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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum concentrations of insulin-like growth factor 1 (IGF-1) and growth hormone were measured in 25 cats with untreated diabetes mellitus (11 of which were used for follow-up measurements, one to three, four to eight, nine to 12 and 13 to 16 weeks after their treatment with insulin began), 14 diabetic cats that had previously been treated with insulin, and seven diabetic cats that also had hypersomatotropism, two of which had not previously been treated with insulin; 18 healthy cats were used as controls. In the untreated diabetic cats the concentration of IGF-1 ranged from 13.0 to 433.0 ng/ml (median 170.5 ng/ml), which was significantly lower than the concentrations in the control cats (196.0 to 791.0 ng/ml, median 452.0 ng/ml). Their IGF-1 concentrations increased significantly when they were treated with insulin and after four to eight weeks were not different from those in the control cats. In the diabetic cats that had previously been treated with insulin the IGF-1 concentrations were 33.0 to 476.0 ng/ml (median 316.0 ng/ml), which was significantly lower than the concentrations in the control cats, but significantly higher than in the untreated diabetic cats. The IGF-1 concentrations in the two previously untreated diabetic cats with hypersomatotropism were low and low-normal but increased markedly after treatment with insulin. In the five previously treated cats with hypersomatotropism the concentration of IGF-1 was above the normal range. The concentrations of growth hormone in the treated and untreated diabetic cats without hypersomatotropisms were not significantly different and there was an overlap in its concentrations in the diabetic cats with and without hypersomatotropism.
Vet Rec 2006 Feb 11
PMID:Measurements of growth hormone and insulin-like growth factor 1 in cats with diabetes mellitus. 1647 53

Previous studies have shown that connexin (Cx) expression is considerably higher in the preglomerular compared to postglomerular vasculature and that these differences are accentuated during diabetes. Since nitric oxide (NO) has been reported to alter Cx expression in endothelial cells and muscle cells and NO bioavailability is altered in diabetes, we hypothesized that NO may be responsible for the changes during diabetes. Cx expression was studied using immunohistochemistry in mice in which eNOS expression was either upregulated (eNOS transgenic) or downregulated (eNOS knockout). Diabetes was induced intraperitoneally with a single dose of alloxan or multiple low doses of streptozotocin. Expression of Cx40 in smooth muscle cells of afferent arterioles was increased, while expression of Cx43 in endothelial cells of efferent arterioles was absent in eNOS transgenic mice, similar to the changes occurring in wild-type mice during diabetes. Expression of Cx40 and Cx43 in eNOS knockout mice was not different from control; however, induction of diabetes in eNOS knockout mice failed to produce any changes in Cx40 or Cx43 in either afferent or efferent arterioles. Immunohistochemistry showed that eNOS expression was increased in the endothelium of renal arterioles in wild-type diabetic and eNOS transgenic mice, but absent from arterioles of eNOS knockout mice. We conclude that changes occurring in Cx expression in afferent and efferent arterioles during diabetes may result from increased eNOS.
Anat Rec A Discov Mol Cell Evol Biol 2006 Sep
PMID:Increased eNOS accounts for changes in connexin expression in renal arterioles during diabetes. 1689 22

Valproic acid, a drug commonly used to treat seizures and other psychiatric disorders, causes neural tube defects (NTDs) in exposed fetuses at a rate 20 times higher than in the general population. Failure of the neural tube to close during development results in exencephaly or anencephaly, as well as spina bifida. In mice, nonspecific activation of the maternal immune system can reduce fetal abnormalities caused by diverse etiologies, including diabetes-induced NTDs. We hypothesized that nonspecific activation of the maternal immune system with interferon-gamma (IFN-gamma) and granulocyte-macrophage colony-stimulating factor (GM-CSF) could reduce valproic acid (VA)-induced defects as well. Female CD-1 mice were given immune stimulant prebreeding: either IFN-gamma or GM-CSF. Approximately half of the control and immune-stimulated pregnant females were then exposed to 500 mg/kg VA on the morning of gestational day 8. The incidence of developmental defects was determined on gestational day 17 from at least eight litters in each of the following treatment groups: control, VA only, IFN-gamma only, IFN-gamma+VA, GM-CSF only, and GM-CSF+VA. The incidence of NTDs was 18% in fetuses exposed to VA alone, compared to 3.7% and 2.9% in fetuses exposed to IFN-gamma+VA, or GM-CSF+VA respectively. Ocular defects were also significantly reduced from 28.0% in VA exposed groups to 9.8% in IFN-gamma+VA and 12.5% in GM-CSF+VA groups. The mechanisms by which maternal immune stimulation prevents birth defects remain unclear, but may involve maternal or fetal production of cytokines or growth factors which protect the fetus from the dysregulatory effects of teratogens.
Anat Rec A Discov Mol Cell Evol Biol 2006 Dec
PMID:Valproic acid-induced fetal malformations are reduced by maternal immune stimulation with granulocyte-macrophage colony-stimulating factor or interferon-gamma. 1707 42

Clinical measurements, including a subjective clinical score and water intake, and biochemical measurements, including blood glucose, fructosamine, beta-hydroxybutyrate, cholesterol, triglycerides, triglycerides corrected for free glycerol, glycerol and urine glucose were compared for monitoring diabetic cats treated with porcine insulin zinc suspension. The data were grouped by subjective clinical score and the sensitivity of each measurement in differentiating the grouped data was assessed. None of the measurements was able to differentiate between the ranked clinical score groups, but two-hourly measurements of blood glucose over 24 hours, water intake, urine glucose and fructosamine were useful in differentiating cats that subjectively had the water and food consumption and general appearance of a normal cat from cats in which the signs of diabetes were less well controlled. Measurements of plasma lipids were not well correlated with the other measurements. The measurements that were most closely correlated with apparently perfect clinical control were the J index, water intake and maximum and mean blood glucose concentrations. In practice, water intake, maximum blood glucose concentration, mean blood glucose concentration and urine glucose would be the most useful indicators of clinical control in diabetic cats treated with porcine insulin zinc suspension.
Vet Rec 2007 Jul 14
PMID:Comparisons of different measurements for monitoring diabetic cats treated with porcine insulin zinc suspension. 1763 Apr 18

The NeuroScope, a specific and sensitive indicator of cardiac vagal tone, was used to look for differences in autonomic tone between 25 dogs with naturally occurring diabetes mellitus and 23 healthy control dogs, to determine whether there was any correlation between the dogs' cardiac vagal tone, the duration of diabetes and the adequacy of glycaemic control. The cardiac index of parasympathetic activity (cipa) was determined for each dog over a period of 2600 heartbeats. The mean, median and modal cipa values were significantly lower in the diabetic dogs than in the healthy dogs. There was no significant relationship between the cipa values and the duration of disease or the adequacy of recent glycaemic control in the diabetic dogs, but there was a significant inverse relationship between the cipa values and the bodyweight of the diabetic dogs that was not evident in the normal dogs. The conclusions were based on a 500-heartbeat interval selected from the 2600 heartbeats recorded.
Vet Rec 2007 Jul 21
PMID:Evidence of cardiac autonomic neuropathy in dogs with diabetes mellitus. 1765 33

The required dose rate of porcine insulin zinc suspension to control the signs of diabetes mellitus in 25 cats was assessed, and their response to insulin treatment was investigated over 12 months. The cats required a median dose of 0.5 iu/kg bodyweight twice a day, and only two of the cats required doses higher than 1.0 iu/kg twice a day. Their lowest blood glucose concentration was on average significantly higher during the night than during the day. Seven of the cats went into diabetic remission during the study, and the control of the clinical signs in the others was either excellent or good by the end of the study.
Vet Rec 2007 Jul 21
PMID:Control of diabetes mellitus in cats with porcine insulin zinc suspension. 1765 34

Recent studies show that podocyte nuclear density (N(V)) and numbers of renal podocytes per glomerulus (N) are altered in experimental and spontaneous diabetes mellitus. N(V) and N are generally reduced, and it has been hypothesized that these morphological changes may relate to the loss of glomerular permselectivity in diabetic nephropathy (DN). In the current study, OVE26 transgenic diabetic mice and age-matched (FVB) controls (60, 150, or 450 days) were fixed by vascular perfusion and renal cortical tissues were prepared for morphometric analyses. ImageJ software and point counting analyses were carried out on light and transmission electron micrographs to determine glomerular volume (V(G)), N(V), and N. As expected, mean V(G) in OVE26 mice increased substantially ( approximately 134%) over the course of the study and was significantly increased over FVB mice at all ages. At 60 days, N(V) and N were not statistically distinguishable in OVE26 and control mice, while at 150 days, N(V) was significantly reduced in diabetics but not N. In 450-day-old OVE26 animals, however, N(V) and N were both significantly decreased ( approximately 231% and approximately 99%, respectively) relative to age-matched FVB mice. These data suggest that in the OVE26 model of diabetes, significant podocyte loss occurs relatively late in the course of the disease. Moreover, it seems possible that these podocytic changes could play a role in sustaining the increased permeability of the blood-urine barrier in the later stages of diabetic renal decompensation.
Anat Rec (Hoboken) 2008 Jan
PMID:Podocyte loss in aging OVE26 diabetic mice. 1808 29

Diabetes affects retinal and nervous glial cells, especially the astrocytes. A key indicator of this response is the alteration in the level of intermediate filament glial fibrillary acidic protein (GFAP) and number of GFAP-immunoreactive astrocytes. To date, no study has investigated the effect of diabetes on the distribution of GFAP-immunoreactive astrocytes in the spinal cord. Therefore, the present study investigated the effect of diabetes on the number of GFAP-immunoreactive astrocytes in the gray matter of the spinal cord of streptozotocin-induced diabetic Wistar rats. Animals were divided into six groups (n = 7); 6 weeks and 12 weeks diabetic duration groups and their respective age-matched normal control and sham control groups. Our results demonstrated a significant (P < 0.001) decrease in the number of GFAP-immunoreactive astrocytes in different areas of the spinal cord sections of the 6 weeks and 12 weeks long diabetic rats when compared with the spinal cord of normal and sham control groups of comparable age. The mean percentage in total number of GFAP-immunoreactive astrocytes in the whole gray matter areas of the spinal cord of the 6 and 12 weeks diabetic groups were approximately 28% and 41% less than control groups. Furthermore, the 12 weeks diabetic group showed a significant (P < 0.001) reduction in the number of GFAP-immunoreactive astrocytes when compared with the 6 weeks diabetic animals. These results suggest that the induction of diabetes is associated with a reduction in GFAP-positive astrocytes in the spinal cord, which may affect the functional support and role of astrocytic cells in the nervous tissue. This in turn may contribute to the pathological changes associated with diabetic state in the central nervous system.
Anat Rec (Hoboken) 2008 Apr
PMID:Alteration of glial fibrillary acidic proteins immunoreactivity in astrocytes of the spinal cord diabetic rats. 1836 Aug 86

Some coxsackievirus B serotypes are potentially diabetogenic. Previous studies revealed that the virulence and the tissue damage varied with the genetics of the virus strain as well as with the genetics of the mice. A single amino acid variation can alter virulence and tropism in both murine and in vitro models. However, the genetic determinants of this phenomenon have not been determined. In this study, infections with a laboratory strain of coxsackievirus B4 resulted in a diabetes-like syndrome in ICR mice, characterized by chronic pancreatic inflammation together with dysregulation in glucose metabolism, loss of pancreatic acinar tissue and persistent infection in islets. To characterize the genetic determinants involved in the mouse pancreas adaptation, the laboratory strain of coxsackievirus B4 was cloned for molecular characterization. Comparing the whole genome sequence of this virus strain with the other coxsackievirus B4 strains revealed some differences. Altogether 15 nucleotides were changed, resulting in 10 amino acid substitutions, which might be responsible for the pathogenic phenotype of this strain in mice.
Anat Rec (Hoboken) 2008 May
PMID:Complete nucleotide sequence of a coxsackievirus B4 strain that establishes infection in ICR mice pancreas and induces glucose intolerance. 1838 52

Amyloid formation is cytotoxic and can activate the caspase cascade. Here, we monitor caspase-3-like activity as reduction of fluorescence resonance energy transfer (FRET) using the contstruct pFRET2-DEVD containing enhanced cyan fluorescent protin (EYFP) linked by the caspase-3 specific cleavage site residues DEVD. Beta-TC-6 cells were transfected, and the fluoorescence was measured at 440 nm excitation and 535 nm (EYFP) and 480 nm (ECFP) emission wavelength. Cells were incubated with recombinant pro lset Amyloid Polypeptide (rec prolAPP) or the processing metabolites of prolAPP; the N-terminal flanking peptide withIAPP (recN+IAPP); IAPP with the C-terminal flanking peptied (recIAPP+C) and lslet Amyloid Polypeptide (recIAPP) . Peptides were added in solubilized from (50 microM) or as performed amyloid-like fibrils, or as a combination of these. FRET was measured and incubation with a mixture of solubilized peptide and performed fibrils resulted in loss of FRET and apoptosis was determined to occure in cells incubated with recproIAPP (49%), recN+IAPP (46%), recIAPP (72%) and recIAPP+C (59%). These results show that proIAPP and the processing intermediates reside the same cell toxic capacity as IAPP, and they can all have a central role in the reduction of beta-cell number in type 2 diabetes.
Exp Diabetes Res 2008
PMID:Real-time monitoring of apoptosis by caspase-3-like protease induced FRET reduction triggered by amyloid aggregation. 1856 81


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