Oral Subacute Exposure to Cadmium LOAEL Dose Induces Insulin Resistance and Impairment of the Hormonal and Metabolic Liver-Adipose Axis in Wistar Rats

Author(s):  
Victor Enrique Sarmiento-Ortega ◽  
Diana Moroni-González ◽  
Alfonso Díaz ◽  
Brambila Eduardo ◽  
Treviño Samuel
Author(s):  
Elvine P. Nguelefack-Mbuyo ◽  
Fernande P. Peyembouo ◽  
Christian K. Fofié ◽  
Télesphore B. Nguelefack

Abstract Objectives Dexamethasone is used experimentally to induce insulin resistance and type 2 diabetes. However, data concerning the dose, the duration of treatment, and the associated comorbidities are inconsistent. The aim of this study was to compare the effects of different doses of dexamethasone and the duration of treatment necessary for the development of a model of insulin resistance that mimics the clinical condition with the associated comorbidities. Methods Dexamethasone was administered intramuscularly to male Wistar rats, at doses of 500 and 1,000 µg/kg/day for the subchronic treatment (eight consecutive days) and at doses of 5, 25, 50, and 100 µg/kg/day in chronic treatment (28 consecutive days). Effects on body weight, metabolism, hemodynamics, renal function, and redox status were evaluated. Results Both treatments induced a progressive body weight loss that was drastic in subchronic treatment, improved glucose tolerance without affecting fasting glycemia. Doses of 1,000 and 100 µg/kg were associated with hypertriglyceridemia, hypertension, and increased heart rate, cardiac and renal hypertrophy. Increased creatinemia associated with reduced creatinuria were observed in sub-chronic treatment while increased proteinuria and reduced creatinuria were noticed in chronic treatment. 1,000 µg/kg dexamethasone caused an increase in hepatic, and renal malondialdehyde (MDA) and glutathione (GSH) coupled with a reduction in catalase activity. The dose of 100 µg/kg induced a rise in GSH and catalase activity but reduced MDA levels in the kidney. Conclusions Doses of 1,000 µg/kg for subchronic and 100 µg/kg for chronic treatment exhibited similar effects and are the best doses to respective time frames to induce the model.


Author(s):  
Shehu-Tijani Toyin Shittu ◽  
Taye Jemilat Lasisi ◽  
Seyid Alli-Sisse Shittu ◽  
Adeyinka Adeyemi ◽  
Tolulope James Adeoye ◽  
...  

Appetite ◽  
2016 ◽  
Vol 96 ◽  
pp. 604-610 ◽  
Author(s):  
Kelly Carraro Foletto ◽  
Bruna Aparecida Melo Batista ◽  
Alice Magagnin Neves ◽  
Fernanda de Matos Feijó ◽  
Cíntia Reis Ballard ◽  
...  

2008 ◽  
Vol 4 (3) ◽  
pp. 176-180
Author(s):  
Mohammad Jafar Golalipour ◽  
Anneh Mohammad Gharravi ◽  
Abbas Ali Keshtkar ◽  
Abdoljalal Marjani

2011 ◽  
Vol 26 (suppl 2) ◽  
pp. 45-50 ◽  
Author(s):  
Gabriela S. F. Castro ◽  
João F. R. Cardoso ◽  
Helio Vannucchi ◽  
Sérgio Zucoloto ◽  
Alceu Afonso Jordão

PURPOSE: The increase in fructose consumption is paralleled by a higher incidence of obesity worldwide. This monosaccharide is linked to metabolic syndrome, being associated with hypertriglyceridemia, hypertension, insulin resistance and diabetes mellitus. It is metabolized principally in the liver, where it can be converted into fatty acids, which are stored in the form of triglycerides leading to NAFLD. Several models of NAFLD use diets high in simple carbohydrates. Thus, this study aimed to describe the major metabolic changes caused by excessive consumption of fructose in humans and animals and to present liver abnormalities resulting from high intakes of fructose in different periods of consumption and experimental designs in Wistar rats. METHODS: Two groups of rats were fasted for 48 hours and reefed for 24 or 48 hours with a diet containing 63% fructose. Another group of rats was fed an diet with 63% fructose for 90 days. RESULTS: Refeeding for 24 hours caused accumulation of large amounts of fat, compromising 100% of the hepatocytes. The amount of liver fat in animals refed for 48 hours decreased, remaining mostly in zone 2 (medium-zonal). In liver plates of Wistar rats fed 63% fructose for 45, 60 and 90 days it's possible to see that there is an increase in hepatocytes with fat accumulation according to the increased time; hepatic steatosis, however, is mild, compromising about 20% of the hepatocytes. CONCLUSIONS: Fructose is highly lipogenic, however the induction of chronic models in NAFLD requires long periods of treatment. The acute supply for 24 or 48 hours, fasted rats can cause big changes, liver steatosis with macrovesicular in all lobular zones.


2017 ◽  
Vol 26 (3) ◽  
pp. 261-267 ◽  
Author(s):  
Hideki Tanaka ◽  
Kumiko Nakai ◽  
Fumiko Murakami ◽  
Toyoko Morita ◽  
Yoji Yamazaki ◽  
...  

2018 ◽  
Vol 7 (4) ◽  
pp. 516-524
Author(s):  
Anoka A. Njan ◽  
Chloe O. Fatigun ◽  
Abdul-Musawwir Alli-Oluwafuyi ◽  
Olufunke E. Olorundare ◽  
Olarenwaju S. Afolabi ◽  
...  

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3070
Author(s):  
Halina Zofia Staniek ◽  
Ewelina Król ◽  
Rafał Wojciech Wójciak

The aim of the study was to evaluate the main and interactive effects of chromium(III) propionate complex (Cr3) supplementation and different iron supply on the carbohydrate metabolism, lipid profile and other selected biochemical parameters of rats. The experiment was carried out in a two-factor design, in which rats were fed a diet with different proportions of Fe(III) and Cr(III) for six weeks. Fifty-four healthy female Wistar rats were divided into nine experimental groups with different Fe(III) levels, i.e. adequate—control group (45 mg/kg)—100% recommended daily dietary dose of Fe for rodents, deficient (5 mg/kg) and oversupply (180 mg/kg—400%). At the same time they were supplemented with Cr(III) of doses 1 (adequate), 50 and 500 mg/kg of diet. The activity and concentrations of most biochemical parameters were measured with standard enzymatic, kinetic, and colorimetric methods. HOMA-IR and QUICKI indexes were calculated according to appropriate formulas. It was found that there was an interactive effect of high Cr(III) doses and different Fe(III) levels in the diet on the carbohydrate metabolism and insulin resistance indexes. The presented results suggested that iron deficient diet fed animals led to insulin resistance; however, an effect is attenuated by Cr(III) supplementation at high doses. There were no significant changes in the rats’ lipid profile (except for the high density lipoprotein cholesterol (HDL-C) level) and most of the other biochemical parameters, such as the leptin, aspartate aminotransferase (AST), alanine transaminase (ALT), total protein (TP), creatinine (Crea) and the urea (BUN) concentrations. The study proved that the Cr(III) supplementation, independently and in combination with diversified Fe(III) content in the diet, affected the carbohydrate metabolism and insulin resistance indexes but did not affect lipid profile and most of the other biochemical parameters in healthy rats. The findings proved the role of Fe and Cr(III) and their interactions on disturbances carbohydrates metabolism.


Sign in / Sign up

Export Citation Format

Share Document