Diabetic Rat Model (diabetic + rat_model)

Distribution by Scientific Domains

Selected Abstracts

Expression Of O-Acetyl Sialic Acid On Cerebral Microcirculation In A Glycine Or Taurine Treated Diabetic Rat Model

A Noe
Expression of sialic acid is altered in Diabetes mellitus. This modification has also been involved with both vascular and neurologic diseases, and with the increase of no enzymatic glycosylation of proteins. In our opinion, the lectins were very useful with specificity for sialic acids in order to determine the level of sialic acid expression on cerebral microcirculation in a diabetic Wistar rat model with streptozotocin. In this model, the glycine (1%) and taurine (0.5%) aminoacids were placed in drinking-water by six months. At the end of this time, the animals were sacrificed, their brains surgically removed and frozen in liquid nitrogen, and the specimens cut in serial sections. Immediately, the sections were incubated with different biotin-labelled lectins specific to sialic acid using peroxidase-labelled avidin as second ligand and H2O2 chromogen. The results showed greater O-acetyl sialic acid expression in cerebral capillaries of untreated diabetic rats than in glycine-, taurine-treated diabetic rats or than in control animals. The minor sialic acid expression may be an indicator of degenerative diseases such as Alzheimer's or the vascular disease of diabetic patients and probably is related to cellular protective properties of the glycine and taurine aminoacids. These first protective characteristics that have been observed in both ischemia with cellular ATP depletion models, suggest the utilization of aminoacids glycine or taurine in diabetic patient in order to avoid the development of microinfarcts. [source]

Comparative analysis of global gene expression profiles between diabetic rat wounds treated with vacuum-assisted closure therapy, moist wound healing or gauze under suction

Kathleen L Derrick
Abstract How differential gene expression affects wound healing is not well understood. In this study, Zucker diabetic fatty (fa/fa) male inbred rats were used to investigate gene expression during wound healing in an impaired wound-healing model. Whole genome microarray surveys were used to gain insight into the biological pathways and healing processes in acute excisional wounds treated with vacuum-assisted closure (V.A.C.) Therapy, moist wound healing (MWH) or gauze under suction (GUS). Global gene expression analyses after 2 days of healing indicated major differences with respect to both number of genes showing fold changes and pathway regulation between the three different wound treatments. Statistical analysis of expression profiles indicated that 5072 genes showed a >16-fold change with V.A.C. Therapy compared with 3601 genes with MWH and 3952 genes with GUS. Pathways and related genes associated with the early phases of wound healing diverged between treatment groups. For example, pathways involving angiogenesis, cytoskeletal regulation and inflammation were associated with elevated gene expression following V.A.C. Therapy. This study is the first to assess wound healing by whole genome interrogation in a diabetic rat model treated with different healing modalities. [source]

Recombinant human platelet-derived growth factor BB (rhPDGF-BB) and beta-tricalcium phosphate/collagen matrix enhance fracture healing in a diabetic rat model

Loay Al-Zube
Abstract Diabetes mellitus is a common systemic disease that has been associated with poor fracture healing outcomes. The mechanism through which diabetes impairs bone regeneration is unknown. One possible mechanism may be related to either decreased or uncoordinated release of local growth factors at the fracture site. Indeed, previous studies have found reduced platelet-derived growth factor (PDGF) levels in the fracture callus of diabetic rats, suggesting that local application of PDGF may overcome the negative effects of diabetes and promote fracture healing. To test this hypothesis, low (22 g) and high (75 ug) doses of recombinant human PDGF-BB (rhPDGF-BB) were applied directly to femur fracture sites in BB Wistar diabetic rats that were then compared to untreated or vehicle-treated animals. rhPDGF-BB treatment significantly increased early callus cell proliferation compared to that in control specimens. Low dose rhPDGF-BB treatment significantly increased callus peak torque values (p,<,0.05) at 8 weeks after fracture as compared to controls. High dose rhPDGF-BB treatment increased callus bone area at 12 weeks postfracture. These data indicate that rhPDGF-BB treatment ameliorates the effects of diabetes on fracture healing by promoting early cellular proliferation that ultimately leads to more bone formation. Local application of rhPDGF-BB may be a new therapeutic approach to treat diabetes-impaired fracture healing. 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 27: 1074,1081, 2009 [source]

Effects of insulin-mimetic vanadyl-poly(,-glutamic acid) complex on diabetic rat model

Rongzhang Hu
Abstract Poly-,-glutamic acid (,-PGA) prepared by fermentation of microbe was used as drug carrier for vanadium sulfate to obtain vanadyl-poly-,-glutamic acid (VO-,-PGA) complex. The FI-IR spectrum of the complex demonstrated that the expected VO-,-PGA complex is formed by the coordination of VO2+ through the side chain carboxylic groups of the ,-PGA. Studies of the complex in treating type I diabetes were carried out on alloxan induced diabetes rats. The results of treating the rats in 2 weeks and then stopping administration for 10 days showed that VO-,-PGA can effectively lower blood glucose levels of diabetic rats during administration. But after ceasing treatment there were no differences between groups in blood glucose level and water intake. The results of oral glucose tolerance and some serum parameters also demonstrated that VO-,-PGA was more effective than vanadium sulfate in treating diabetic rats. 2010 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 99:3041,3047, 2010 [source]

Evidence for lymphatic transport of insulin by topically applied biphasic vesicles

Martin J. King
ABSTRACT The cutaneous delivery pathway through the lymphatics of a novel transdermal lipid-based delivery system (biphasic vesicles), which was previously shown to deliver sustained physiological levels of basal insulin in a pain-free manner across the skin, was evaluated in a diabetic rat model. Transdermal patches (one per rat) containing insulin in biphasic vesicles (1,10 mg recombinant human insulin dose) were applied to the shaved abdominal skin of streptozotocin-induced diabetic rats for 73 h. Blood glucose was monitored approximately every 2,10 h using a Lifescan glucose meter. Inguinal lymph node insulin levels were analysed by ELISA. Insulin in the lymph nodes increased in a dose- and time-dependent manner. Maximal transdermal insulin concentrations in the lymph nodes were observed with both 140 IU (5 mg: 43.0 + 18.0 ,IU mg,1 (mean + s.e.m., n = 4)) and 280 IU (10 mg: 48.0 + 19.6 ,IU mg,1 (mean + s.e.m., n = 4)) doses of recombinant insulin at t = 73 h. The level of insulin in the lymph nodes after subcutaneous injection of 1 mg insulin at the peak blood glucose response was 35.8 ,IU mg,1 (n = 2), before falling to 0.35 ,IU mg,1 by t = 48 h (n = 2). The lymphatics is involved in the transdermal insulin delivery by biphasic vesicles. This is the first report on the lymphatic transport of a protein after non-invasive topical application on the skin. [source]

The differential regulation of Smad7 in kidney tubule cells by connective tissue growth factor and transforming growth factor-beta1

NEPHROLOGY, Issue 3 2007
Summary: Aims: Smad7 is an inhibitory Smad that regulates transforming growth factor-, (TGF-,) signaling. Connective tissue growth factor (CTGF) is recognized as a potent downstream mediator of the fibrogenic effects of TGF-,1. SMAD binding sites have been identified in both TGF-, and CTGF promoters. The effect of CTGF on Smad7 expression and its role in the regulation of Smad7 induced by TGF-,1 in renal tubular cells is unknown. Methods: Human model of proximal tubular cells (HK-2 cells) was used and confirmed using a diabetic rat model. RT-PCR was performed to measure Smad7, TGF-,1 and Smad2 and ELISA was performed to measure active TGF-,1. CTGF or TGF-,1 was silenced in HK-2 cells using siRNA methodology. Results: TGF-,1 induced Smad7 in a time-dependent manner, peaking at 30 min (P < 0.0005) but sustained up to 24 hrs (p < 0.005). Conversely, CTGF reduced Smad7, which was maximal at 24 hrs (p < 0.05). This was supported by our in vivo data demonstrating that CTGF protein significantly increased while Smad7 mRNA level was reduced in a diabetic rat model. The basal expression level of Smad7 decreased in TGF-,1 silenced cells compared to cells transfected with non-specific siRNA (p < 0.0005). The basal expression level of Smad7 increased in CTGF silenced cells (p < 0.05), which was increased by TGF-,1 (p < 0.005). Both mRNA and protein levels of TGF-,1 decreased in CTGF silenced cells (p < 0.05 and p < 0.005 respectively) accompanied by reduction in Smad2 mRNA level in CTGF silenced cells. Conclusions: Smad7 is induced rapidly by TGF-,1 limiting the response to TGF-,1. CTGF likely plays a key role in promoting TGF-,1 activity by decreasing the availability of Smad7 and increasing Smad2. [source]

Effect of exposure to 50,Hz magnetic field with or without insulin on blood,brain barrier permeability in streptozotocin-induced diabetic rats,

Sefa Gulturk
Abstract We investigated the effect of long-term exposure to modulation magnetic field (MF), insulin, and their combination on blood,brain barrier (BBB) permeability in a diabetic rat model. Fifty-three rats were randomly assigned to one of six groups: sham, exposed to no MF; MF, exposed to MF; diabetes mellitus (DM), DM induced with streptozotocin (STZ); DM plus MF (DMMF); DM plus insulin therapy (DMI); and DM plus insulin therapy plus MF (DMIMF). All the rats underwent Evans blue (EB) measurement to evaluate the BBB 30 days after the beginning of experiments. The rats in MF, DMMF, and DMIMF groups were exposed to MF (B,=,5,mT) for 165,min every day for 30 days. Mean arterial blood pressure (MABP), body mass, and serum glucose level of the study rats were recorded. The extravasation of brain EB of the MF, DM, DMMF, DMI, and DMIMF groups was higher than that of the sham group and the extravasation of right hemisphere of the DMIMF group was highest (P,<,0.05). The post-procedure body mass of the sham and MF groups were significantly higher than those of the DM and DMMF groups (P,<,0.05). In the DM, DMMF, DMI, and DMIMF groups, the baseline glucose was significantly lower than the post-procedure glucose (P,<,0.05). DM and MF increase BBB permeability; in combination, they cause more increase in BBB permeability, and insulin decreases their effect on BBB. Improved glucose metabolism may prevent body mass loss and the hypoglycemic effect of MF. DM increases MABP but MF causes no additional effect. Bioelectromagnetics 31:262,269, 2010. 2009 Wiley-Liss, Inc. [source]