1045: Pioglitazone Ameliorates Penile Corpora Veno-Occlusive Dysfunction (CVOD) in a Rat Model of Type 2 Diabetes

2005 ◽  
Vol 173 (4S) ◽  
pp. 283-284
Author(s):  
Istvan Kovanecz ◽  
Monica G. Ferrini ◽  
Hugo H. Davila ◽  
Jacob Rajfer ◽  
Nestor F. Gonzalez-Cadavid
Keyword(s):  
2021 ◽  
Vol 49 (3) ◽  
pp. 030006052199759
Author(s):  
Jiajia Tian ◽  
Yanyan Zhao ◽  
Lingling Wang ◽  
Lin Li

Aims To analyze expression of members of the Toll-like receptor (TLR)4/myeloid differentiation primary response 88 (MyD88)/nuclear factor (NF)-κB signaling pathway in the heart and liver in a rat model of type 2 diabetes mellitus (T2DM). Our overall goal was to understand the underlying pathophysiological mechanisms. Methods We measured fasting blood glucose (FBG) and insulin (FINS) in a rat model of T2DM. Expression of members of the TLR4/MyD88/NF-κB signaling pathway as well as downstream cytokines was investigated. Levels of mRNA and protein were assessed using quantitative real-time polymerase chain reaction and western blotting, respectively. Protein content of tissue homogenates was assessed using enzyme-linked immunosorbent assays. Results Diabetic rats had lower body weights, higher FBG, higher FINS, and higher intraperitoneal glucose tolerance than normal rats. In addition, biochemical indicators related to heart and liver function were elevated in diabetic rats compared with normal rats. TLR4 and MyD88 were involved in the occurrence of T2DM as well as T2DM-related heart and liver complications. TLR4 caused T2DM-related heart and liver complications through activation of NF-κB. Conclusions TLR4/MyD88/NF-κB signaling induces production of tumor necrosis factor-α, interleukin-6, and monocyte chemoattractant protein-1, leading to the heart- and liver-related complications of T2DM.


2015 ◽  
Vol 60 (1) ◽  
pp. 94-100 ◽  
Author(s):  
Raziye Akcılar ◽  
Sebahat Turgut ◽  
Vildan Caner ◽  
Aydın Akcılar ◽  
Ceylan Ayada ◽  
...  
Keyword(s):  

2016 ◽  
Vol 62 (6) ◽  
pp. 416-424
Author(s):  
Kazuhiro KUBO ◽  
Ayano KOIDO ◽  
Misako KITANO ◽  
Hirotaka YAMAMOTO ◽  
Morio SAITO

2013 ◽  
Vol 12 (1) ◽  
pp. 136 ◽  
Author(s):  
Latt S Mansor ◽  
Eileen R Gonzalez ◽  
Mark A Cole ◽  
Damian J Tyler ◽  
Jessica H Beeson ◽  
...  

2015 ◽  
Vol 228 (1) ◽  
pp. 13-23 ◽  
Author(s):  
Xinrong Zhou ◽  
Bangguo Qian ◽  
Ning Ji ◽  
Conghui Lui ◽  
Zhiyuan Liu ◽  
...  

Gastric bypass surgery produces clear antidiabetic effects in a substantial proportion of morbidly obese patients. In view of the recent trend away from ‘bariatric’ surgery and toward ‘metabolic’ surgery, it is important to elucidate the enhancing effect of bypass surgery on pancreatic β-cell mass, which is related to diabetes remission in non-obese patients. We investigated the effects of gastric bypass surgery on glycemic control and other pancreatic changes in a spontaneous non-obese type 2 diabetes Goto-Kakizaki rat model. Significant improvements in postprandial hyperglycemia and plasma c-peptide level were observed when glucose was administered orally post-surgery. Other important events observed after surgery were enhanced first phase insulin secretion in a in site pancreatic perfusion experiment, pancreatic hyperplasia, improved islet structure (revealed by immunohistochemical analysis), striking increase in β-cell mass, slight increase in ratio of β-cell area to total pancreas area, and increased number of small islets closely related to exocrine ducts. No notable changes were observed in ratio of β-cell to non-β endocrine cell area, β-cell apoptosis, or β-cell proliferation. These findings demonstrate that gastric bypass surgery in this rat model increases endocrine cells and pancreatic hyperplasia, and reflect the important role of the gastrointestinal system in regulation of metabolism.


2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Jeanine J Prompers ◽  
Bart Wessels ◽  
Jolita Ciapaite ◽  
Klaas Nicolay

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