scholarly journals Lipid‐lowering effect on glucose metabolism in the type 2 diabetes mouse model of TALLYHO/Jng

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Jennifer M. Fortuna ◽  
Ola A. Mostafa ◽  
Taryn P. Stewart ◽  
Jung Han Kim
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Metabolism ◽  
Mouse Model ◽  
Lipid Lowering ◽  
Lowering Effect ◽  
Lipid Lowering Effect ◽  
Diabetes Mouse

Structural analysis of tooth and jawbone in a type 2 diabetes mouse model

2014 ◽  
Author(s):  
Silvia Pabisch ◽  
Tsuguno Yamaguchi ◽  
Yasushi Koike ◽  
Kenji Egashira ◽  
Shinsuke Kataoka ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Structural Analysis ◽  
Mouse Model ◽  
Diabetes Mouse

scholarly journals Pharmacological Sirt6 inhibition improves glucose tolerance in a type 2 diabetes mouse model

2017 ◽  
Vol 31 (7) ◽  
pp. 3138-3149 ◽  
Author(s):  
Giovanna Sociali ◽  
Mirko Magnone ◽  
Silvia Ravera ◽  
Patrizia Damonte ◽  
Tiziana Vigliarolo ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Tolerance ◽  
Mouse Model ◽  
Diabetes Mouse

scholarly journals Porphyromonas gingivalis induces entero-hepatic metabolic derangements with alteration of gut microbiota in a type 2 diabetes mouse model

2021 ◽  
Author(s):  
Yoichiro Kashiwagi ◽  
Syunsuke Aburaya ◽  
Naoyuki Sugiyama ◽  
Yuki Narukawa ◽  
Yuta Sakamoto ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Mouse Model ◽  
Gut Microbiota ◽  
Porphyromonas Gingivalis ◽  
Alveolar Bone ◽  
Periodontal Pathogens ◽  
Periodontal Infection ◽  
Related Enzyme ◽  
Diabetes Mouse

Abstract Periodontal infection is thought to generate systemic inflammation, thus aggravating diabetes. Furthermore, orally administered periodontal pathogens may directly alter the gut microbiota. To elucidate this, using an obese db/db diabetes mice, orally treated with Porphyromonas gingivalis (Pg), we screened for Pg-specific peptides in intestinal fecal specimens and examined whether Pg localization affected the intestinal microbiota profile altering gut metabolite levels. Finally, we screened whether deterioration of fasting hyperglycemia was related to changes in intrahepatic glucose metabolism, using proteome and metabolome analyses. As results; (1) Oral Pg treatment aggravated both fasting and postprandial hyperglycemia (P < 0.05) with a significant (P < 0.01) increase in dental alveolar bone resorption. (2) Pg-specific peptides were identified in fecal specimens after oral Pg treatment and intestinal Pg profoundly altered gut microbiome profiles at the phylum, family, and genus levels. Prevotella showed the largest increase in abundance. Furthermore, Pg-treatment significantly altered intestinal metabolite levels. (3) Fasting hyperglycemia was associated with increases in gluconeogenesis-related enzyme and metabolite levels without changes in proinflammatory cytokine expressions and insulin resistance. This work reveals that oral Pg administration induced gut microbiota changes, leading to entero-hepatic metabolic derangements, thereby aggravating hyperglycemia in an obese type 2 diabetes mouse model.

scholarly journals Porphyromonas gingivalis induces entero-hepatic metabolic derangements with alteration of gut microbiota in a type 2 diabetes mouse model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yoichiro Kashiwagi ◽  
Shunsuke Aburaya ◽  
Naoyuki Sugiyama ◽  
Yuki Narukawa ◽  
Yuta Sakamoto ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Mouse Model ◽  
Gut Microbiota ◽  
Porphyromonas Gingivalis ◽  
Alveolar Bone ◽  
Postprandial Hyperglycemia ◽  
Periodontal Pathogens ◽  
Periodontal Infection ◽  
Diabetes Mouse

AbstractPeriodontal infection induces systemic inflammation; therefore, aggravating diabetes. Orally administered periodontal pathogens may directly alter the gut microbiota. We orally treated obese db/db diabetes mice using Porphyromonas gingivalis (Pg). We screened for Pg-specific peptides in the intestinal fecal specimens and examined whether Pg localization influenced the intestinal microbiota profile, in turn altering the levels of the gut metabolites. We evaluated whether the deterioration in fasting hyperglycemia was related to the changes in the intrahepatic glucose metabolism, using proteome and metabolome analyses. Oral Pg treatment aggravated both fasting and postprandial hyperglycemia (P < 0.05), with a significant (P < 0.01) increase in dental alveolar bone resorption. Pg-specific peptides were identified in fecal specimens following oral Pg treatment. The intestinal Pg profoundly altered the gut microbiome profiles at the phylum, family, and genus levels; Prevotella exhibited the largest increase in abundance. In addition, Pg-treatment significantly altered intestinal metabolite levels. Fasting hyperglycemia was associated with the increase in the levels of gluconeogenesis-related enzymes and metabolites without changes in the expression of proinflammatory cytokines and insulin resistance. Oral Pg administration induced gut microbiota changes, leading to entero-hepatic metabolic derangements, thus aggravating hyperglycemia in an obese type 2 diabetes mouse model.

Molecular and cellular bases of diabetes: Focus on type 2 diabetes mouse model-TallyHo

2019 ◽  
Vol 1865 (9) ◽  
pp. 2276-2284 ◽  
Author(s):  
Kavya Tamarai ◽  
Jasvinder Singh Bhatti ◽  
P. Hemachandra Reddy
Keyword(s):  
Type 2 Diabetes ◽  
Mouse Model ◽  
Diabetes Mouse

scholarly journals Effects of Sodium-Glucose Cotransporter 2 Inhibition on Glucose Metabolism, Liver Function, Ascites, and Hemodynamics in a Mouse Model of Nonalcoholic Steatohepatitis and Type 2 Diabetes

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Koichi Yabiku ◽  
Keiko Nakamoto ◽  
Maho Tsubakimoto
Keyword(s):  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Heart Rate ◽  
Blood Glucose ◽  
Glucose Metabolism ◽  
Mouse Model ◽  
Nonalcoholic Steatohepatitis ◽  
Blood Glucose Monitoring ◽  
Sodium Glucose Cotransporter

Many blood glucose-lowering drugs cannot be used once patients with type 2 diabetes (T2D) and nonalcoholic fatty liver disease develop nonalcoholic steatohepatitis (NASH). Therefore, such patients often require insulin treatment. We aimed to determine the effect of sodium-glucose cotransporter 2 inhibitor (SGLT2i) dapagliflozin monotherapy on glucose metabolism in a mouse model of NASH/T2D, with a focus on its diuretic effects. To imitate ascites and to determine its severity by imaging, meglumine sodium amidotrizoate (MSA) was infused into the abdominal cavities of mice. The reduction in ascites induced by dapagliflozin was compared with that induced by furosemide using microcomputed tomography. The effects of each drug on hemodynamics were also compared. A dapagliflozin-related improvement in glucose tolerance was achieved in mice fed a high-fat diet (HFD) or an HFD + methionine-and-choline-deficient diet (MCDD). In dapagliflozin-treated NASH mice, hypoglycemia was not identified during 24-hour casual blood glucose monitoring. In the dapagliflozin and furosemide-treated groups, the time taken for the resolution of artificial ascites was significantly shorter than in the untreated group, and there were no significant differences between these groups. Furosemide significantly reduced the blood pressure and significantly increased the heart rate of the mice. Dapagliflozin caused a mild decrease in systolic, but not diastolic blood pressure, and the heart rate and circulating catecholamine and renin-aldosterone concentrations were unaffected. Dapagliflozin treatment improved glycemic control in the NASH mice versus untreated mice. Thus, dapagliflozin had a prompt diuretic effect but did not adversely affect the hemodynamics of mice with NASH and T2D. Therefore, it may be useful for the treatment of patients with both T2D and liver cirrhosis.

Structural analysis of tooth and jawbone in a type 2 diabetes mouse model

2014 ◽  
Author(s):  
Felix Repp ◽  
Philip Kollmannsberger ◽  
Andreas Roschger ◽  
Paul Roschger ◽  
Wolfgang Wagermaier ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Structural Analysis ◽  
Mouse Model ◽  
Diabetes Mouse
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