Stage-dependent effect of pancreatic transplantation on diabetic ocular complications in the spontaneously diabetic torii rat

Miao, Gang; Ito, Toshinori; Uchikoshi, Fumihiro; Kamei, Motohiro; Akamaru, Yusuke; Kiyomoto, Tetsuma; Komoda, Hiroshi; Nozawa, Masumi; Matsuda, Hikaru

doi:10.1097/01.tp.0000113790.88730.41

Cited by 20 publications

(19 citation statements)

References 27 publications

(27 reference statements)

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“…The male SDT rats develop hyperglycemia more frequently than female rats [10], and the hyperglycemia and glucosuria occurs spontaneously at about 20-weeks-of-age. Cataracts in SDT rats are detected at around 40-weeks-of-age [10,12,13]. Some male animals have tractional retinal detachment with fibrous proliferation, and massive hemorrhaging in the anterior chamber at around 40-50-weeks-of-age [10,12].…”

Section: Introductionmentioning

confidence: 97%

Electroretinographic study of spontaneously diabetic Torii rats

et al. 2008

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Spontaneously diabetic Torii (SDT) rats are an inbred strain of rats with a non-obese type 2 diabetes mellitus that were isolated from an outbred colony of Sprague-Dawley (SD) rats. Electroretinograms (ERGs) were recorded from SDT and SD (controls) rats at 10- and 44-weeks-of-age to determine their retinal function. The amplitudes and implicit times of the ERGs of the right and left eyes were not significantly different indicating that the intra-individual variation was small. Both amplitudes and implicit times of the ERGs in the SDT rats were not significantly different from those of SD rats at 10-weeks-of-age. At 44-weeks-of-age, however, the a- and b-waves and the oscillatory potentials were significantly reduced with prolonged implicit times in the SDT rats compared to SD rats. These depressed ERGs may reflect vascular and neuronal damage throughout the retina as are seen in the advanced stages of human diabetic retinopathy. Thus, the SDT rat can be used to study the retinal physiology of diabetic retinopathy.

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Section: Introductionmentioning

confidence: 97%

Electroretinographic study of spontaneously diabetic Torii rats

et al. 2008

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“…In our previous report regarding insulin resistance of the SDT rats, insulin (Humulin N, 4 U/kg/d) was administered daily from the onset of diabetes and demand for insulin was gradually increased from 8 weeks after the onset of diabetes under nonfasting conditions [9]. In another one of our studies, we continued insulin treatment at a variable rate adjusted for glucose concentration, leading to increasing demand for as much as insulin of 30 U/kg/d (Humulin N) at 15 weeks after the onset of diabetes in the SDT rats (data not shown).…”

Section: Figmentioning

confidence: 99%

“…The diabetic SDT rats were defined as having a blood glucose level Ͼ250 mg/dL. In our previous study, SDT rats developed diabetes at a mean onset time of 25.2 Ϯ 3.9 weeks of age [9]. After PTx, blood glucose measurements were performed once per week during the first 5 weeks and then at least twice per week thereafter.…”

Section: Blood Glucose Measurementmentioning

confidence: 99%

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Development of β-Cells in the Native Pancreas After Pancreas Allo-Transplantation in the Spontaneously Diabetic Torii Rat

Shimada

Ito

Tanemura

et al. 2008

Journal of Surgical Research

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“…Unlike other studies (7,25), which used age-matched male SDT rats with different diabetes onsets and durations, we used male SDT rats with the same diabetes onsets and durations and characterized their diabetic features at 0, 8, and 16 wk after diabetes onset. At 0 wk, the ages of the control, SDT, and Olm groups of rats used in the study were 22.7 Ϯ 1.1, 22.2 Ϯ 0.7, and 22.6 Ϯ 0.7 wk (n ϭ 25 rats/group), respectively; this did not differ statistically among the groups.…”

Section: Characteristics Of Sdt Rats As a Model Of Human Nonobese Typmentioning

confidence: 99%

Heart angiotensin II-induced cardiomyocyte hypertrophy suppresses coronary angiogenesis and progresses diabetic cardiomyopathy

Masuda¹,

Muto²,

Fujisawa

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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Heart angiotensin II-induced cardiomyocyte hypertrophy suppresses coronary angiogenesis and progresses diabetic cardiomyopathy. Am J Physiol Heart Circ Physiol 302: H1871-H1883, 2012. First published March 2, 2012; doi:10.1152/ajpheart.00663.2011.-To examine whether and how heart ANG II influences the coordination between cardiomyocyte hypertrophy and coronary angiogenesis and contributes to the pathogenesis of diabetic cardiomyopathy, we used Spontaneously Diabetic Torii (SDT) rats treated without and with olmesartan medoxomil (an ANG II receptor blocker). In SDT rats, left ventricular (LV) ANG II, but not circulating ANG II, increased at 8 and 16 wk after diabetes onset. SDT rats developed LV hypertrophy and diastolic dysfunction at 8 wk, followed by LV systolic dysfunction at 16 wk, without hypertension. The SDT rat LV exhibited cardiomyocyte hypertrophy and increased hypoxia-inducible factor-1␣ expression at 8 wk and to a greater degree at 16 wk and interstitial fibrosis at 16 wk only. In SDT rats, coronary angiogenesis increased with enhanced capillary proliferation and upregulation of the angiogenic factor VEGF at 8 wk but decreased VEGF with enhanced capillary apoptosis and suppressed capillary proliferation despite the upregulation of VEGF at 16 wk. In SDT rats, the phosphorylation of VEGF receptor-2 increased at 8 wk alone, whereas the expression of the antiangiogenic factor thrombospondin-1 increased at 16 wk alone. All these events, except for hyperglycemia or blood pressure, were reversed by olmesartan medoxomil. These results suggest that LV ANG II in SDT rats at 8 and 16 wk induces cardiomyocyte hypertrophy without affecting hyperglycemia or blood pressure, which promotes and suppresses coronary angiogenesis, respectively, via VEGF and thrombospondin-1 produced from hypertrophied cardiomyocytes under chronic hypoxia. Thrombospondin-1 may play an important role in the progression of diabetic cardiomyopathy in this model. angiogenic factor; antiangiogenic factor; thrombospondin-1; vascular endothelial growth factor; vascular endothelial growth factor receptor-2 THE RISING INCIDENCE of type 2 diabetes mellitus raises major public health concerns because of the increased risk of cardiovascular complications (1, 2). Diabetic cardiomyopathy (DCM) is defined as left ventricular (LV) dysfunction that occurs independently of coronary artery disease and hypertension (1, 2). Its functional alterations are LV hypertrophy (LVH) and LV diastolic dysfunction, which may precede the development of LV systolic dysfunction (1, 2). Its pathological features involve cardiomyocyte hypertrophy and apoptosis, microvascular pathology, including abnormal capillary density and permeability, and interstitial fibrosis (1, 2, 6).The activation of the renin-angiotensin system (RAS) is well recognized in DCM. The circulating RAS is downregulated in diabetes (24, 35). Nevertheless, pharmacological blockade of the RAS with ANG II type 1 receptor blockers (ARBs) or angiotensin-converting enzyme inhibitors prevents cardiac damage in ...

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Stage-dependent effect of pancreatic transplantation on diabetic ocular complications in the spontaneously diabetic torii rat

Abstract: Our results indicate that the potential use of the SDT rat for diabetes study and the positive effect of PTx performed before the "point of no return" could prevent and cure diabetic ocular complications.

Cited by 20 publications

References 27 publications

Electroretinographic study of spontaneously diabetic Torii rats

Electroretinographic study of spontaneously diabetic Torii rats

Development of β-Cells in the Native Pancreas After Pancreas Allo-Transplantation in the Spontaneously Diabetic Torii Rat

Heart angiotensin II-induced cardiomyocyte hypertrophy suppresses coronary angiogenesis and progresses diabetic cardiomyopathy

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