scholarly journals The HND mouse, a nonobese model of type 2 diabetes mellitus with impaired insulin secretion

2005 ◽  
Vol 153 (6) ◽  
pp. 971-979 ◽  
Author(s):  
Fumihiko Horio ◽  
Shin Teradaira ◽  
Tsunehiko Imamura ◽  
Rea Victoria P Anunciado ◽  
Misato Kobayashi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Insulin Release ◽  
Neural Control ◽  
Serum Insulin ◽  
The Philippines

Objectives: This study aimed to develop a novel type 2 diabetes model designated the HND (Horio–Niki diabetic) mouse, by transferring diabetogenic genes from wild castaneus mice (Mus musculus castaneus) captured in the Philippines into laboratory mice (C57BL/6J:B6). Methods: Offspring from the cross between a wild male and a B6 female were backcrossed to the sire. One male backcross which exhibited fasting hyperglycemia was crossed with a B6 female to comprise the fundamental stock (F0). Thereafter, full-sib mating was performed, and mice with impaired glucose tolerance were selected and bred from the F2 generation. Characterization of the phenotype of HND mice and insulin release from their islets was evaluated with F12 generation males. Results: The male HND mice were lean, and spontaneously exhibited impaired glucose tolerance at a high incidence rate at 6 weeks of age. Their serum insulin levels in response to intraperitoneal glucose were markedly attenuated. However, glucose-induced insulin release from isolated HND islets was not affected. Notably, inhibition of glucose-induced insulin release by epinephrine was more pronounced in HND islets than in B6 islets. Moreover, in vivo treatment of HND mice with the α2-adrenergic receptor agonist clonidine resulted in marked hypoinsulinemic hyperglycemia. Conclusions: We suggest the HND mouse may be a distinctive and useful model for type 2 diabetes with impaired neural control of insulin secretion.

scholarly journals TRAIL reduces impaired glucose tolerance and NAFLD in the high-fat diet fed mouse

2018 ◽  
Vol 132 (1) ◽  
pp. 69-83 ◽  
Author(s):  
Stella Bernardi ◽  
Barbara Toffoli ◽  
Veronica Tisato ◽  
Fleur Bossi ◽  
Stefania Biffi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
High Fat Diet ◽  
Disease Onset ◽  
High Fat ◽  
Primary Hepatocytes

Recent studies suggest that a circulating protein called TRAIL (TNF-related apoptosis inducing ligand) may have an important role in the treatment of type 2 diabetes. It has been shown that TRAIL deficiency worsens diabetes and that TRAIL delivery, when it is given before disease onset, slows down its development. The present study aimed at evaluating whether TRAIL had the potential not only to prevent, but also to treat type 2 diabetes. Thirty male C57BL/6J mice were randomized to a standard or a high-fat diet (HFD). After 4 weeks of HFD, mice were further randomized to receive either placebo or TRAIL, which was delivered weekly for 8 weeks. Body weight, food intake, fasting glucose, and insulin were measured at baseline and every 4 weeks. Tolerance tests were performed before drug randomization and at the end of the study. Tissues were collected for further analyses. Parallel in vitro studies were conducted on HepG2 cells and mouse primary hepatocytes. TRAIL significantly reduced body weight, adipocyte hypertrophy, free fatty acid levels, and inflammation. Moreover, it significantly improved impaired glucose tolerance, and ameliorated non-alcoholic fatty liver disease (NAFLD). TRAIL treatment reduced liver fat content by 47% in vivo as well as by 45% in HepG2 cells and by 39% in primary hepatocytes. This was associated with a significant increase in liver peroxisome proliferator-activated receptor (PPAR) γ (PPARγ) co-activator-1 α (PGC-1α) expression both in vivo and in vitro, pointing to a direct protective effect of TRAIL on the liver. The present study confirms the ability of TRAIL to significantly attenuate diet-induced metabolic abnormalities, and it shows for the first time that TRAIL is effective also when administered after disease onset. In addition, our data shed light on TRAIL therapeutic potential not only against impaired glucose tolerance, but also against NAFLD.

scholarly journals Xenin-25 Amplifies GIP-Mediated Insulin Secretion in Humans With Normal and Impaired Glucose Tolerance but Not Type 2 Diabetes

Diabetes ◽  
2012 ◽  
Vol 61 (7) ◽  
pp. 1793-1800 ◽  
Author(s):  
B. M. Wice ◽  
D. N. Reeds ◽  
H. D. Tran ◽  
D. L. Crimmins ◽  
B. W. Patterson ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance

scholarly journals Effects of Hydrogen Sulfide on Carbohydrate Metabolism in Obese Type 2 Diabetic Rats

Molecules ◽  
2019 ◽  
Vol 24 (1) ◽  
pp. 190 ◽  
Author(s):  
Sevda Gheibi ◽  
Sajad Jeddi ◽  
Khosrow Kashfi ◽  
Asghar Ghasemi
Keyword(s):  
Type 2 Diabetes ◽  
Hydrogen Sulfide ◽  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Carbohydrate Metabolism ◽  
Serum Insulin ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Type 2 Diabetic

Hydrogen sulfide (H2S) is involved in the pathophysiology of type 2 diabetes. Inhibition and stimulation of H2S synthesis has been suggested to be a potential therapeutic approach for type 2 diabetes. The aim of this study was therefore to determine the effects of long-term sodium hydrosulfide (NaSH) administration as a H2S releasing agent on carbohydrate metabolism in type 2 diabetic rats. Type 2 diabetes was established using high fat-low dose streptozotocin. Rats were treated for 9 weeks with intraperitoneal injections of NaSH (0.28, 0.56, 1.6, 2.8, and 5.6 mg/kg). Serum glucose was measured weekly for one month and then at the end of the study. Serum insulin was measured before and after the treatment. At the end of the study, glucose tolerance, pyruvate tolerance and insulin secretion were determined and blood pressure was measured. In diabetic rats NaSH at 1.6–5.6 mg/kg increased serum glucose (11%, 28%, and 51%, respectively) and decreased serum insulin, glucose tolerance, pyruvate tolerance and in vivo insulin secretion. In controls, NaSH only at 5.6 mg/kg increased serum glucose and decreased glucose tolerance, pyruvate tolerance and insulin secretion. Chronic administration of NaSH in particular at high doses impaired carbohydrate metabolism in type 2 diabetic rats.

1501-P: Reproducibility of Glycemic Measures among Youth and Adults with Impaired Glucose Tolerance (IGT) or Recently Diagnosed Type 2 Diabetes (T2D) in the Restoring Insulin Secretion (RISE) Study

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1501-P
Author(s):  
ASHLEY H. TJADEN ◽  
SHARON EDELSTEIN ◽  
SILVA A. ARSLANIAN ◽  
ELENA BARENGOLTS ◽  
SONIA CAPRIO ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance
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