We want to study some antioxidants and assess their relative effectiveness. However we wish to induce oxidative stress preferably using dietary additives.
The attached publications demonstrate the effect of inducing oxidative stress (experimentally) on rats:
1-EPMA J. 2014; 5(1): 2.
Published online 2014 Jan 13. doi: 10.1186/1878-5085-5-2
PMCID: PMC3922789
The efficacy of probiotics for monosodium glutamate-induced obesity: dietology concerns and opportunities for prevention
Oleksandr A Savcheniuk,1 Oleksandr V Virchenko,1 Tetyana M Falalyeyeva,1 Tetyana V Beregova,1 Lidia P Babenko,2 Liudmyla M Lazarenko,2 Olga M Demchenko,3 Rostyslav V Bubnov,corresponding author2,4 and Mykola Ya Spivak
Abstract
Introduction
Obesity becomes endemic today. Monosodium glutamate was proved as obesogenic food additive. Probiotics are discussed to impact on obesity development.
Aims and objectives
The aim was to study the effects of probiotics on the development of monosodium glutamate (MSG)-induced obesity in rats.
Material and methods
We included 45 Wistar male rats and divided into three groups (n = 15). Newborn rats of group 1 (control) received subcutaneously 8 μl/g saline. Group 2 received 3 to 4 mg/g MSG subcutaneously on the second, fourth, sixth, eighth and tenth day of life. Within 4 months after birth, rats were on a standard diet. Group 3 received an aqueous solution of probiotics mixture (2:1:1 Lactobacillus casei IMVB-7280, Bifidobacterium animalis VKL, B. animalis VKB) at the dose of 5 × 109 CFU/kg (50 mg/kg) intragastrically. Administration of probiotics was started at the age of 4 weeks just after weaning and continued for 3 months during 2-week courses. Group 2 received intragastrically 2.5 ml/kg water. Organometric and biochemical parameters in all groups of rats were analyzed over 4 months. The concentration of adiponectin was determined in serum, and leptin - in adipose tissue.
Results
Administration of MSG led to the development of obesity in rats; body weight had increased by 7.9% vs controls (p < 0.05); body length had increased by 5.4% (p < 0.05). Body mass index and Lee index and visceral fat mass had increased (p < 0.001). Under the neonatal injection of MSG, the concentration of total cholesterol, triglycerides, VLDL cholesterol and LDL cholesterol significantly increased (p < 0.001), in comparison with controls. Adipose-derived hormones changed in MSG obesity rats: adiponectin decreased by 58.8% (p < 0.01), and leptin concentration in adipose tissue had increased by 74.7% (p < 0.01). The probiotic therapy of rats from group 3 prevented obesity development. Parameters of rats treated with probiotic mixture did not differ from that in the control.
Conclusions
The introduction of MSG to newborn rats caused the obesity in adulthood. Periodic administration of probiotic mixture to rat injected with MSG neonatally resulted in recovery of lipid metabolism and prevention of the obesity development.
3- itation: Clinical and Translational Gastroenterology (2013) 4, e39; doi:10.1038/ctg.2013.11
Published online 11 July 2013
Functional GI Disorders
The Effect of High-Fat Diet-Induced Pathophysiological Changes in the Gut on Obesity: What Should be the Ideal Treatment?
Open
Chooi Y Lee PhD1
Abstract
Obesity is a metabolic disorder and fundamental cause of other fatal diseases including atherosclerosis and cancer. One of the main factor that contributes to the development of obesity is high-fat (HF) consumption. Lipid ingestion will initiate from the gut feedback mechanisms to regulate glucose and lipid metabolisms. But these lipid-sensing pathways are impaired in HF-induced insulin resistance, resulting in hyperglycemia. Besides that, duodenal lipid activates mucosal mast cells, leading to the disruption of the intestinal tight junction. Lipopolysaccharide that is co-transited with dietary fat postprandially, promotes the release of cytokines and the development of metabolic syndrome. HF-diet also alters microbiota composition and enhances fat storage. Although gut is protected by immune system and contains high level of antioxidants, obesity developed presumably when this protective mechanism is compromised by the presence of excessive fat. Several therapeutic approaches targeting different pathways have been proposed. There may be no one single most effective treatment, but all aimed to prevent obesity. This review will elaborate on the physiological and molecular changes in the gut that lead to obesity, and will provide a summary of potential treatments to manage these pathophysiological changes.
The attached publications demonstrate the effect of inducing oxidative stress (experimentally) on rats:
1-EPMA J. 2014; 5(1): 2.
Published online 2014 Jan 13. doi: 10.1186/1878-5085-5-2
PMCID: PMC3922789
The efficacy of probiotics for monosodium glutamate-induced obesity: dietology concerns and opportunities for prevention
Oleksandr A Savcheniuk,1 Oleksandr V Virchenko,1 Tetyana M Falalyeyeva,1 Tetyana V Beregova,1 Lidia P Babenko,2 Liudmyla M Lazarenko,2 Olga M Demchenko,3 Rostyslav V Bubnov,corresponding author2,4 and Mykola Ya Spivak
Abstract
Introduction
Obesity becomes endemic today. Monosodium glutamate was proved as obesogenic food additive. Probiotics are discussed to impact on obesity development.
Aims and objectives
The aim was to study the effects of probiotics on the development of monosodium glutamate (MSG)-induced obesity in rats.
Material and methods
We included 45 Wistar male rats and divided into three groups (n = 15). Newborn rats of group 1 (control) received subcutaneously 8 μl/g saline. Group 2 received 3 to 4 mg/g MSG subcutaneously on the second, fourth, sixth, eighth and tenth day of life. Within 4 months after birth, rats were on a standard diet. Group 3 received an aqueous solution of probiotics mixture (2:1:1 Lactobacillus casei IMVB-7280, Bifidobacterium animalis VKL, B. animalis VKB) at the dose of 5 × 109 CFU/kg (50 mg/kg) intragastrically. Administration of probiotics was started at the age of 4 weeks just after weaning and continued for 3 months during 2-week courses. Group 2 received intragastrically 2.5 ml/kg water. Organometric and biochemical parameters in all groups of rats were analyzed over 4 months. The concentration of adiponectin was determined in serum, and leptin - in adipose tissue.
Results
Administration of MSG led to the development of obesity in rats; body weight had increased by 7.9% vs controls (p < 0.05); body length had increased by 5.4% (p < 0.05). Body mass index and Lee index and visceral fat mass had increased (p < 0.001). Under the neonatal injection of MSG, the concentration of total cholesterol, triglycerides, VLDL cholesterol and LDL cholesterol significantly increased (p < 0.001), in comparison with controls. Adipose-derived hormones changed in MSG obesity rats: adiponectin decreased by 58.8% (p < 0.01), and leptin concentration in adipose tissue had increased by 74.7% (p < 0.01). The probiotic therapy of rats from group 3 prevented obesity development. Parameters of rats treated with probiotic mixture did not differ from that in the control.
Conclusions
The introduction of MSG to newborn rats caused the obesity in adulthood. Periodic administration of probiotic mixture to rat injected with MSG neonatally resulted in recovery of lipid metabolism and prevention of the obesity development.
3- itation: Clinical and Translational Gastroenterology (2013) 4, e39; doi:10.1038/ctg.2013.11
Published online 11 July 2013
Functional GI Disorders
The Effect of High-Fat Diet-Induced Pathophysiological Changes in the Gut on Obesity: What Should be the Ideal Treatment?
Open
Chooi Y Lee PhD1
Abstract
Obesity is a metabolic disorder and fundamental cause of other fatal diseases including atherosclerosis and cancer. One of the main factor that contributes to the development of obesity is high-fat (HF) consumption. Lipid ingestion will initiate from the gut feedback mechanisms to regulate glucose and lipid metabolisms. But these lipid-sensing pathways are impaired in HF-induced insulin resistance, resulting in hyperglycemia. Besides that, duodenal lipid activates mucosal mast cells, leading to the disruption of the intestinal tight junction. Lipopolysaccharide that is co-transited with dietary fat postprandially, promotes the release of cytokines and the development of metabolic syndrome. HF-diet also alters microbiota composition and enhances fat storage. Although gut is protected by immune system and contains high level of antioxidants, obesity developed presumably when this protective mechanism is compromised by the presence of excessive fat. Several therapeutic approaches targeting different pathways have been proposed. There may be no one single most effective treatment, but all aimed to prevent obesity. This review will elaborate on the physiological and molecular changes in the gut that lead to obesity, and will provide a summary of potential treatments to manage these pathophysiological changes.
Thanks Rafik for the answer. I will investigate the third option. But basically these and other compounds may induce other pathways too. We are looking for some more specific oxidative stress inducers. Doxorubicin was also suggested to us as a useful inducer. Has anyone used this compound for induction of oxidative stress?