Improvement in glucose tolerance and insulin sensitivity by probiotic strains of Indian gut origin in high-fat diet-fed C57BL/6J mice

Balakumar, Mahalingam; Prabhu, Durai; Chandrakumar, Sathishkumar; Prabu, Paramasivam; Rokana, Namita; Kumar, Ramesh; Raghavan, Srividhya; Soundarajan, Avinash; Grover, Sunita; Batish, V. K.; Mohan, Viswanathan; Balasubramanyam, Muthuswamy

doi:10.1007/s00394-016-1317-7

Cited by 161 publications

(156 citation statements)

References 57 publications

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“…In the present study, the glucose tolerance was unimpaired and the huge increases in HOMA‐IR was abrogated in HFD/STZ‐T2DM rats fed on L. paracasei NL41, suggesting that oral administration of live probiotic strain NL41 could prevent or delay the onset of T2DM by ameliorating insulin resistance. Previous studies have reported that a diet supplemented with L. casei strain CCFM419 increases glucose tolerance in HFD/STZ‐induced T2DM rats, L. rhamnosus GG improves glucose tolerance in STZ‐induced diabetic rats and that the impaired glucose tolerance in HFD‐fed mice is alleviated by L. fermentum strain MTCC 5689 administration, consistent with our studies. PI3K/Akt signalling pathway plays a crucial role in insulin action to regulate glucose and lipid metabolism and a long‐term HFD blunts this pathway .…”

Section: Discussionsupporting

confidence: 92%

Ameliorative Effects of Probiotic Lactobacillus paracasei NL41 on Insulin Sensitivity, Oxidative Stress, and Beta‐Cell Function in a Type 2 Diabetes Mellitus Rat Model

Zeng

Yuan

et al. 2019

Molecular Nutrition Food Res

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Scope The present study aims to assess the antidiabetic effect of Lactobacillus paracasei strain NL41 and its potential mechanisms in rats with type 2 diabetes mellitus (T2DM) induced by a high‐fat diet and low‐dose streptozotocin administration (HFD/STZ). Methods and results Eighteen Sprague–Dawley (SD) rats are randomly assigned to three groups: one control, one HFD/STZ model, and one HFD/STZ‐Lactobacillus protection group with administration of strain NL41 for 12 weeks. Blood is collected for biochemical parameters analysis and tissue samples for histological analysis. Treatment with strain NL41 results in excellent blood glucose regulation and significantly decreases insulin resistance, and HbA1c, glucagon, and leptin levels, accompanied by remarkable improvement of dyslipidemia and oxidative stress status in the animals. Islets of Langerhans, liver, and kidney are significantly protected in the NL41‐treated rats compared to the HFD/STZ‐T2DM model rats. Histochemistry shows that strain NL41 inhibits beta‐cell loss and alpha‐cell expansion, indicating pancreatic islets as the targeted tissues for the primary ameliorative effect of the probiotic strain on HFD/STZ‐T2DM rats. Crosstalk between the gut–liver and liver–pancreas endocrine axes is discussed. Conclusion Probiotic strain NL41 prevents HFD/STZ‐T2DM by decreasing insulin resistance and oxidative stress status, and protecting beta‐cell function.

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Section: Discussionsupporting

confidence: 92%

Ameliorative Effects of Probiotic Lactobacillus paracasei NL41 on Insulin Sensitivity, Oxidative Stress, and Beta‐Cell Function in a Type 2 Diabetes Mellitus Rat Model

Zeng

Yuan

et al. 2019

Molecular Nutrition Food Res

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“…Furthermore, a meta-analysis suggests that the supplementation of probiotics has a modest effect on the serum level of fasting blood sugar as well as oxidative stress biomarkers [211]. Mechanisms that have been proposed are as follows: improved intestinal integrity, decreased systemic lipopolysaccharide levels, decreased endoplasmic reticulum stress and improved peripheral insulin sensitivity [204,212]. Data from clinical studies and animal models have shown a reduction in lipopolysaccharide translocation, endotoxemia and inflammation, reducing stimulation of the proinflammatory genes like tumor necrosis factor alpha (TNF-α), IL-6 and IL-1β [204,213].…”

Section: Probiotic Administration Microbiota Bile Acids and Cardiovmentioning

confidence: 99%

The Gut Microbiota and Its Implication in the Development of Atherosclerosis and Related Cardiovascular Diseases

et al. 2020

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The importance of gut microbiota in health and disease is being highlighted by numerous research groups worldwide. Atherosclerosis, the leading cause of heart disease and stroke, is responsible for about 50% of all cardiovascular deaths. Recently, gut dysbiosis has been identified as a remarkable factor to be considered in the pathogenesis of cardiovascular diseases (CVDs). In this review, we briefly discuss how external factors such as dietary and physical activity habits influence host-microbiota and atherogenesis, the potential mechanisms of the influence of gut microbiota in host blood pressure and the alterations in the prevalence of those bacterial genera affecting vascular tone and the development of hypertension. We will also be examining the microbiota as a therapeutic target in the prevention of CVDs and the beneficial mechanisms of probiotic administration related to cardiovascular risks. All these new insights might lead to novel analysis and CVD therapeutics based on the microbiota.

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“…This microbiota transfer could alter the microbial community in the upper small intestine, contributing to this insulin-sensitizing effect. Similarly, pre-and probiotics improve glucose regulation and robustly alter distal intestinal and fecal microbiota of rodents and humans (Balakumar et al, 2016;Cani et al, 2006a;Ejtahed et al, 2012;Everard and Cani, 2013); however, these substances must first pass the upper small intestine where they could elicit their glucoregulatory effects. This is in line with the fact that most probiotics are derived from Lactobacillus (Asemi et al, 2013;Balakumar et al, 2016;Ejtahed et al, 2012;Yadav et al, 2007), which is a prominent inhabitor of the small intestine (Gu et al, 2013;Wirth et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Lactobacillus gasseri in the Upper Small Intestine Impacts an ACSL3-Dependent Fatty Acid-Sensing Pathway Regulating Whole-Body Glucose Homeostasis

et al. 2018

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Long-chain acyl-CoA synthetase (ACSL)-dependent upper small intestinal lipid metabolism activates pre-absorptive pathways to regulate metabolic homeostasis, but whether changes in the upper small intestinal microbiota alter specific fatty acid-dependent pathways to impact glucose homeostasis remains unknown. We here first find that upper small intestinal infusion of Intralipid, oleic acid, or linoleic acid pre-absorptively increases glucose tolerance and lowers glucose production in rodents. High-fat feeding impairs pre-absorptive fatty acid sensing and reduces upper small intestinal Lactobacillus gasseri levels and ACSL3 expression. Transplantation of healthy upper small intestinal microbiota to high-fat-fed rodents restores L. gasseri levels and fatty acid sensing via increased ACSL3 expression, while L. gasseri probiotic administration to non-transplanted high-fat-fed rodents is sufficient to restore upper small intestinal ACSL3 expression and fatty acid sensing. In summary, we unveil a glucoregulatory role of upper small intestinal L. gasseri that impacts an ACSL3-dependent glucoregulatory fatty acid-sensing pathway.

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Improvement in glucose tolerance and insulin sensitivity by probiotic strains of Indian gut origin in high-fat diet-fed C57BL/6J mice

Abstract: Native probiotic strains MTCC 5690 and MTCC 5689 appear to have potential against insulin resistance and type 2 diabetes with mechanistic, multiple tissue-specific mode of actions.

Cited by 161 publications

References 57 publications

Ameliorative Effects of Probiotic Lactobacillus paracasei NL41 on Insulin Sensitivity, Oxidative Stress, and Beta‐Cell Function in a Type 2 Diabetes Mellitus Rat Model

Ameliorative Effects of Probiotic Lactobacillus paracasei NL41 on Insulin Sensitivity, Oxidative Stress, and Beta‐Cell Function in a Type 2 Diabetes Mellitus Rat Model

The Gut Microbiota and Its Implication in the Development of Atherosclerosis and Related Cardiovascular Diseases

Lactobacillus gasseri in the Upper Small Intestine Impacts an ACSL3-Dependent Fatty Acid-Sensing Pathway Regulating Whole-Body Glucose Homeostasis

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