scholarly journals Analysis of Urine Composition in Type II Diabetic Mice after Intervention Therapy Using Holothurian Polypeptides

2017 ◽  
Vol 5 ◽  
Author(s):  
Yanyan Li ◽  
Jiajie Xu ◽  
Xiurong Su
Keyword(s):  
Type Ii ◽  
Diabetic Mice ◽  
Urine Composition ◽  
Analysis Of Urine

scholarly journals The tissue origin of human mesenchymal stem cells dictates their therapeutic efficacy on glucose and lipid metabolic disorders in type II diabetic mice

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yinzhong Ma ◽  
Lisha Wang ◽  
Shilun Yang ◽  
Dongyu Liu ◽  
Yi Zeng ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Therapeutic Efficacy ◽  
Metabolic Disorders ◽  
Human Mscs ◽  
Dependent Manner ◽  
Type Ii ◽  
Diabetic Mice ◽  
Histological Lesion ◽  
Insulin Levels

Abstract Background The therapeutic efficacy of mesenchymal stem cells (MSCs) of different tissue origins on metabolic disorders can be varied in many ways but remains poorly defined. Here we report a comprehensive comparison of human MSCs derived from umbilical cord Wharton’s jelly (UC-MSCs), dental pulp (PU-MSCs), and adipose tissue (AD-MSCs) on the treatment of glucose and lipid metabolic disorders in type II diabetic mice. Methods Fourteen-to-fifteen-week-old male C57BL/6 db/db mice were intravenously administered with human UC-MSCs, PU-MSCs, and AD-MSCs at various doses or vehicle control once every 2 weeks for 6 weeks. Metformin (MET) was given orally to animals in a separate group once a day at weeks 4 to 6 as a positive control. Body weight, blood glucose, and insulin levels were measured every week. Glucose tolerance tests (GTT) and insulin tolerance tests (ITT) were performed every 2 weeks. All the animals were sacrificed at week 6 and the blood and liver tissues were collected for biochemical and histological examinations. Results UC-MSCs showed the strongest efficacy in reducing fasting glucose levels, increasing fasting insulin levels, and improving GTT and ITT in a dose-dependent manner, whereas PU-MSCs showed an intermediate efficacy and AD-MSCs showed the least efficacy on these parameters. Moreover, UC-MSCs also reduced the serum low-density lipoprotein cholesterol (LDL-C) levels with the most prominent potency and AD-MSCs had only very weak effect on LDL-C. In contrast, AD-MSCs substantially reduced the lipid content and histological lesion of liver and accompanying biomarkers of liver injury such as serum aspartate transaminase (AST) and alanine aminotransferase (ALT) levels, whereas UC-MSCs and PU-MSCs displayed no or modest effects on these parameters, respectively. Conclusions Taken together, our results demonstrated that MSCs of different tissue origins can confer substantially different therapeutic efficacy in ameliorating glucose and lipid metabolic disorders in type II diabetes. MSCs with different therapeutic characteristics could be selected according to the purpose of the treatment in the future clinical practice.

scholarly journals A Soybean Peptide Isolate Diet Promotes Postprandial Carbohydrate Oxidation and Energy Expenditure in Type II Diabetic Mice

2003 ◽  
Vol 133 (3) ◽  
pp. 752-757 ◽  
Author(s):  
Kengo Ishihara ◽  
Shinichi Oyaizu ◽  
Yoshiko Fukuchi ◽  
Wataru Mizunoya ◽  
Kikumi Segawa ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Carbohydrate Oxidation ◽  
Type Ii ◽  
Diabetic Mice

Abstract 890: Feed-forward Signaling of TNF alpha and NFkappa B Produces Endothelial Dysfunction in Coronary Arterioles In Type Ii Diabetic Mice.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Jiyeon Yang ◽  
Xiangbin Xu ◽  
Glen A Laine ◽  
Cuihua Zhang
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Nuclear Factor Κb ◽  
Inhibitory Effect ◽  
Type Ii ◽  
Diabetic Mice ◽  
Necrosis Factor Alpha ◽  
Paramagnetic Resonance ◽  
Feed Forward ◽  
Coronary Arterioles

Nuclear factor-κB (NFκB) signaling reportedly increases tumor necrosis factor-alpha (TNF expression), and the oxidative stress induced by TNF may then lead to further increase NFκB expression, i.e., a feed-forward interaction. Accordingly, we hypothesized that this feed-forward interaction between TNF and NFκB may amplify one another toward the evolution of vascular disease in diabetes. To test this hypothesis, we assessed the role of NFκB in endothelial dysfunction in Lepr db mice by evaluation of endothelial function of isolated coronary resistance vessels of m Lepr db (heterozygote, normal) and Lepr db (homozygote, diabetic) mice. Coronary arterioles (40 –100 μm) were isolated and pressurized (60 cmH2O) without flow. Although dilation of vessels to the endothelium-independent vasodilator, sodium nitroprusside (SNP) was not different between Lepr db and m Lepr db mice (n = 6), dilation to the endothelium-dependent agonist, acetycholine (ACh) was reduced (n = 5, P < 0.05). Electron Paramagnetic Resonance (EPR) results show that superoxide production was reduced by NFκB antagonist (MG-132), or anti-TNF in Lepr db mice suggesting that NFκB and TNF were contributing to elevated oxidative stress. MG-132 (1 μM, n = 4) antagonized the inhibitory effect of Lepr db mice on ACh-induced dilation vs. Lepr db without treatment, but did not affect dilation in m Lepr db mice. To better understand the basis for enhanced contributions of TNF and NFκB in diabetes, we used Western analysis to assess expression of major proteins involved in TNF-mediated signaling. Previous studies have provided compelling evidence that IKK beta plays an essential role in NFκB activation in response to TNF, whereas IKK alpha appears to play a lesser role; therefore, we examined the expression levels of IKK alpha and IKK beta mRNA and protein in Lepr db null for TNF. The protein concentration and mRNA expression level of IKK alpha were increased in Lepr db mice null for TNF (db TNF- /db TNF- ) mice. One intriguing finding of this study is that the roles of IKK alpha and IKK beta appear reversed in the inflammatory response in diabetic Lepr db mice. Furthermore, our results indicate that NFκB and TNF signaling interact to amplify the oxidative stress and induce endothelial dysfunction in type II diabetes.

The inhibiting effect of the Coptis chinensis polysaccharide on the type II diabetic mice

2016 ◽  
Vol 81 ◽  
pp. 111-119 ◽  
Author(s):  
Lijuan Cui ◽  
Min Liu ◽  
XiangYun Chang ◽  
Kan Sun
Keyword(s):  
Type Ii ◽  
Diabetic Mice ◽  
Coptis Chinensis ◽  
Inhibiting Effect

Management of metabolic syndrome and reduction in body weight in type II diabetic mice by inhibiting glycosphingolipid synthesis

2020 ◽  
Vol 525 (2) ◽  
pp. 455-461
Author(s):  
Subroto Chatterjee ◽  
Lucy Zheng ◽  
Sijia Ma ◽  
Djahida Bedja ◽  
Veera Venkata Ratnam Bandaru ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Body Weight ◽  
Type Ii ◽  
Diabetic Mice

A novel Alaska pollack-derived peptide, which increases glucose uptake in skeletal muscle cells, lowers the blood glucose level in diabetic mice

2015 ◽  
Vol 6 (8) ◽  
pp. 2749-2757 ◽  
Author(s):  
Tatsuhiro Ayabe ◽  
Takafumi Mizushige ◽  
Wakana Ota ◽  
Fuminori Kawabata ◽  
Kohsuke Hayamizu ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Glucose ◽  
Blood Glucose Level ◽  
Glucose Uptake ◽  
Type Ii ◽  
Diabetic Mice ◽  
Glucose Lowering ◽  
Tryptic Digest ◽  
Glucose Lowering Effect ◽  
Ay Mice

We found that the tryptic digest of Alaska pollack protein (APP) and novel APP-derived peptide exhibited a glucose-lowering effect in KK-Ay mice, a type II diabetic mice.

scholarly journals Role of diabetes in lung injury from acute exposure to electronic cigarette, heated tobacco product, and combustible cigarette aerosols

2020 ◽  
Author(s):  
Michella Abi Zeid Daou ◽  
Alan Shihadeh ◽  
Yasmine Hashem ◽  
Hala Bitar ◽  
Alaa Kassir ◽  
...  
Keyword(s):  
Lung Injury ◽  
Electronic Cigarettes ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Tobacco Product ◽  
Albumin Concentration ◽  
Type Ii ◽  
Diabetic Mice ◽  
Tnf Α ◽  
Patients With Diabetes

Abstract Background Patients with diabetes are more vulnerable to the detrimental respiratory effects of combustible cigarette smoke (CS) when compared to the general population. Electronic cigarettes (ECIG) and heated tobacco products (HTP) are marketed as less harmful alternatives to CS. In this study, we compared the effects of acute ECIG, HTP and CS exposure on the lungs of type II diabetes versus non-diabetic mice in an animal model Methods Type II Diabetic (Diab) and Non-Diabetic (Non-Diab) mice were divided into Control, ECIG, HTP and CS groups. Animals were exposed for 6 hrs./day to either air, ECIG, HTP or CS for seven days. Lung injury was determined by a) histopathology, b) wet to dry ratio, c) albumin concentration in bronchoalveolar lavage fluid, d) expression of TNF-α, IL-6, and IL-1 β, e) reactive oxygen species production (ROS), and f) assessment of cellular apoptosis. Results Lung histology revealed increased edema and inflammatory cells in diabetic mice exposed to ECIG, HTP and CS. The expression of Inflammatory mediators was, in general, more significant in the Diabetic groups as well. TNF-α expression, for example, was upregulated in Diab + HTP and Diab + ECIG but not in Non-Diab + HTP. ROS was significantly increased in Diab + CS, less in Non-Diab + CS and weakly noted in ECIG + Diab. Significant albumin leak was observed in HTP-exposed animals. CS exposure worsened lung injury in Diab when compared to Non-Diab mice. Conclusion Comorbid medical conditions like diabetes may amplify ill effects CS, ECIG or HTP exposure.

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