Administration of Lactobacillus paracasei ameliorates type 2 diabetes in mice

2018 ◽  
Vol 9 (7) ◽  
pp. 3630-3639 ◽  
Author(s):  
Fangfang Dang ◽  
Yujun Jiang ◽  
Ruili Pan ◽  
Yanhong Zhou ◽  
Shuang Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Lipid Metabolism ◽  
Glucose Metabolism ◽  
Lactobacillus Paracasei ◽  
Akt Pathway ◽  
Diabetic Mice ◽  
Diabetes In Mice ◽  
Dose Dependent

Lactobacillus paracasei TD062 with high inhibitory activity ameliorated lipid metabolism, oxidative stress, glucose metabolism and the PI3K/Akt pathway in diabetic mice, and the effects were dose-dependent to some extent.

scholarly journals Decreased glycolytic and tricarboxylic acid cycle intermediates coincide with peripheral nervous system oxidative stress in a murine model of type 2 diabetes

2012 ◽  
Vol 216 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Lucy M Hinder ◽  
Anuradha Vivekanandan-Giri ◽  
Lisa L McLean ◽  
Subramaniam Pennathur ◽  
Eva L Feldman
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Sciatic Nerve ◽  
Peripheral Nerves ◽  
Sural Nerve ◽  
Tca Cycle ◽  
Tricarboxylic Acid ◽  
Diabetic Mice ◽  
Type 2 Diabetic

Diabetic neuropathy (DN) is the most common complication of diabetes and is characterized by distal-to-proximal loss of peripheral nerve axons. The idea of tissue-specific pathological alterations in energy metabolism in diabetic complications-prone tissues is emerging. Altered nerve metabolism in type 1 diabetes models is observed; however, therapeutic strategies based on these models offer limited efficacy to type 2 diabetic patients with DN. Therefore, understanding how peripheral nerves metabolically adapt to the unique type 2 diabetic environment is critical to develop disease-modifying treatments. In the current study, we utilized targeted liquid chromatography–tandem mass spectrometry (LC/MS/MS) to characterize the glycolytic and tricarboxylic acid (TCA) cycle metabolomes in sural nerve, sciatic nerve, and dorsal root ganglia (DRG) from male type 2 diabetic mice (BKS.Cg-m+/+Leprdb;db/db) and controls (db/+). We report depletion of glycolytic intermediates in diabetic sural nerve and sciatic nerve (glucose-6-phosphate, fructose-6-phosphate, fructose-1,6-bisphosphate (sural nerve only), 3-phosphoglycerate, 2-phosphoglycerate, phosphoenolpyruvate, and lactate), with no significant changes in DRG. Citrate and isocitrate TCA cycle intermediates were decreased in sural nerve, sciatic nerve, and DRG from diabetic mice. Utilizing LC/electrospray ionization/MS/MS and HPLC methods, we also observed increased protein and lipid oxidation (nitrotyrosine; hydroxyoctadecadienoic acids) indb/dbtissue, with a proximal-to-distal increase in oxidative stress, with associated decreased aconitase enzyme activity. We propose a preliminary model, whereby the greater change in metabolomic profile, increase in oxidative stress, and decrease in TCA cycle enzyme activity may cause distal peripheral nerves to rely on truncated TCA cycle metabolism in the type 2 diabetes environment.

scholarly journals Beneficial Effects of Poplar Buds on Hyperglycemia, Dyslipidemia, Oxidative Stress, and Inflammation in Streptozotocin-Induced Type-2 Diabetes

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Shiqin Peng ◽  
Ping Wei ◽  
Qun Lu ◽  
Rui Liu ◽  
Yue Ding ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Blood Glucose ◽  
Crude Extract ◽  
Liver Homogenate ◽  
Control Group ◽  
Diabetic Mice ◽  
Model Control

The effects of propolis on blood glucose regulation and the alleviation of various complications caused by diabetes have been widely studied. The main source of propolis in the northern temperate zone is poplar buds. However, there is limited research on the antidiabetic activity of poplar buds. In order to evaluate the effect of poplar buds on type-2 diabetes, crude extract and 50% fraction of poplar buds were used to feed streptozotocin-induced type-2 diabetic mice. The results showed that 50% fraction could increase insulin sensitivity and reduce insulin resistance, as well as decrease the levels of fasting blood glucose, glycated hemoglobin, and glycosylated serum proteins in diabetic mice. Compared with the model control group, the 50% fraction-treated group showed significant decreases of malondialdehyde (MDA) and increases of superoxide dismutase (SOD) in serum and liver homogenate. Moreover, 50% fraction could significantly decrease total cholesterol (TC), alleviate abnormal lipid metabolism, and enhance antioxidant capacity in the serum. For inflammatory factors, feeding of 50% fraction could also reduce the levels of interleukin 6 (IL-6), tumor necrosis factorα(TNF-α), monocyte chemotactic protein 1 (MCP-1), and cyclooxygenase-2 (COX-2) in liver homogenate. Taken together, our results suggest that crude extract and 50% fraction of poplar buds, particularly the latter, can decrease blood glucose levels and insulin resistance, and 50% fraction can significantly relieve dyslipidemia, oxidative stress, and inflammation caused by type-2 diabetes.

scholarly journals Hypolipidaemic and antioxidative effects of oligonol, a low-molecular-weight polyphenol derived from lychee fruit, on renal damage in type 2 diabetic mice

2010 ◽  
Vol 104 (8) ◽  
pp. 1120-1128 ◽  
Author(s):  
Jeong Sook Noh ◽  
Hyun Young Kim ◽  
Chan Hum Park ◽  
Hajime Fujii ◽  
Takako Yokozawa
Keyword(s):  
Type 2 Diabetes ◽  
Lipid Peroxidation ◽  
Lipid Metabolism ◽  
Regulatory Element ◽  
Advanced Glycation Endproducts ◽  
Receptor Expression ◽  
Diabetic Mice ◽  
Element Binding Protein ◽  
Abnormal Lipid Metabolism

Oligonol was orally administered at 10 or 20 mg/kg body weight per d for 8 weeks to db/db mice with type 2 diabetes, and its effects were compared with those of the vehicle in db/db and m/m (misty, non-diabetic) mice. Serum and renal biochemical factors, protein expressions related to lipid metabolism and inflammation, and advanced glycation endproducts were measured. There were significant reductions in the serum lipid concentration, reactive oxygen species (ROS) and lipid peroxidation, as well as improvements in renal function parameters. In addition, oligonol treatment significantly decreased ROS levels and lipid peroxidation in the kidney. In particular, the renal lipid contents such as TAG and total cholesterol were significantly reduced in the oligonol-administered groups through the up-regulation of PPARα and down-regulation of sterol regulatory element-binding protein-1 in db/db mice. Moreover, oligonol inhibited non-fluorescent AGE formation and their receptor expression, suggesting that it could effectively inhibit AGE development caused by oxidative stress and/or dyslipidaemia in the kidney of db/db mice. Furthermore, augmented expressions of NF-κBp65, cyclo-oxygenase-2 and inducible NO synthase were down-regulated to the levels of m/m mice in the group given oligonol at 20 mg/kg. This means that oligonol would act as a regulator in the inflammatory response of type 2 diabetes. The present results suggest that oligonol could have renoprotective effects against abnormal lipid metabolism and ROS-related AGE formation in type 2 diabetes.

scholarly journals Intermittent injections of osteocalcin improve glucose metabolism and prevent type 2 diabetes in mice

Bone ◽  
2012 ◽  
Vol 50 (2) ◽  
pp. 568-575 ◽  
Author(s):  
Mathieu Ferron ◽  
Marc D. McKee ◽  
Robert L. Levine ◽  
Patricia Ducy ◽  
Gérard Karsenty
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Metabolism ◽  
Diabetes In Mice

Lactobacillus plantarum X1 with α-glucosidase inhibitory activity ameliorates type 2 diabetes in mice

RSC Advances ◽  
2016 ◽  
Vol 6 (68) ◽  
pp. 63536-63547 ◽  
Author(s):  
Xiangfei Li ◽  
Na Wang ◽  
Boxing Yin ◽  
Dongsheng Fang ◽  
Jianxin Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Gut Microbiota ◽  
Lactobacillus Plantarum ◽  
Inhibitory Activity ◽  
Diabetes In Mice

Lactobacillus plantarum X1 is of potential beneficial utility to counter diabetes via five potential pathways, which including dyslipidemia, oxidative stress, α-glucosidase, gut microbiota, and inflammatory.

scholarly journals Gentiopicroside Ameliorates Glucose and Lipid Metabolism in T2DM by Activating PI3K/AKT Pathway Via FGFR1

2021 ◽  
Author(s):  
Zhanchi Xu ◽  
Zeyuan Lin ◽  
Jingran Zeng ◽  
Rui Chen ◽  
Chuting Li ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Glucose Metabolism ◽  
Hepg2 Cells ◽  
Growth Factor Receptor ◽  
Akt Pathway ◽  
Phosphatidylinositol 3 Kinase ◽  
Glucose And Lipid Metabolism ◽  
Lipid Metabolism Disorders

Abstract Background: Abnormalities in lipid and glucose metabolism are are constantly occured in type 2 diabetes (T2DM). However, it can be ameliorated by gentiopicroside (GPS). Considering the key role of fibroblast growth factor receptor 1/phosphatidylinositol 3-kinase/protein kinase B (FGFR1/PI3K/AKT) pathway in T2DM, we explore the possible mechanism of GPS on lipid and glucose metabolism through its effects on FGFR1/PI3K/AKT pathway.Methods: Palmitic acid (PA)-induced HepG2 cells and a db/db mice were used to clarify the role and mechanism of polydatin on lipid and glucose metabolism.Results: GPS ameliorated glucose and lipid metabolism disorders in db/db mice and PA-induced HepG2 cells. Furthermore, GPS activated FGFR1/PI3K/AKT pathway including increased the protein expression of FGFR1 and promoted the phosphorylation of PI3K, AKT and FoxO1. Additionally, knockdown of FGFR1 reversed the activation of PI3K/AKT pathway by GPS.Conclusions: The present study demontrates that GPS ameliorates glucose and lipid metabolism disorders via activation of FGFR1/PI3K/AKT pathway.

scholarly journals Evidence and Potential Mechanisms of Jin-Gui Shen-Qi Wan as a Treatment for Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis

2021 ◽  
Vol 12 ◽  
Author(s):  
Zhipeng Hu ◽  
Xiaoke Liu ◽  
Maoyi Yang
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Lipid Metabolism ◽  
Glucose Metabolism ◽  
Combination Treatment ◽  
Meta Analysis ◽  
Hypoglycemic Agents ◽  
Current Evidence

Background: Type 2 diabetes mellitus (T2DM) is a subtype of diabetes mellitus characterized by progressive dysfunction of β-cell insulin secretion and insulin resistance. Jīn-Guì Shèn-Qì Wán (JGSQW) has for many years been widely used in clinical practice as a treatment for T2DM. However, its effect remains unknown.Objectives: This study aims to summarize the clinical evidence of the effect of JGSQW on glucose and lipid metabolism in T2DM and the potential mechanisms underlying this effect.Methods: Six databases were searched without language or publication status restrictions. Data were extracted to a predefined template for synthesis.Results: Fourteen studies with 1586 participants were included in this meta-analysis. All 14 studies were judged to be at high risk of bias. JGSQW is safe for T2DM patients. Pooled results indicated that combination treatment results in a reduction in glycated hemoglobin (HbA1c) (mean difference (MD) −0.49%; 95% CI −0.67 to −0.31), fasting blood glucose (FBG) (MD −0.84; 95% CI −1.19 to −0.49), and 2-hour postprandial glucose 2hBG (MD −1.38; 95% CI −1.60 to −1.16). No significant difference in glucose metabolism was observed between JGSQW and hypoglycemic agents. The available evidence was insufficient to determine the effects on lipid metabolism. Sensitivity analyses indicated that these results were robust.Conclusion: By combining the available evidence, we found that JGSQW is safe for T2DM patients. Compared with hypoglycemic agents alone, combination treatment with JGSQW enhances the effect on glucose metabolism in patients with T2DM. We found no difference in the efficacy of JGSQW alone compared to hypoglycemic agents alone. In terms of lipid metabolism, the current evidence is insufficient and too inconsistent for us to draw firm conclusions, so further studies are needed.

scholarly journals Empagliflozin prevents cardiomyopathy via sGC-cGMP-PKG pathway in type 2 diabetes mice

2019 ◽  
Vol 133 (15) ◽  
pp. 1705-1720 ◽  
Author(s):  
Mei Xue ◽  
Ting Li ◽  
Yue Wang ◽  
Yunpeng Chang ◽  
Ying Cheng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Soluble Guanylate Cyclase ◽  
Therapeutic Option ◽  
Guanosine Monophosphate ◽  
Protective Effects ◽  
Diabetic Mice ◽  
Mortality And Morbidity ◽  
Urinary Glucose

Abstract Cardiovascular complications contribute to the major mortality and morbidity in type 2 diabetes. Diabetic cardiomyopathy (DCM) is increasingly recognized as an important cause of heart failure. EMPA-REG OUTCOME trial has reported that empagliflozin, the sodium-glucose cotransporter 2 inhibitor, exerts cardiovascular benefits on diabetic population. However, the mechanism by which empagliflozin alleviates DCM still remains unclear. In the current study, we investigated the cardiac protective effects of empagliflozin on spontaneous type 2 diabetic db/db mice and its potential mechanism. Eight weeks of empagliflozin treatment (10 mg/kg/day) decreased body weight and blood glucose level, and increased urinary glucose excretion (UGE) in diabetic mice. Echocardiography revealed that both systolic and diastolic functions of db/db mice were also obviously improved by empagliflozin. Furthermore, empagliflozin-treated diabetic mice presented with amelioration of cardiac hypertrophy and fibrosis. In addition, diabetic hearts exhibited the deterioration of oxidative stress, apoptosis and pyroptosis, while these effects were significantly counteracted after empagliflozin treatment. Moreover, empagliflozin rescued diabetes-induced suppression of sGC (soluble guanylate cyclase enzyme)-cGMP (cyclic guanosine monophosphate)-PKG (cGMP-dependent protein kinase) pathway. However, when sGC-β expression of hearts was inhibited by transvascular delivery of small interfering RNA, cardiac dysfunction was aggravated and the advantages of empagliflozin were reversed through inhibiting sGC-cGMP-PKG pathway. Collectively, these findings indicate that empagliflozin improves cardiac function involving the inhibition of oxidative stress-induced injury via sGC-cGMP-PKG pathway and may be a promising therapeutic option for DCM.

scholarly journals Protective Effects and Mechanisms of Polyethylene Glycol Loxenatide Against Hyperglycemia and Liver Injury in db/db diabetic Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Yu Zhang ◽  
Yufeng Li ◽  
Junjun Zhao ◽  
Cong Wang ◽  
Bin Deng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Polyethylene Glycol ◽  
Liver Injury ◽  
Serum Insulin ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Akt Pathway ◽  
Inflammatory Factor

Background: Type 2 diabetes mellitus (T2DM) is a metabolic disorder with insulin resistance and impaired insulin secretion that can cause complications, including liver injury. Polyethylene glycol loxenatide (PEG-Loxe), a glucagon-like peptide-1 (GLP-1) analog, is widely used to treat T2DM. However, its specific glucose-lowering and hepatoprotective mechanisms of action have not been established yet.METHODS: Using a high glucose-induced hepatocyte injury model and a type 2 diabetic db/db mouse model, we assessed PEG-Loxe’s impact on reducing blood glucose and improving liver injury in T2DM and revealed its mechanism.RESULTS: PEG-Loxe treatment significantly reduced body weight and fasting glucose, increased glucose tolerance, improved serum and liver biochemical parameters (glycated hemoglobin, serum insulin, triglycerides, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, alanine aminotransferase, and aspartate aminotransferase), and attenuated hepatic steatosis and liver and pancreatic tissue damages in db/db mice. Additionally, PEG-Loxe considerably inhibited oxidative stress, decreased pro-inflammatory factor (TNF-α, IL-6, and MCP-1) levels, and increased anti-inflammatory factor IL-10 levels. PEG-Loxe possibly inhibits hepatic lipid synthesis, oxidative stress, and inflammatory response by upregulating Sirt1, p-AMPK, and p-ACC expressions in the Sirt1/AMPK/ACC pathway of lipid metabolism, thereby improving T2DM liver injury. PEG-Loxe most likely also promotes GLP-1R expression by inhibiting β-cell apoptosis, which in turn activates the insulin PI3K/AKT pathway to promote insulin synthesis and secretion, thereby exerting hypoglycemic effects. In vitro cellular experiments further confirmed that PEG-Loxe possibly exerts hypoglycemic effects by activating the insulin PI3K/AKT pathway.Conclusion: PEG-Loxe improved liver injury in T2DM probably by activating Sirt1/AMPK/ACC lipid metabolism pathway, and exerted hypoglycemic effects through activation of insulin PI3K/AKT pathway.

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