Decreased cortical bone thickness in spontaneously non-insulin-dependent diabetic GK rats

Östenson, Claes Göran; Fière, Vincent; Ahmed, Mahmood; Lindström, Per; Brismar, Kerstin; Brismar, Tom; Kreicbergs, Andris

doi:10.1016/s1056-8727(96)00079-7

Cited by 15 publications

(7 citation statements)

References 25 publications

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“…We investigated the influence of insulin-induced hypoglycaemia on islet blood perfusion in Type 2 diabetic GK rats. Although neuropathic changes are known to occur in diabetic GK rats [49,50], an even more pronounced decrease in islet blood flow occurred in the GK rats than in normal rats. Of interest, diabetic GK rats and their hybrids have been shown to have an increased islet blood flow during normal conditions dependent on a glucose-dependent mechanism mediated by the vagus nerve [11,13].…”

Section: Discussionmentioning

confidence: 82%

Hypoglycaemia induces decreased islet blood perfusion mediated by the central nervous system in normal and Type 2 diabetic GK rats

et al. 2003

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Aims/hypothesis. The aim of this study was to evaluate the effects of induced hypoglycaemia on pancreatic-islet blood flow in normal rats and in the GK rat, an animal model of Type 2 diabetes which normally has an increased islet blood perfusion. Methods. A 50% reduction in blood glucose concentrations was achieved by intravenous administration of a rapidly acting insulin (15 IU/kg body weight). Blood flows were measured by a non-radioactive microsphere technique. Results. A pronounced decrease in islet blood flow was observed in all animals, but preferentially in the Type 2 diabetic GK rats. When a similar dose of insulin was given to whole-pancreas transplanted rats only islet blood flow in the native pancreas was decreased, whereas that of the transplanted, i.e. denervated, pancreas was unchanged. Administration of 2-deoxy-Dglucose, which induces intracellular glucopenia especially in neurons, also decreased islet blood flow despite a systemic hyperglycaemia. Conclusion/interpretation. Hypoglycaemia leads to a preferential decrease in pancreatic-islet blood perfusion. The effect is probably mediated by the central nervous system, since 2-deoxy D-glucose-induced neuronal glucopenia caused a similar decrease in blood flow. The effects of islet blood flow are not likely to be mediated by nervous stimulation of the adrenal glands, with an associated release of catecholamines, because the transplanted pancreas was not affected by hypoglycaemia. The decreased islet blood perfusion could possibly diminish the output of insulin from the islets, thereby preventing a further decrease in blood glucose concentrations. [Diabetologia (2003[Diabetologia ( ) 46:1124[Diabetologia ( -1130

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Section: Discussionmentioning

confidence: 82%

Hypoglycaemia induces decreased islet blood perfusion mediated by the central nervous system in normal and Type 2 diabetic GK rats

et al. 2003

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“…However, this is a model of type 1 diabetes and, hence, inappropriate for analysis of type 2 diabetes because the pathophysiological status is very different. Several rat models of type 2 diabetes are available, such as the Wistar fatty rat, Otsuka Long-Evans Tokushima fatty rat, Goto-Kakizaki rat, Zucker diabetic fatty (ZDF) rat, and ZSF1 rat [6,14,15,16,17]. However, these are obese type 2 diabetic model rats.…”

Section: Discussionmentioning

confidence: 99%

Oxidative and Nitrosative Stress and Progression of Diabetic Nephropathy in Type 2 Diabetes

Fujii¹,

Kono²,

Nakai³

et al. 2010

Am J Nephrol

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Background: The role of nitric oxide (NO) is controversial in diabetes nephropathy progression and the mechanisms remain unknown, especially in non-obese type 2 diabetes. To examine mechanisms of nephropathy progression in non-obese type 2 diabetes, we used spontaneously diabetic Torii (SDT) rats, a newly established model of non-obese type 2 diabetes. Methods: Fourteen male Sprague-Dawley rats were used as a control (20 weeks, n = 6; 30 weeks, n = 8), and 20-week-old male SDT rats were divided into 2 groups: diabetic (DM, n = 8) and DM + insulin (n = 8) groups. Twenty- and 36-week-old rats were sacrificed, and blood, urine, and histomorphometric analyses, mRNA expression analysis of endothelial NO synthase (eNOS) and NADPH oxidase, and blood pressure measurement were performed. Results: At 36 weeks, NO metabolites, and 8-hydroxydeoxyguanosine (8-OHdG) were significantly higher in the diabetic group than in the other 2 groups. Further renal studies showed increased glomerular volume and mesangial area, and intensified eNOS, 8-OHdG, and nitrotyrosine immunostaining in the diabetic group. Oxidative and nitrosative stress were positively associated with increased glomerular volume and mesangial area, which were mostly recovered by insulin therapy. Conclusions: NO and oxidative stress increased in SDT rats, suggesting that these play key roles in nephropathy progression in non-obese type 2 diabetes.

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“…To determine serum insulin and glucose levels, the blood samples were centrifuged at 7 g at 4°C (Ostenson et al., 1997) for 15 min. Serum glucose and insulin levels were determined by the clinical test laboratory in the Department of Kitasato University (OLYMPUS AU510, DH‐UV method), and serum insulin levels were determined by radioimmunoassay in SRL Co. Ltd (Tokyo, Japan).…”

Section: Methodsmentioning

confidence: 99%

Expression of Nestin and IGF‐1 in Rat Pancreas after Streptozotocin Administration

Nagasao

Yoshioka

Amasaki

et al. 2004

Anat Histol Embryol

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The present study examines whether centroacinar (CA) and intercalated duct (ICD) cells can serve as stem cells, after administration of the diabetogenic agent streptozotocin (STZ). Thirty rats were divided into five experimental groups: (1) control, (2) 1 day after STZ (STZ-1), (3) 3 days after STZ (STZ-3), (4) 7 days after STZ (STZ-7) and (5) 14 days after STZ (STZ-14). Many small pancreatic islets were observed in the STZ-7 group than in the other experimental groups, and many of these small islets were in close contact with ICD and CA cells. A higher number of nestin, insulin-like growth factor-1 (IGF-1) and IGF-1-receptor positive ICD and CA cells were observed at STZ-3 and STZ-7 than at the others. These expression patterns coincided well with the proliferating cell nuclear antigen pattern. The results suggest that rat pancreatic endocrine cells after damage by STZ administration might be recovered from newly generated cells derived from ICD and CA cells.

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Decreased cortical bone thickness in spontaneously non-insulin-dependent diabetic GK rats

Cited by 15 publications

References 25 publications

Hypoglycaemia induces decreased islet blood perfusion mediated by the central nervous system in normal and Type 2 diabetic GK rats

Hypoglycaemia induces decreased islet blood perfusion mediated by the central nervous system in normal and Type 2 diabetic GK rats

Oxidative and Nitrosative Stress and Progression of Diabetic Nephropathy in Type 2 Diabetes

Expression of Nestin and IGF‐1 in Rat Pancreas after Streptozotocin Administration

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