Insulin resistance induced by high-fructose diet potentiates carbon tetrachloride hepatotoxicity

2010 ◽  
Vol 26 (2) ◽  
pp. 89-104 ◽  
Author(s):  
M. Pooranaperundevi ◽  
MS Sumiyabanu ◽  
P. Viswanathan ◽  
R. Sundarapandiyan ◽  
CV Anuradha

Insulin resistance (IR) is recognized as a contributory factor for a variety of liver diseases. The present study investigates the susceptibility of liver to the toxic actions of carbon tetrachloride (CCl4) in a rat model of IR, induced by feeding a high-fructose diet (60 g/100 g) for 30 days. A sub-lethal dose of CCl4 (2 mL/kg intraperitoneally [i.p.], in corn oil) was administered and the outcome of hepatotoxicity was assessed at 0 hour and at 6, 12, 24 and 36 hours after CCl4 administration. After 30 days of fructose feeding, the rats showed IR, decline in liver antioxidant status and rise in lipid peroxidation. Liver dysfunction in fructose-fed rats was evident from a rise in transaminases, total bilirubin and a decrease in albumin/globulin ratio in plasma and decreases in nitrite, arginase and increase in protein carbonyl and nitrosothiol content in liver. Increased staining for 3-nitro tyrosine (3-NT) antibody was observed in fructose-fed rat liver as compared to control. CCl4 (2 mL/kg) caused 100% mortality in fructose-fed rats within 48 hours, while no death of animals occurred in control. CCl 4 caused liver damage in both control and fructose-fed rats. Time-based studies showed that progressive liver injury occurred only in fructose-fed rats from 0, 6, 12, 24 hours, with a peak at 36 hours. In control diet—fed rats, the extent of damage was maximum at 24 hours, which declined at 36 hours. Thus, the toxic effects of CCl4 are potentiated due to compromised liver function in the setting of IR.

2021 ◽  
Author(s):  
Ryohei Nishiguchi ◽  
Srijani Basu ◽  
Hannah A Staab ◽  
Naotake Ito ◽  
Xi Kathy Zhou ◽  
...  

Abstract Diet is believed to be an important factor in the pathogenesis of Inflammatory Bowel Disease. High consumption of dietary fructose has been shown to exacerbate experimental colitis, an effect mediated through the gut microbiota. This study evaluated whether dietary alterations could attenuate the detrimental effects of a high fructose diet (HFrD) in experimental colitis. First, we determined whether the pro-colitic effects of a HFrD could be reversed by switching mice from a HFrD to a control diet. This diet change completely prevented HFrD-induced worsening of acute colitis, in association with a rapid normalization of the microbiota. Second, we tested the effects of dietary fiber, which demonstrated that psyllium was the most effective type of fiber for protecting against HFrD-induced worsening of acute colitis, compared to pectin, inulin or cellulose. In fact, supplemental psyllium nearly completely prevented the detrimental effects of the HFrD, an effect associated with a shift in the gut microbiota. We next determined whether the protective effects of these interventions could be extended to chronic colitis and colitis-associated tumorigenesis. Using the azoxymethane/dextran sodium sulfate model, we first demonstrated that HFrD feeding exacerbated chronic colitis and increased colitis-associated tumorigenesis. Using the same dietary changes tested in the acute colitis setting, we also showed that mice were protected from HFrD-mediated enhanced chronic colitis and tumorigenesis, upon either diet switching or psyllium supplementation. Taken together, these findings suggest that high consumption of fructose may enhance colon tumorigenesis associated with long-standing colitis, an effect that could be reduced by dietary alterations.


Marine Drugs ◽  
2015 ◽  
Vol 13 (4) ◽  
pp. 1864-1881 ◽  
Author(s):  
Gabriela Salim de Castro ◽  
Rafael Deminice ◽  
Livia Cordeiro Simões-Ambrosio ◽  
Philip C. Calder ◽  
Alceu A. Jordão ◽  
...  

2020 ◽  
Vol ahead-of-print (ahead-of-print) ◽  
Author(s):  
Yasmina Bahlil ◽  
Djamil Krouf ◽  
Zoheir Mellouk ◽  
Nawal Taleb-Dida ◽  
Akila Guenzet

Purpose This study aims to examine whether Globularia alypum (Ga) lyophilized aqueous leaves extract treatment improves cardiometabolic syndromes such as hyperglycemia, lipid profiles and oxidative damage resulting from a high-fructose diet induced in hypertriglyceridemic rats. Design/methodology/approach A total of 24 male Wistar rats weighing 80 ± 5 g were first randomly divided into 2 groups. A total of 12 control rats (C) were fed a standard-diet (St-D) and 12 high fructose (HF) rats were fed a high-fructose diet (HF-D) containing St-D in which cornstarch was substituted by fructose (61.4%). After 15 weeks of feeding, body weight (BW) was about 320 ± 20 g and hypertriglyceridemia was noted in HF vs C group (2.69 ± 0.49 mmol/L) vs (1.25 ± 0.33 mmol/L). Each group of rats was then divided into two equal groups (n = 6) and fed during four weeks either a St-D or HF-D, treated or not with 1% of Ga extract (C-Ga) and (HF-Ga). After 28 days, fasting rats were anesthetized and blood and tissues were removed to measure biochemical parameters. Findings The results showed no significant differences in BW and insulinemia between all groups. Ga extract supplementation reduced glycemia (−36%), glycosylated hemoglobin (−37%), Homeostasis Model of Assessment-Insulin Resistance index (−34%) and triacylglycerol’s contents in plasma (−33%), very low density lipoproteins–low density lipoproteins (VLDL-LDL) (−48%), liver (−52%) and aorta (−39%); total cholesterol concentrations in aorta was 3.7-fold lower in HF-Ga vs HF group. Ga treatment reduced lipid peroxidation in plasma, VLDL-LDL, red blood cells (RBC), liver, muscle and kidney by improving superoxide dismutase (SOD) activity and glutathione peroxidase (GPx) in RBC and catalase (CAT) activity in kidney (p < 0.05). Moreover, Ga ameliorates glutathione (GSH) production in RBC (+41%) and kidney tissues (+35%). Originality/value Ga extract ameliorated cardiometabolic syndrome by its hypotriglyceridemic effect and prevented development of insulin resistance. It reduces lipid peroxidation by enhancing non-enzymatic (GSH) and enzymatic (SOD, GPx and CAT) antioxidant defense systems in high-fructose hypertriglyceridemic rats. Therefore, supplementation of Ga leaves extract as an adjuvant could be used for the treatment of hypertriglyceridemia and the prevention and/or the management of cardio-metabolic adverse effects.


2020 ◽  
Vol 160 ◽  
pp. 105191
Author(s):  
Hui-Juan Zhang ◽  
Cheng Chen ◽  
Lin Ding ◽  
Hao-Hao Shi ◽  
Cheng-Cheng Wang ◽  
...  

2020 ◽  
Vol 19 (10) ◽  
pp. 2137-2146
Author(s):  
Beatrice N. Kiage-Mokua ◽  
Michael De Vrese ◽  
Ina Kraus-Stojanowic ◽  
Annegret Nielsen ◽  
Patrick Kareru ◽  
...  

Purpose: To examine the potential of extracts from selected herbs used in African traditional medicine in diabetes patients, and to determine their effect on traits of metabolic syndrome in rats fed a high-fat and high-fructose diet.Methods: Ethanol and aqueous extracts were prepared from Mangifera indica (MI), Lonchocarpus eriocalyx (LE), Urtica massaica (UM), Schkuhria pinnata (SP) and Launaea cornuta (LC). Ethanol extracts (1:100 dilution) were examined for inhibition of pancreatic lipase and α-glucosidase activity invitro. Furthermore, aqueous extracts were administered for 74 days to male Wistar rats fed a high-fat and high-fructose diet to assess their effect on traits of metabolic syndrome.Results: Ethanol extracts showed at least 30 % inhibition of pancreatic lipase in vitro but no effect on α- glucosidase activity. Administration of the aqueous extracts caused significant reduction in liver triglycerides (except for LE). Muscle triglycerides and fat were also reduced, with the most pronounced effect elicited by LE. Urinary glucose excretion and plasma triglycerides, but not hyperinsulinemia and insulin resistance, were reduced by UM compared to control.Conclusion: This exploratory study indicates that UM may be considered a candidate for the prevention and management of type 2 diabetes. Keywords: Kenyan traditional medicine, High-fat diet, High fructose, Insulin resistance, Triglycerides, Diabetes, Liver steatosis


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