Choroidal vasculature in diabetic rats

This study aims to evaluate the diabetic influence on the choroidal vessels morphology. Twenty Wistar rats were divided into a control (CG) and a diabetic group (DG). The animals had the diabetes induced by an intra-venous injection of Alloxan (42 mg/kg). Transmission electron microscopy analysis focusing the choroidal vessels was done one (T2) and twelve (T3) months after the diabetes induction. The CG rats in T3 showed vesicles and dense bodies in the endothelial and pericytic cells; the same structures were observed in the DG at T2. The DG rats in T3 had even more and intense changes than the T2DG rats. The morphological evaluation indicates that the choroidal vessels are affected in diabetes and the disease accelerates degenerative processes in the rat choroidal vasculature.

Alterações morfológicas nos vasos da íris de ratos normais e diabéticos aloxânicos

Pós-graduação em Bases Gerais da Cirurgia - FMB

Histoquímica e ultra-estrutura da musculatura ventricular esquerda de ratos diabéticos: efeitos do exercício físico

Pós-graduação em Ciências Biológicas (Biologia Celular e Molecular) - IBRC

Avaliação ultra-estrutural do endotélio corneal de ratos normais e de diabéticos aloxânicos

Pós-graduação em Bases Gerais da Cirurgia - FMB

Efeitos do treinamento físico moderado nas concentrações de grelina, leptina e no eixo GH-IGF em ratos diabéticos

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Treinamento físico aeróbio e o eixo de crescimento GH/IGF-1 em ratos diabéticos experimentais

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Estudo da cicatrização de anastomoses realizadas no íleo terminal e cólon distal de ratos normais e diabéticos: análise morfométrica e ultraestrututral do colágeno

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Peer-led diabetes self-management programme for community-dwelling older people in China : study protocol for a quasi-experimental design

Aim. A protocol for a new peer-led self-management programme for communitydwelling older people with diabetes in Shanghai, China. Background. The increasing prevalence of type 2 diabetes poses major public health challenges. Appropriate education programmes could help people with diabetes to achieve self-management and better health outcomes. Providing education programmes to the fast growing number of people with diabetes present a real challenge to Chinese healthcare system, which is strained for personnel and funding shortages. Empirical literature and expert opinions suggest that peer education programmes are promising. Design. Quasi-experimental. Methods. This study is a non-equivalent control group design (protocol approved in January, 2008). A total of 190 people, with 95 participants in each group, will be recruited from two different, but similar, communities. The programme, based on Social Cognitive Theory, will consist of basic diabetes instruction and social support and self-efficacy enhancing group activities. Basic diabetes instruction sessions will be delivered by health professionals, whereas social support and self-efficacy enhancing group activities will be led by peer leaders. Outcome variables include: self-efficacy, social support, self-management behaviours, depressive status, quality of life and healthcare utilization, which will be measured at baseline, 4 and 12 weeks. Discussion. This theory-based programme tailored to Chinese patients has potential for improving diabetes self-management and subsequent health outcomes. In addition, the delivery mode, through involvement of peer leaders and existing community networks,is especially promising considering healthcare resource shortage in China.

Implant healing in experimental animal models of diabetes.

Diabetes mellitus is becoming increasingly prevalent worldwide. Additionally, there is an increasing number of patients receiving implantable devices such as glucose sensors and orthopedic implants. Thus, it is likely that the number of diabetic patients receiving these devices will also increase. Even though implantable medical devices are considered biocompatible by the Food and Drug Administration, the adverse tissue healing that occurs adjacent to these foreign objects is a leading cause of their failure. This foreign body response leads to fibrosis, encapsulation of the device, and a reduction or cessation of device performance. A second adverse event is microbial infection of implanted devices, which can lead to persistent local and systemic infections and also exacerbates the fibrotic response. Nearly half of all nosocomial infections are associated with the presence of an indwelling medical device. Events associated with both the foreign body response and implant infection can necessitate device removal and may lead to amputation, which is associated with significant morbidity and cost. Diabetes mellitus is generally indicated as a risk factor for the infection of a variety of implants such as prosthetic joints, pacemakers, implantable cardioverter defibrillators, penile implants, and urinary catheters. Implant infection rates in diabetic patients vary depending upon the implant and the microorganism, however, for example, diabetes was found to be a significant variable associated with a nearly 7.2% infection rate for implantable cardioverter defibrillators by the microorganism Candida albicans. While research has elucidated many of the altered mechanisms of diabetic cutaneous wound healing, the internal healing adjacent to indwelling medical devices in a diabetic model has rarely been studied. Understanding this healing process is crucial to facilitating improved device design. The purpose of this article is to summarize the physiologic factors that influence wound healing and infection in diabetic patients, to review research concerning diabetes and biomedical implants and device infection, and to critically analyze which diabetic animal model might be advantageous for assessing internal healing adjacent to implanted devices.

Retinopathy is reduced during experimental diabetes in a mouse model of outer retinal degeneration

PURPOSE. Diabetic patients who also have retinitis pigmentosa (RP) appear to have fewer and less severe retinal microvascular lesions. Diabetic retinopathy may be linked to increased inner retinal hypoxia, with the possibility that this is exacerbated by oxygen usage during the dark-adaptation response. Therefore, patients with RP with depleted rod photoreceptors may encounter proportionately less retinal hypoxia, and, when diabetes is also present, there may be fewer retinopathic lesions. This hypothesis was tested in rhodopsin knockout mice (Rho(-/-)) as an RP model in which the diabetic milieu is superimposed. The study was designed to investigate whether degeneration of the outer retina has any impact on hypoxia, to examine diabetes-related retinal gene expression responses, and to assess lesions of diabetic retinopathy.

The AGE inhibitor pyridoxamine inhibits development of retinopathy in experimental diabetes

We examined the ability of pyridoxamine (PM), an inhibitor of formation of advanced glycation end products (AGEs) and lipoxidation end products (ALEs), to protect against diabetes-induced retinal vascular lesions. The effects of PM were compared with the antioxidants vitamin E (VE) and R-alpha-lipoic acid (LA) in streptozotocin-induced diabetic rats. Animals were given either PM (1 g/l drinking water), VE (2,000 IU/kg diet), or LA (0.05%/kg diet). After 29 weeks of diabetes, retinas were examined for pathogenic changes, alterations in extracellular matrix (ECM) gene expression, and accumulation of the immunoreactive AGE/ALE N-epsilon-(carboxymethyl)lysine (CML). Acellular capillaries were increased more than threefold, accompanied by significant upregulation of laminin immunoreactivity in the retinal microvasculature. Diabetes also increased mRNA expression for fibronectin (2-fold), collagen IV (1.6-fold), and laminin beta chain (2.6-fold) in untreated diabetic rats compared with nondiabetic rats. PM treatment protected against capillary drop-out and limited laminin protein upregulation and ECM mRNA expression and the increase in CML in the retinal vasculature. VE and LA failed to protect against retinal capillary closure and had inconsistent effects on diabetes-related upregulation of ECM mRNAs. These results indicate that the AGE/ALE inhibitor PM protected against a range of pathological changes in the diabetic retina and may be useful for treating diabetic retinopathy.

CD11b+ bone marrow-derived monocytes are the major leukocyte subset responsible for retinal capillary leukostasis in experimental diabetes in mouse and express high levels of CCR5 in the circulation

We investigated the phenotype of cells involved in leukostasis in the early stages of streptozotocin-induced diabetes in mice by direct observation and by adoptive transfer of calcein-AM-labeled bone marrow-derived leukocytes from syngeneic mice. Retinal whole mounts, confocal microscopy, and flow cytometry ex vivo and scanning laser ophthalmoscopy in vivo were used. Leukostasis in vivo and ex vivo in retinal capillaries was increased after 2 weeks of diabetes (Hb A(1c), 14.2 ± 1.2) when either donor or recipient mice were diabetic. Maximum leukostasis occurred when both donor and recipient were diabetic. CD11b(+), but not Gr1(+), cells were preferentially entrapped in retinal vessels (fivefold increase compared with nondiabetic mice). In diabetic mice, circulating CD11b(+) cells expressed high levels of CCR5 (P = 0.04), whereas spleen (P = 0.0001) and retinal (P = 0.05) cells expressed increased levels of the fractalkine chemokine receptor. Rosuvastatin treatment prevented leukostasis when both recipient and donor were treated but not when donor mice only were treated. This effect was blocked by treatment with mevalonate. We conclude that leukostasis in early diabetic retinopathy involves activated CCR5(+)CD11b(+) myeloid cells (presumed monocytes). However, leukostasis also requires diabetes-induced changes in the endothelium, because statin therapy prevented leukostasis only when recipient mice were treated. The up-regulation of the HMG-CoA reductase pathway in the endothelium is the major metabolic dysregulation promoting leukostasis.

Induction of alloxan/streptozotocin diabetes in dogs: a revised experimental technique

The diabetic dog represents an excellent model for use in many aspects of diabetic research. The present paper describes, in detail, a reproducible experimental protocol for the successful induction of chemical diabetes in beagles using a combination of the 2 pancreatic beta-cell cytoxic agents alloxan and streptozotocin.