the cristae, and reduction of matrix density.Conclusion.We conclude that in male Wistar rat 8-week consumption of FDW 20% leads to NAFLD likely via mitochondrial structural alteration.


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