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

We address the question whether oxygen metabolism of polymorphonuclear neutrophils (PMN) is influenced by disease duration in patients with insulin-dependent diabetes mellitus (IDDM). PMN were isolated from patients with IDDM of various durations and from healthy controls. We measured PMN production of superoxide anions (O2-) by cytochrome c reduction (see Babior, B.M. et al. (1973) J. Clin. Invest. 52, 741-746) and PMN production of hydrogen peroxide (H2O2) by phenol red oxygenation (see Pick, E. (1980) J. Immunol. Methods 38, 161-169) in three groups of IDDM patients subdivided according to disease duration (group A: IDDM less that 10 years; group B: IDDM of 10-15 years; group C: IDDM of more than 15 years) and in control healthy subjects (group H). Unstimulated O2- production in all IDDM patients was not statistically different from control values (A: 4.3 +/- 0.4 nmol/10(6) PMN per 30 min, nmol/10(6) PMN per 30 min; C: 4.9 +/- 0.9 nmol/10(6) PMN per 30 min; and H: 3.5 +/- 0.2 nmol/10(6) PMN per 30 min, respectively). In contrast, stimulated O2- production was significantly lower in both patients with 10-15 years, and patients with more than 15 years, duration of IDDM than in controls (B: 25.7 +/- 2.5 nmol/10(6) PMN per 30 min; C: 21.1 +/- 3.4 nmol/10(6) PMN per 30 min and H: 42.2 +/- 1.1 nmol/10(6) PMN per 30 min, respectively) correlating with disease duration (r = -0.44, P < 0.033). The stimulated O2- production in patients with less than 10 years duration of IDDM (A: 35.7 +/- 1.9 nmol/10(6) PMN per 30 min) was slightly lower than in controls. H2O2 production of unstimulated PMN (A: 4.0 +/- 0.5 nmol/10(6) PMN per 30 min; B: 4.4 +/- 0.8 nmol/10(6) PMN per 30 min and C: 4.4 +/-1.0 nmol/10(6) PMN per 30 min, respectively) was much higher than those in controls. In contrast, stimulated H2O2 production did not differ statistically from the value noticed in healthy subjects. The results obtained might indicate that production of H2O2 by unstimulated cells is increased in diabetic patients while generation of O2- by stimulated neutrophils is markedly impaired, suggesting that toxic oxygen species production might be influenced by disease duration.
Diabetes Res Clin Pract 1996 Aug
PMID:The influence of insulin-dependent diabetes mellitus (IDDM) duration on superoxide anion and hydrogen peroxide production by polymorphonuclear neutrophils. 892 34

The aim of this study was to describe the safety and effectiveness associated with phenol matricectomy in patients with diabetes. To date, the medical literature is devoid of information regarding the use of chemical toenail matricectomies performed on patients with diabetes. Sixty-six consecutive patients with diabetes and ingrown toenails were evaluated. The procedure was performed on 57 of these patients. The results demonstrate a 5% regrowth rate, no significant complications, and limited risk in this patient population.
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PMID:Phenol matricectomy in patients with diabetes. 943 4

Experiments were conducted on an alloxan diabetes model to study the preventive effects of the phenol antioxidants ionol and probucol. Ionol showed a tendency towards inhibition of glycemia and free radical oxidation of lipids. Probucol effectively inhibited the development of glycemia, hyperlipidemia, and intensification of autooxidation in the vascular wall. On the grounds of the results it is concluded that inclusion of probucol into complex treatment of patients suffering from diabetes mellitus with vascular complications is expedient.
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PMID:[The effect of phenol antioxidants on the development of alloxan diabetes in rats]. 932

Amylin, a 37-amino acid peptide hormone co-secreted with insulin, potently governs the rate of gastric emptying. Hypoglycemia, in the absence of agents such as amylin, is reported to accelerate gastric emptying. We asked whether hypoglycemia had a similar action on gastric emptying in the presence of amylin. In preliminary experiments using a phenol red gavage technique in fasted SD rats, we showed that insulin administration accelerated gastric emptying in a dosage-dependent manner. This acceleration was totally prevented by coadministration of glucose in dosages that prevented a change in plasma glucose, indicating that insulin per se did not affect gastric emptying. The effect on gastric emptying of hypoglycemia induced by a 5 mU/min insulin infusion (t = 5-90 min) was assessed in conscious rats continuously infused with amylin (50 pmol x kg-1 x min-1; t = -30 to 90 min). Gastric emptying was indicated by the appearance in plasma of label from 3-O-methyl-[3H]glucose gavaged at t = 0 min. Label appearance was markedly inhibited in rats preinfused with amylin (84% reduced vs. saline controls at t = 30 min), indicating amylin inhibition of gastric emptying. In amylin-treated rats that were subsequently infused with insulin, gavaged label abruptly appeared in plasma when plasma glucose had fallen to 2.1 +/- 0.1 mmol/l (at t approximately 45 min), consistent with a reversal by hypoglycemia of amylin's inhibition of gastric emptying. These data support the idea of a central "fail-safe" mechanism whereby hypoglycemia can override the slowing of gastric emptying by amylin.
Diabetes 1998 Jan
PMID:Hypoglycemia overrides amylin-mediated regulation of gastric emptying in rats. 942 80

The present investigation was carried out to understand the effect of metal catalyzed oxidation on glycation and crosslinking of collagen. Tail tendons obtained from rats weighing 200-225 g were incubated with glucose (250 mM) and increasing concentrations of copper ions (5, 25, 50 and 100 microM) under physiological conditions of temperature and pH. Early glycation, crosslinking and late glycation (fluorescence) of collagen samples were analyzed periodically. Early glycation was estimated by phenol sulfuric acid method, and the crosslinking was assessed by pepsin and cyanogen bromide digestion. A concentration-dependent effect of metal ions on the rate of glycation and crosslinking of collagen was observed. Tendon collagen incubated with glucose and 100 microM copper ions showed 80% reduction in pepsin digestion within seven days, indicating extensive crosslinking, whereas collagen incubated with glucose alone for the same period showed only 7% reduction. The presence of metal ions in the incubation medium accelerated the development of Maillard reaction fluorescence on collagen, and the increase was dependent on the concentration of metal ions used. The metal chelator diethylene triamine penta-acetate significantly prevented the increase in collagen crosslinking by glucose and copper ions. Free radical scavengers benzoate and mannitol effectively prevented the increased crosslinking and browning of collagen by glucose. The results indicate that the metal catalyzed oxidation reactions play a major role in the crosslinking of collagen by glucose. It is also suggested that the prevention of increased oxidative stress in diabetes may prevent the accelerated advanced glycation and crosslinking of collagen.
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PMID:An in vitro study on the role of metal catalyzed oxidation in glycation and crosslinking of collagen. 1039 Nov 48

Benzene is a ubiquitous environmental pollutant primarily metabolized by a cytochrome P-450 (CYP-450) isoenzyme, CYP-450 IIE1. A consistent induction of CYP450 IIE1 has been observed in both rat and human affected by diabetes mellitus. The aim of this study was to evaluate whether streptozotocin (STZ)-induced diabetes determines modifications in the metabolic pathways of benzene in rat. Benzene (100 mg/kg per day, dissolved in corn oil) was administered i.p. once a day for 5 days. Urine samples were collected every day in STZ-treated and normoglycaemic animals, treated and untreated with benzene (n = 10). Urinary levels of trans,trans-muconic acid and of phenol, catechol and hydroquinone (free and conjugated with sulphuryl and glucuronic group) were measured by high-performance liquid chromatography (HPLC). In normoglycaemic rats during the 5 days of treatment with benzene we observed a progressive and significant decrement in the urinary excretion of phenol, phenyl sulphate and glucuronide, catechol, catechol glucuronide, hydroquinone, hydroquinone glucuronide and t,t-muconic acid (P < 0. 05). In the diabetic animals, conversely, the same metabolites showed progressively increasing urinary levels (P < 0.05). Catechol sulphate and hydroquinone sulphate levels were below the instrument's detection limit. In the comparison between diabetic and normoglycaemic benzene treated rats, the inter-group difference was significant (P < 0.05) from day 3 of treatment for t,t-muconic acid, and from day 1 for free and conjugated phenol, free and glucuronide catechol and free hydroquinone. In the normoglycaemic rat exposed to benzene the decreasing trend observed in urinary excretion of free and conjugated metabolites may be due to their capability to reduce cytochromial activity. Conversely, in the diabetic rat, urinary levels of benzene metabolites tended to increase progressively, probably due to the consistent induction of CYP-450 IIE1 observed in diabetes, which would overwhelm the inhibition of this isoenzyme caused by phenolic metabolites. Furthermore, the metabolic switch towards detoxification metabolites observed after administration of high doses of benzene is not allowed in the diabetic because of reduced glutathione-S-transferase activity. As a consequence, higher levels of hydroquinone, phenol and catechol, considered the actual metabolites responsible for benzene toxicity, will accumulate in the diabetic rat. Extrapolating these data to human, we may thus suggest that occupational exposure to benzene of a diabetic subject poses a higher risk level, as his metabolism tends to produce and accumulate higher levels of reactive benzene catabolites.
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PMID:Modifications in the metabolic pathways of benzene in streptozotocin-induced diabetic rat. 1044 56

We sought to elucidate the role of the portal vein afferents in the sympathetic response to hypoglycemia. Laparotomy was performed on 27 male Wistar rats. Portal veins were painted with either 90% phenol (denervation group [PDN]) or 0.9% saline solution (sham-operated group [SHAM]). Rats were chronically cannulated in the carotid artery (sampling), jugular vein (infusion), and portal vein (infusion). After a recovery period of 5 days, animals were exposed to a hyperinsulinemic-hypoglycemic clamp, with glucose infused either portally (POR) or peripherally (PER). In all animals, systemic hypoglycemia (2.48+/-0.09 mmol/l) was induced via jugular vein insulin infusion (50 mU x kg(-1) x min(-1)). Arterial plasma catecholamines were assessed at basal (-30 and 0 min) and during sustained hypoglycemia (60, 75, 90, and 105 min). By design, portal vein glucose concentrations were significantly elevated during POR versus PER (4.4+/-0.14 vs. 2.5+/-0.07 mmol/l; P<0.01, respectively) for both PDN and SHAM. There were no significant differences in arterial glucose or insulin concentration between the four experimental conditions at any point in time. When portal glycemia and systemic glycemia fell concomitantly (SHAM-PER), epinephrine increased 12-fold above basal (3.75+/-0.34 and 44.56+/-6.1 nmol/l; P<0.001). However, maintenance of portal normoglycemia (SHAM-POR) caused a 50% suppression of the epinephrine response, despite cerebral hypoglycemia (22.2+/-3.1 nmol/l, P<0.001). Portal denervation resulted in a significant blunting of the sympathoadrenal response to whole-body hypoglycemia (PDN-PER 27.6+/-3.8 nmol/l vs. SHAM-PER; P<0.002). In contrast to the sham experiments, there was no further suppression in arterial epinephrine concentrations observed during PDN-POR versus PDN-PER (P = 0.8). These findings indicate that portal vein afferent innervation is critical for hypoglycemic detection and normal sympathoadrenal counterregulation.
Diabetes 2000 Jan
PMID:Portal vein afferents are critical for the sympathoadrenal response to hypoglycemia. 1061 43

So far little is known about the importance of different types of non-diabetic hyperglycemia for the development of macrovascular disease. The aim of this work was to examine the intima-media thickness (IMT) of the common carotid artery (CCA), a well-accepted marker of atherosclerosis, as well as various risk factors for atherosclerosis in non-diabetic subjects with isolated fasting (IFH; n=67), isolated postchallenge (IPH; n=82) and combined hyperglycemia (CH; n=88) in comparison to normoglycemic (NG; n=265) controls. Subjects were participants of the RIAD study (Risk Factors in IGT for Atherosclerosis and Diabetes). IMT in the IPH (IMTmean: 0.89+/-0.02 mm; IMTmax: 1.01+/-0.02 mm; mean+/-SEM) and CH group (IMTmean: 0.91+/-0.02 mm; IMTmax: 1.03+/-0.02 mm) was significantly increased vs. the NG (IMTmean: 0.82+/-0.01 mm; IMTmax: 0.94+/-0.01 mm) and IFH group (IMTmean: 0.81+/-0.02 mm; IMTmax: 0.90+/-0.03 mm). IMT of the IFH group was similar to the normoglycemic controls. Subjects in the first and second tertile for postchallenge plasma glucose have similar carotid IMT irrespective of the level of fasting plasma glucose. The individuals of the third tertile for 2 h plasma glucose, whether in the first, second or third tertile of fasting plasma glucose, showed the same carotid IMT, which was significantly higher than all other groups, except for the one with lowest tertile for fasting and postchallenge plasma glucose. Except for total cholesterol and von Willebrand factor the levels of all other risk parameters were significantly higher in the hyperglycemic groups in comparison to the normoglycemic controls. Among the hyperglycemic subjects the CH group was at the highest risk for atherosclerosis with significantly increased levels of plasma triglycerides, fibrinogen, PAI-1, albuminuria, HDL-triglycerides, free fatty acids, insulin and proinsulin, and significantly reduced HDL-cholesterol in comparison to the normoglycemic controls. In summary, postchallenge hyperglycemia within the non-diabetic range is associated with atherosclerosis, as measured by the increased intima-media thickness of the common carotid artery. Furthermore, cardiovascular risk factors are significantly raised in all types of non-diabetic hyperglycemia.
Exp Clin Endocrinol Diabetes 2000
PMID:Prevalence and atherosclerosis risk in different types of non-diabetic hyperglycemia. Is mild hyperglycemia an underestimated evil? 1082 15

Alterations of gastric calcitonin gene-related peptide and substance P content and gastric emptying in early stages of streptozotocin-induced diabetic rats were investigated. Diabetes was induced by intravenous injection of streptozotocin (50 mg/kg) in male Wistar rats. Gastric emptying of phenol red solution and calcitonin gene-related peptide and substance P content of gastric walls, measured by radioimmunoassay, was assessed two and four weeks after streptozotocin injection. Gastric emptying two weeks after streptozotocin was delayed (32+/-9%) and that four weeks after was enhanced (73+/-2%) compared with nondiabetic control rats (50+/-3%). Calcitonin gene-related peptide content of the gastric antrum and corpus was increased two weeks after and decreased four weeks after streptozotocin, while gastric substance P content was not changed at any time in diabetic rats. Insulin treatment reversed alterations of gastric emptying and calcitonin gene-related peptide content. The delayed gastric emptying in two-week diabetic rats was reversed by CGRP antagonist and the enhanced gastric emptying in four-week diabetic rats was reversed by CGRP pretreatment. These results suggest a possible relationship between gastric calcitonin gene-related peptide and abnormal gastric motility in diabetic state.
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PMID:Gastric neuropeptides and gastric motor abnormality in streptozotocin-induced diabetic rats: observation for four weeks after streptozotocin. 1150 55

Using data on history of diabetes, fasting glucose (FG) and the oral glucose tolerance test (OGTT), the authors contrasted cardiovascular disease (CVD) risk factors (body mass index, blood pressure, lipids and glycated hemoglobin) in 3052 African-American and White adults aged 70-79 in mutually exclusive categories of diagnosed diabetes, undiagnosed diabetes defined by the American Diabetes Association (ADA), isolated post-challenge hyperglycemia (IPH; FG < 126 mg/dL and 2 h post-OGTT > or = 200 mg/dL), impaired fasting glucose (IFG; FG > or = 110 but < 126 mg/dL), and individuals who were non-diabetic by both ADA and World Health Organization (WHO) criteria (FG < 126 mg/dL and 2 h post-challenge glucose < 200 mg/dL). The prevalence of diagnosed diabetes, undiagnosed ADA diabetes and IPH were 15.2, 3.8 and 4.7%, respectively, with more diagnosed and undiagnosed ADA diabetes in African-Americans than Whites. Compared to mean glycated hemoglobin (HbA(1c)) among ADA/WHO non-diabetic individuals (6.0%), HbA(1c) was substantially higher in the diagnosed diabetes and undiagnosed ADA diabetes groups (8.0% and 7.7%), but not in the IPH group (6.3%). The diagnosed and undiagnosed ADA diabetic groups had worse CVD risk factor profiles than the ADA/WHO non-diabetic group. IPH subjects had elevated levels of some CVD risk factors, but differences were more modest than those for the diabetic groups. Among people with IPH, those who also had IFG had worse CVD profiles than those with IPH alone. Although the OGTT may identify additional adults with more CVD risk factors than normals, these differences appear to be clustered among those who also have IFG.
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PMID:Prevalence and clinical implications of American Diabetes Association-defined diabetes and other categories of glucose dysregulation in older adults: the health, aging and body composition study. 1152 Jun 45


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