Protective and curative effects of Bacillus subtilis SPB1 biosurfactant on high-fat-high-fructose diet induced hyperlipidemia, hypertriglyceridemia and deterioration of liver function in rats

Zouari, Raida; Hamden, Khaled; Feki, Abdelfattah El; Chaabouni, Khansa; Makni‐Ayadi, Fatma; Kallel, Choumous; Sallemi, Fahima; Ellouze-Chaâbouni, Semia; Ghribi-Aydi, Dhouha

doi:10.1016/j.biopha.2016.09.023

Cited by 34 publications

(35 citation statements)

References 22 publications

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“…in male Sprague Dawley rats (350–360 g upon commencement of the feeding period), following 13 weeks of high‐fructose, high‐fat diet feeding (25% fructose and 25% lard in the diet) compared to those on a control diet. Zouari et al . also observed significant hypercholesterolemia in male, Wistar rats fed a high‐fructose, high‐fat diet (10% fructose and 10% sheep fat in the diet) for a period of 75 days compared to those receiving the control diet.…”

Section: Discussionmentioning

confidence: 91%

“…Significantly increased serum total cholesterol concentrations were also observed by Wang et al 23 in male Sprague Dawley rats (350-360 g upon commencement of the feeding period), following 13 weeks of high-fructose, high-fat diet feeding (25% fructose and 25% lard in the diet) compared to those on a control diet. Zouari et al 30 also observed significant hypercholesterolemia in male, Wistar rats fed a high-fructose, high-fat diet (10% fructose and 10% sheep fat in the diet) for a period of 75 days compared to those receiving the control diet. In the current study, both quercetin and fenofibrate were not successful in ameliorating the high-fructose, high-cholesterol diet-induced hypercholesterolemia.…”

Section: Discussionmentioning

confidence: 92%

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Quercetin administration post‐weaning attenuates high‐fructose, high‐cholesterol diet‐induced hepatic steatosis in growing, female, Sprague Dawley rat pups

et al. 2019

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BACKGROUND Fructose and cholesterol‐rich diets have been implicated in the upsurge of metabolic syndrome (MetS). Phytochemicals are being explored as alternatives for the prevention and management of MetS. Thirty‐six 21‐day‐old, female Sprague Dawley rats fed a high‐fructose, high‐cholesterol diet post‐weaning were used to investigate the prophylactic potential of quercetin. Group 1 was given standard rat chow (SRC); Group 2: SRC and quercetin (75 mg kg−1 daily); Group 3: SRC and fenofibrate (100 mg kg−1 daily); Group 4 was given a high cholesterol diet (HCD) (2% added dietary cholesterol in SRC), 20% fructose drinking solution (FS); Group 5 was given HCD, 20% FS and quercetin (75 mg kg−1 daily); Group 6: HCD, 20% FS and fenofibrate (100 mg kg−1 daily). Rats were fed ad libitum for 8 weeks, euthanized, and blood and liver samples were collected. RESULTS The HCD and FS significantly increased (P < 0.05) absolute and relative liver masses and serum cholesterol. Fasting blood glucose, serum triglycerides, alanine transaminase, creatinine, and urea were not significantly different (P > 0.05) between groups. The HCD and FS significantly increased liver lipid yield compared to the SRC and rats receiving SRC with fenofibrate (P < 0.05). Quercetin or fenofibrate together with HCD and FS attenuated the diet‐induced increase in liver lipids by approximately 50%, although this was not statistically significant. Liver macro‐ and micro‐steatosis scores were significantly increased (P < 0.05) in rats receiving HCD and FS. Quercetin or fenofibrate administration together with HCD and FS significantly decreased (P < 0.05) liver macro‐steatosis scores. CONCLUSION The prophylactic effect of quercetin on fructose and cholesterol diet‐induced liver lipid accumulation may be exploited in the fight against non‐alcoholic fatty liver disease (NAFLD). © 2019 Society of Chemical Industry

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 92%

Quercetin administration post‐weaning attenuates high‐fructose, high‐cholesterol diet‐induced hepatic steatosis in growing, female, Sprague Dawley rat pups

et al. 2019

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“…), antifungal activity against phytopathogenic fungi (Mnif and Ghribi ) and antidiabetic and antilipidemic properties in alloxan‐induced diabetic rats (Zouari et al . ).…”

Section: Health‐related Applicationsmentioning

confidence: 97%

Microbial biosurfactants: current trends and applications in agricultural and biomedical industries

et al. 2019

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Synthetic surfactants are becoming increasingly unpopular in many applications due to previously disregarded effects on biological systems and this has led to a new focus on replacing such products with biosurfactants that are biodegradable and produced from renewal resources. Microbially derived biosurfactants have been investigated in numerous studies in areas including: increasing feed digestibility in an agricultural context, improving seed protection and fertility, plant pathogen control, antimicrobial activity, antibiofilm activity, wound healing and dermatological care, improved oral cavity care, drug delivery systems and anticancer treatments. The development of the potential of biosurfactants has been hindered somewhat by the myriad of approaches taken in their investigations, the focus on pathogens as source species and the costs associated with large‐scale production. Here, we focus on various microbial sources of biosurfactants and the current trends in terms of agricultural and biomedical applications.

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“…During insulin resistance (IR), proteins associated with this signaling pathway are abnormally modified, which may therefore serve as intracellular markers for hypoglycemia ( 16 , 17 ). HFSD has also been suggested to induce dysfunction in lipid metabolism ( 18 ). In addition, previous studies have revealed that an HFSD results in free fatty acid accumulation, which may be toxic and trigger the mitogen activated protein kinase (MAPK) inflammation signaling pathway, resulting in the increase of interleukin (IL)6 and tumor necrosis factor (TNF)α, which may lead to insulin signaling pathway damage, exacerbating IR ( 1 ).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of type 2 diabetic mellitus animal models via interactions between insulin and mitogen‑activated protein kinase signaling pathways induced by a high fat and sugar diet and streptozotocin

Zhuo

Zeng

Cai³

et al. 2018

Mol Med Report

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Type 2 diabetic mellitus (T2DM), which is characterized by insulin resistance (IR), hyperglycemia and hyperlipidemia, is a comprehensive dysfunction of metabolism. The insulin receptor (INSR)/phosphoinositide 3-kinase (PI3K)/AKT signaling pathway is well acknowledged as a predominant pathway associated with glucose uptake; however, the effect of streptozotocin (STZ) plus a high fat and sugar diet (HFSD) on the proteins associated with this pathway requires further elucidation. In order to explore this effect, a T2DM rat model was constructed to investigate T2DM pathogenesis and potential therapeutic advantages. Rats were randomly divided into control and model groups, including normal diet (ND) and HFSD types. ND types were administered intraperitoneal (IP) injections of STZ (35 mg/kg) or a combination of STZ and alloxan monohydrate (AON) (40 mg/kg), whereas HFSD types were composed of HFSD pre-given, post-given and simul-given groups, and were modeled as follows: IP or intramuscular (IM) injection of STZ (35 mg/kg) or a combination of STZ and AON (40 mg/kg). Results indicated that, compared with controls, blood glucose, insulin, homeostatic model assessment-insulin resistance and total triglyceride were significantly elevated in groups with HFSD and modeling agents (P<0.05 or P<0.01), whereas total cholesterol and low-density lipoprotein levels were significantly elevated in groups simultaneously administered HFSD and modeling agents (P<0.05 or P<0.01), in addition to downregulation of the expression of insulin signaling pathway proteins in the liver, including INSR, PI3K, AKT1, phosphatidylinositol-5-phosphate 4-kinase type-2α (PIP5Kα) and glucose transporter (GLUT)2, and increased expression of inflammatory factors, including p38, tumor necrosis factor (TNF)α and interleukin (IL)6. Furthermore, compared with other two HFSD types including pre-given and post-given group, the simul-given group that received IM injection with STZ exhibited decreased expression levels of major insulin signal pathway proteins INSR, PI3K, AKT1, PIP5Kα, GLUT2 or GLUT4 in the liver and pancreas (P<0.05 or P<0.01), whereas the opposite was observed in the skeletal muscle. In addition, the protein expression levels of phosphorylated-p38, p38, IL6 and TNFα in the simul-given group that received IM injection with STZ were increased (P<0.05 or P<0.01), and histopathology also indicated inflammation in pancreas and liver. The present findings suggest that a low dose of STZ may partially impair the β cells of the pancreas, whereas long-term excess intake of HFSD may increase lipid metabolites, inhibit the insulin signaling pathway and activate the mitogen-activated protein kinase p38 signaling pathway. The combined action of STZ and AON may result in insulin resistance, which ultimately results in abnormalities in glucose and lipid metabolism. The present model, analogue to T2DM onset of humans, evaluated the medical effect on metabolic dysfunction and provides an insight into the underlining mechanism of IR.

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Protective and curative effects of Bacillus subtilis SPB1 biosurfactant on high-fat-high-fructose diet induced hyperlipidemia, hypertriglyceridemia and deterioration of liver function in rats

Cited by 34 publications

References 22 publications

Quercetin administration post‐weaning attenuates high‐fructose, high‐cholesterol diet‐induced hepatic steatosis in growing, female, Sprague Dawley rat pups

Quercetin administration post‐weaning attenuates high‐fructose, high‐cholesterol diet‐induced hepatic steatosis in growing, female, Sprague Dawley rat pups

Microbial biosurfactants: current trends and applications in agricultural and biomedical industries

Evaluation of type 2 diabetic mellitus animal models via interactions between insulin and mitogen‑activated protein kinase signaling pathways induced by a high fat and sugar diet and streptozotocin

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