scholarly journals Effect of Alpha-Linolenic Acid on Blood Glucose, Insulin and GLUT4 Protein Content of Type 2 Diabetic Mice.

2000 ◽  
Vol 46 (6) ◽  
pp. 489-492 ◽  
Author(s):  
Motoshi Kato ◽  
Toshihiro Miura ◽  
Masami Nakao ◽  
Naoki Iwamoto ◽  
Torao Ishida ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Protein Content ◽  
Linolenic Acid ◽  
Diabetic Mice ◽  
Alpha Linolenic Acid ◽  
Type 2 Diabetic

scholarly journals Suppressive Activity of the Fruit of Momordica charantia with Exercise on Blood Glucose in Type 2 Diabetic Mice

2004 ◽  
Vol 27 (2) ◽  
pp. 248-250 ◽  
Author(s):  
Toshihiro Miura ◽  
Yasushi Itoh ◽  
Naoki Iwamoto ◽  
Motoshi Kato ◽  
Torao Ishida
Keyword(s):  
Blood Glucose ◽  
Momordica Charantia ◽  
Diabetic Mice ◽  
Suppressive Activity ◽  
Type 2 Diabetic

scholarly journals ID: 1080 Adipose-derived stem cells alleviate glucose tolerance in type 2 diabetic mouse

2017 ◽  
Vol 4 (S) ◽  
pp. 166
Author(s):  
Anh Nguyen Tu Bui ◽  
Cong Le Thanh Nguyen ◽  
Anh Thi Minh Nguyen ◽  
Nhat Chau Truong ◽  
Ngoc Kim Phan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Stem Cells ◽  
Blood Glucose ◽  
Glucose Tolerance ◽  
Adipose Derived Stem Cells ◽  
Diabetic Mice ◽  
Human Ascs ◽  
Type 2 Diabetic

Background: Type 2 diabetes (T2D) is the most common form of diabetes and accounts for 90-95% of all existing diabetic cases. The main etiologies of T2D include insulin resistance in target tissues, insufficient secretion of insulin and subsequent decline of pancreatic β-cell function. Recently, many studies have suggested that adipose – derived stem cells (ASCs) were potential to alleviate insulin resistance and hyperglycemia and promote the islets repair. In this study, ASCs were hypothesized that they could have ameliorative effects on type 2 diabetic mice.  Methods: Type 2 diabetic mice were induced by a combination of high-fat diet and injection of STZ 100 mg/kg and NA 120 mg/kg. Thereafter, two doses of 106 human ASCs were transplanted 2 week interval into each mouse via the tail vein. The mice were monitored health condition, rate of mortaity, body weight, consumption of food and water, blood glucose level, serum insulin level and histological structure of pancreatic islets.  Results: Our results indicated that the ASC-treated mice expressed improved condition in comparision with non-treated diabetic mice. The consumption of food and water as well as the blood glucose level decreased. Simultaneously, ASC transplantation improved the impaired glucose tolerance and insulin tolerance in T2D mice. Besides, the total cholesterol have significantly decreased.  Conclusion: it is suggested that human ASCs infusion is safe and effective for type 2 diabetes mellitus in mice regarding the improved glucose metabolism and insulin resistance.

Abstract 279: Stromal Cell-derived Factor-1 Prevents From Diabetic Cardiomyopathy via Cxcr7/ampk-mediated Nrf2 Activation in Type 2 Diabetic Mice

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Shudong Wang ◽  
Junlian Gu ◽  
Xiaoqing Yan ◽  
Jing Chen ◽  
Jun Chen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Glucose ◽  
Cardiac Function ◽  
Stromal Cell ◽  
Normal Diet ◽  
Diabetic Mice ◽  
Nrf2 Activation ◽  
Stromal Cell Derived Factor ◽  
Type 2 Diabetic

We have demonstrated that stromal cell-derived factor 1(SDF-1) protects against palmitate-induced cardiac cell death via CXCR7-mediated activation of AMPK signaling (Diabetes 62:2545-2558, 2013). Whether SDF-1 prevents diabetic cardiomyopathy (DCM) and what the underlying mechanism has not been addressed. Here we evaluated the prevention of SDF-1 from DCM in a high fat diet plus streptozotocin (HFD/STZ)-induced type 2 diabetic model in C57BL/6J mice. After 1 month on HFD, the HFD-fed mice were injected with one low dose STZ (100mg/kg body weight, ip). Five days after STZ injection, mice with blood glucose levels ≥250 mg/dl were defined as diabetic. In parallel, the age-matched normal diet-fed mice injected with a same volume of vehicle were used as control. After onset of diabetes, the mice were maintained on HFD or normal diet for another 4 months with or without SDF-1 treatment. Then cardiac function was assayed again, and the mice were sacrificed and cardiac tissue collected for cardiomyopathic index assay. We found that 1 month HFD feeding induced a significant insulin resistance without effect on cardiac function, but continued HFD feeding after STZ injection significantly increased insulin resistance and blood glucose, as well as blood insulin, triglyceride and cholesterol levels. Furthermore, HFD/STZT significantly impaired cardiac function, which were accompanied by increased cardiac inflammation, oxidative stress and fibrotic remodeling. Treatment with SDF-1 dose-dependently prevented diabetes-induced cardiac dysfunction, inflammation and remodeling, but without significant effects on the above mentioned other pathophysiological changes. Mechanistic study demonstrated that diabetes significantly inhibited the function of AMPK and Nrf2, and the expression of CXCR7, but not CXCR4; while treatment with SDF-1 significantly preserved AMPK and Nrf2 function and CXCR7 expression. Knockout CXCR4 did not affect SDF-1 preservation of AMPK and Nrf2 function, but SiRNA knockdown of AMPK resulted in blockade of SDF-1 preservation of Nrf2 function. These results indicate that SDF-1 prevents from DCM via CXCR7/AMPK-mediated Nrf2 activation in type 2 diabetic mice.

scholarly journals Drinking Watermelon Juice Shift the Gut Microbiome in Diabetic Mice (P20-025-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Siau Yen Wong ◽  
Lei Wu ◽  
Peiran Lu ◽  
Babajide Ojo ◽  
Minghua Tang ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Gut Microbiome ◽  
Tap Water ◽  
Fasting Blood Glucose ◽  
Chow Diet ◽  
Diabetic Mice ◽  
Watermelon Juice ◽  
Type 2 Diabetic

Abstract Objectives Watermelon is a delicious and healthy fruit that contains low calories and is rich in carotenoids, vitamin A, vitamin C, citrulline, and other bioactive compounds. The health benefits of watermelon in diabetes are poorly understood. In the current study, we sought to determine the effects of watermelon juice on gut microbiome profile and blood glucose management in type 1 and type 2 diabetic mice. Methods Six-week-old male C57BL/6 J wild type (WT), db/db type 2 diabetic (db/db), and streptozocin (STZ)-induced type 1 (STZ) diabetic mice were fed a chow diet and given 50% or 100% watermelon juice or tape water during night cycle for 8 weeks. At the termination of the study, mice were fasted for 3 hrs prior to euthanization. Blood, cecal contents, and other tissues were collected for laboratory assessments. Plasma metabolic parameters and pro-inflammatory cytokines were monitored by a clinical analyzer and ELISA, respectively. Cecal microbiome was profiled by 16S rRNA sequencing and followed by bioinformatic analysis. Results Consumption of watermelon juice significantly lowered fasting blood glucose levels in both diabetic mouse models. The fasting insulin level was significantly decreased in db/db consuming watermelon juice, though it was undetectable in STZ mice, with or without watermelon juice. Drinking watermelon juice tremendously changed the gut microbiome composition. At the phylum level, the Firmicutes/Bacteroidetes ratio was significantly associated with genotype (e.g., WT vs STZ vs db/db) and diet (e.g., watermelon juice vs tap water). At the genus level, abundances of Ruminiclostridium_9, Parasutterella, and Clostridium_sensu_stricto_1 were increased in STZ mice with watermelon, and abundances of Oscillibacter and Ruminiclostridium were decreased in db/db mice with watermelon. Watermelon juice induced gut microbiome compositional changes also occurred at the species level. Conclusions Watermelon juice intervention causes a decrease in blood glucose level and shifts of the gut microbiome in both type 1 and type 2 mice. Funding Sources National watermelon board grant.

scholarly journals 104 Dietary α-Linolenic Acid Does Not Modify Caveolar Proteins Yet Limits Cardioprotective Dysfunction in Type 2 Diabetic Mice

2020 ◽  
Vol 29 ◽  
pp. S83
Author(s):  
J. Russell ◽  
T. Griffith ◽  
S. Naghipour ◽  
J. Vider ◽  
E. Du Toit ◽  
...  
Keyword(s):  
Linolenic Acid ◽  
Diabetic Mice ◽  
Type 2 Diabetic

The plasma 5′-AMP acts as a potential upstream regulator of hyperglycemia in type 2 diabetic mice

2012 ◽  
Vol 302 (3) ◽  
pp. E325-E333 ◽  
Author(s):  
Ying Zhang ◽  
Zhongqiu Wang ◽  
Yue Zhao ◽  
Ming Zhao ◽  
Shiming Wang ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Blood Glucose ◽  
Adenosine Monophosphate ◽  
Plasma Free Fatty Acid ◽  
Hepatic Glycogen ◽  
Diabetic Mice ◽  
Wild Type ◽  
Upstream Regulator ◽  
Type 2 Diabetic

Increased plasma free fatty acid (FFA) level is a hallmark of type 2 diabetes. However, the underlying molecular basis for FFA-caused hyperglycemia remains unclear. Here we identified plasma 5′-adenosine monophosphate (pAMP) markedly elevated in the plasma of type 2 diabetic mice. High levels of FFAs induced damage in vein endothelial cells and contributed to an increase in pAMP. Administration of synthetic 5′-AMP caused hyperglycemia and impaired insulin action in lean wild-type mice. 5′-AMP elevated blood glucose in mice deficient in adenosine receptors with equal efficiency as wild-type mice. The function of pAMP was initiated by the elevation of cellular adenosine levels, directly stimulating G-6-Pase enzyme activity, attenuating insulin-dependent GLUT4 translocation in skeletal muscle, and displaying a rapid and steep increase in blood glucose and a decrease in hepatic glycogen level. It was followed by an increase in the gene expression of hepatic Foxo1 and its targeting gene Pepck and G6Pase, which was similar to diabetic phenotype in db/db mice. Our results suggest that pAMP is a potential upstream regulator of hyperglycemia in type 2 diabetes.

scholarly journals GLP-1 Gene-Modified Human Umbilical Cord Mesenchymal Stem Cell Line Improves Blood Glucose Level in Type 2 Diabetic Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Ying Chang ◽  
Mingxin Dong ◽  
Yan Wang ◽  
Haotian Yu ◽  
Chengbiao Sun ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Stem Cells ◽  
Blood Glucose ◽  
Cell Line ◽  
Umbilical Cord ◽  
Human Umbilical Cord ◽  
Diabetic Mice ◽  
Type 2 Diabetic

Type 2 diabetes constitutes a serious threat to the health of patients, but there is currently no ideal treatment in the clinic. Glucagon-like peptide-1 and human umbilical cord mesenchymal stem cells have been confirmed to have antidiabetic effects, but both of them have certain defects in the process of antidiabetes, which cannot meet the need of clinical treatment. We hypothesized that human umbilical cord mesenchymal stem cells can be used as a vector to construct a novel cell line that expresses GLP-1 in vivo for a long time. And this cell strain results in lowering blood glucose in type 2 diabetic mice. The results showed that after 3 weeks of intramuscular injection of the new cell line, the fasting blood glucose of type 2 diabetic mice returned to the normal range, and the hypoglycemic effect was maintained within 3 weeks after putting an end to the drug. At the same time, during the administration, the mice lost weight, the food intake decreased, the half-life of GLP-1 in the body prolonged, the IR reduced, and the pancreatic function recovered. The results of this study indicate that the novel cell line can prolong the half-life of GLP-1 in vivo and effectively lower blood sugar, which is a feasible method to improve type 2 diabetes.

scholarly journals PO-062 Acute exercise intervention combined with metformin’s influences on glucose homeostasis in T2D mice

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Wenqing Shen ◽  
Yi Zhang ◽  
Qiang Zhang ◽  
Zhengtang Qi ◽  
Yi Sun ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Resistance Training ◽  
Mrna Expression ◽  
Endurance Training ◽  
Glucose Homeostasis ◽  
Acute Exercise ◽  
High Dose ◽  
Diabetic Mice ◽  
Type 2 Diabetic

Objective Type 2 diabetes mellitus is a common chronic diseases prevailing in the world and the amount of diabetic and pre-diabetic patients is increasing gradually. Exercise combined with hypoglycemic drug is the first recommended therapy to treat type 2 diabetes. Metformin was found from galegine in 1957 and has been used now as the first cheap and effective hypoglycemic guanidines. Our study aims to explore the effects of different ways of acute exercise intervention combined with high dose of metformin on glucose homeostasis and its relative molecular mechanisms in type 2 diabetic mice. Methods Adopt 4-week high fat diet (HFD, 45% fat content) and one-time STZ (Streptozocin, 100mg/kg) intraperitoneal injection to build type 2 diabetic mice. There are 84 mice in total, 24 mice were divided into three groups: normal control (NC) group, normal acute resistance training (NCR) group and normal acute endurance training (NCE) group, N=8 each group, they were fed normal chow. The rest 60 mice were fed HFD as T2D modeling group. 48 mice were developing type 2 diabetes and they were divided into 6 groups: diabetic control (DC) group, diabetic acute resistance training (DCR) group, diabetic acute endurance training (DCE) group, high dose of metformin control (HMC) group, high dose of metformin combined with acute resistance training (HMR) group and high dose of metformin combined with acute endurance training (HME) group, N=8 each group. Acute resistance training is climbing 1 meter ladder from down to up, 5 times a group, 3 groups in total, monitoring the glucose change with extracting mouse tail vein blood during each group, using ACCU-CHEK monitor. Acute endurance training is running at the speed of 18 m/min on the platform for 50 minutes and blood glucose change was monitored every 10 minutes by extracting mouse tail vein blood. HMC, HMR and HME group mice were intraperitoneally injected high dose of metformin (200mg/kg) one hour before the acute exercise intervention. Comparatively, NC, NCR, NCE, DC, DCR, DCE group mice were intraperitoneally injected 0.9% saline one hour before the acute exercise intervention. ELISA, RT-PCR and Western Blot were used to evaluate relative serum indicators, mRNA and protein expression of regulating blood glucose homeostasis. Results 1) 4-week high fat diet and one time 100mg/kg Streptozocin intraperitoneal injection induces mice to develop type 2 diabetes. The fasting blood glucose, IPGTT, ITT, glucose AUC and insulin AUC of T2D group mice are significantly higher than NC group. 2) Compared with DCR group, the blood glucose value and fluctuation of HMR group mice are both significantly decreased, but the blood glucose value of DCR and HMR group mice are significantly higher than NCR group. In the same way, the blood glucose value and fluctuation of HME group mice is lower than DCE group and the whole blood glucose level of both group are higher than NCE group. Acute resistance training and acute endurance training combined with high dose of metformin have not affected the weight of type 2 diabetic mice. Hence compared with HMC group, the eWAT (epididymal white adipose tissue) of HMR and HME group mice is significantly declined. 3) Compared with NC group, the indicators of serum glucose, GSP (glycosylated serum protein), serum TG and serum T-CHO of DC group are notably increased, further reflect that the success model of type 2 diabetic mice. Compared with HMC group, the indicators of serum glucose, GSP, serum TG and serum T-CHO of HMR group mice are notably decreased, in the mean time, the indicators of serum glucose and serum TG of HME group mice are significantly declined. Interestingly, the serum insulin of HME group mice is notably lower than HMR group. 4) Compared with DC group, the indicators of mRNA expression about hepatic gluconeogenesis key rate-limiting enzymes PEPCK and G6pase of HMC group are significantly declined, but mRNA expression of regulating hepatic glucose homeostasis GLUT2 of HMC group is notably raised. Compared with HMC group, G6Pase mRNA expression of HMR and HME group is significantly escalated and Fbp mRNA expression of both groups are significantly declined. Compared with HMC, the indicators of mRNA expression about regulating hepatic glucose homeostasis GLUT2 and Gck of HMR and HME group mice show opposite trend, the former is down and the latter is up. Compared with HMC group, PEPCK mRNA expression of HMR group mice is notably escalated. Compared with HMR group, PEPCK and G6Pase mRNA expression of HME group mice are notably raised. 5) In the liver, there is a signaling pathway of AMPKα-PGC-1α-CREB to regulate glucose homeostasis and hepatic gluconeogenesis. Our study find that compared with HMC group, AMPKα2, PGC-1α and CREB mRNA expression of HMR and HME group mice are notably increased and only AMPKα1 mRNA expression of HMR group mice is significantly increased. Conclusions 1) Acute resistance training and acute endurance training combined with high dose of metformin can effectively reduce glucose fluctuation during exercise in type 2 diabetic mice, therefore these two way can both improve glucose homeostasis during acute exercise intervention in type 2 diabetic mice. 2) Acute resistance training and acute endurance training combined with high dose of metformin can improve serum glucose and lipid metabolism in type 2 diabetic mice, but acute resistance training combined with high dose of metformin are better to improve serum lipid metabolism. 3) Acute exercise intervention combined with high dose of metformin can comparatively increase hepatic gluconeogenesis key rate-limiting enzymes PEPCK and G6Pase and regulating hepatic glucose transport Gck mRNA expression. In the opposite, these two ways inhibit the other hepatic gluconeogenesis key rate-limiting enzyme Fbp and regulating hepatic glucose transport GLUT2 mRNA expression. 4) Compared with acute endurance training combined with high dose of metformin, acute resistance training combined with high dose of metformin can better improve glucose homeostasis and hepatic gluconeogenesis in type 2 diabetic mice via the signaling pathway of AMPKα-PGC-1α-CREB.

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