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PubMed2006

Effect of Japanese radish (Raphanus sativus) sprout (Kaiware-daikon) on carbohydrate and lipid metabolisms in normal and streptozotocin-induced diabetic rats.

No information is available about the effects of Japanese radish sprout (JRS) on diabetes. To clarify the effects, the influence of JRS on carbohydrate and lipid metabolisms was investigated in normal and streptozotocin-induced diabetic rats. The rats were fed a diet containing 0%, 2.5% or 5% of JRS ad libitum for 21 days. Compared with the corresponding control groups, the JRS-fed normal rats showed lower plasma levels of total cholesterol (TC), triglycerides (TG), phospholipids (PL), fructosamine, glucose and insulin and higher plasma levels of low-density lipoprotein-cholesterol, whereas the JRS-fed diabetic rats showed lower plasma levels of fructosamine, glucose and insulin without changes in the plasma lipid parameters. JRS also decreased the hepatic TC, TG and PL levels in the normal rats and the TG level in the diabetic rats. These results showed that JRS had a hypoglycemic activity in both the normal and diabetic rats and partly improved lipid metabolism in the normal rats. JRS has the potential to alleviate hyperglycemia in cases where diabetes is present and to serve in the primary prevention of diabetes mellitus.

Animals↗
PubMed1993

Serum sialic acid and acute phase proteins in type 1 and type 2 diabetes mellitus.

Serum sialic acid is a risk factor for cardiovascular disease in the general population. Serum total sialic acid concentrations were therefore measured in 20 type 1 diabetic patients and in 20 age- and sex-matched non-diabetic subjects. Serum sialic acid were not significantly different in the type 1 diabetic patients and the normal subjects (2.00 +/- 0.37 vs. 1.98 +/- 0.67 mmol/l), but was significantly correlated with serum total cholesterol (r = 0.55, P < 0.02) and serum triglyceride concentration (r = 0.63, P < 0.01) in the type 1 diabetic patients. There was no relationship of sialic acid levels to age, duration of diabetes, smoking, body mass index, systolic or diastolic blood pressure, plasma glucose, serum fructosamine, or daily insulin dosage. Six of the type 1 diabetic patients with retinopathy had higher total serum sialic acid concentrations than those patients without retinopathy (2.38 +/- 0.33 vs. 1.85 +/- 0.26 mmol/l, P < 0.01). A further study of 16 type 1 and 16 type 2 diabetic patients matched for serum fructosamine and blood glucose concentrations and without tissue complications showed that the serum total sialic acid concentration was significantly higher in the type 2 diabetic patients compared with the type 1 patients (2.32 +/- 0.41 vs. 1.84 +/- 0.24 mmol/l, P < 0.001). Although the serum concentrations of the non-sialylated acute phase protein, C-reactive protein, was higher in type 2 than type 1 diabetes, sialylated acute phase protein levels did not explain differences in serum total sialic acid in diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute-Phase Proteins↗
PubMedDate not supplied

Effect of cilazapril therapy on glucose and lipid metabolism in patients with hypertension.

The effects of long-term monotherapy with cilazapril, an angiotensin-converting enzyme inhibitor, on blood pressure, glucose tolerance, and serum lipid profiles were prospectively investigated in 66 patients with hypertension: 23 with normal glucose tolerance and 43 with glucose intolerance (including 9 patients with non-insulin-dependent diabetes mellitus). The levels of plasma glucose, serum insulin, serum lipids, glycated hemoglobin A(lc) (Hb A(lc)), and fructosamine were determined before and during long-term (mean +/- SD, 26.2 +/- 1.2 weeks) therapy with cilazapril. A 75-g oral glucose tolerance test was performed before and during treatment. Significant reductions in both systolic and diastolic blood pressures in both patient groups were maintained during the study. Neither fasting nor post-glucose load venous plasma glucose levels were altered in either group of patients, and no patient with normal glucose tolerance developed diabetes mellitus during the study. There was no significant change in the insulinogenic index (delta serum insulin/delta venous plasma glucose at 30 minutes post-glucose load) in either group, and glucose intolerance was slightly improved with significant reductions (P < 0.01) in Hb A(lc) and fructosamine in the patient group with impaired glucose tolerance. Serum total cholesterol (TC), low-density lipoprotein cholesterol, and triglyceride levels were significantly (P < 0.01) decreased and high-density lipoprotein cholesterol levels increased in patients with hypercholesterolemia (TC levels > or = 5.69 mmol/L). These results suggest that long-term cilazapril therapy may improve glucose and lipid metabolism in hypertensive patients with impaired glucose tolerance. Cilazapril also appears to be useful as an antihypertensive agent for hypertensive patients with either impaired glucose tolerance or hypercholesterolemia.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Oxygen radical generation by Maillard compounds.

Amino sugars such as galactosamine are hepatotoxic. It has been verified that toxic hepatitis induced by galactosamine is similar to that of CCl4 poisoning, and that both were inhibited by O2* scavengers. Fructosamine results from the union of glucose with the epsilon-amine of lysine. A test for fructosamine quantification is based on nitroblue tetrazolium (NBT) reduction, in which O2- is involved, the reduction being inhibited in the presence of superoxide dismutase (SOD). Given these facts, we attempted to elucidate if galactosamine and glucosamine reduce NBT and if that reduction is inhibited by SOD. This was confirmed. Subsequently, we incubated aminoacids (glycine, lysine, alanine) with glucose and galactose for 7 days and studied the action of the incubation products on NBT, using amino acids and sugars as controls. We found that NBT reduction increases proportionally to the length of incubation time of glucose/galactose with lysine, but not with other amino acids. Reduction of NBT by the Amadori compounds formed is inhibited by SOD. We suggest that oxygen radical generation by Amadori compounds must be taken into consideration as one cause of damage in diabetes of long duration.

Amino Sugars↗
PubMedDate not supplied

Plasma prekallikrein as a risk factor for diabetic retinopathy.

BACKGROUND: The aim of the study was to verify the hypothesis that in diabetes there is an increased activation of coagulation system leading in consequence to diabetic retinopathy. METHODS: Thirty three healthy subjects (controls, 16 males and 17 females) and 35 patients with diabetes type 1 (15 males and 20 females) were examined. We monitored plasma prekallikrein (PPK), glycemia, fructosamine, glycosylated hemoglobin, activated partial thromboplastin time (PTT), INR, fibrinolysis in euglobulins time (FET), level of antithrombin III (AT III), fibrinogen (Fb) and fibrinogen degradation products (FDP). RESULTS: In diabetic patients without retinopathy, PKK concentration was 16% higher (p <0.005), in patients with background retinopathy 33% higher (p <0.001), and in patients with proliferative retinopathy PKK concentration was 50% higher (p <0.001) than in controls. In the subgroup of patients with proliferative retinopathy PTT was significantly shorter (p <0.001), and FET was significantly longer (p <0.001) than in control. In patients with diabetes higher FDP concentrations were found than in controls (p <0.05). Significant correlations were found between PPK and fructosamine levels in all diabetic patients (R(S)=+0.57 p <0.001), in diabetic patients without retinopathy (R(S)=+0.61, p <0.05), and in diabetic patients with retinopathy (R(S)=+0.62, p <0.005). We found negative correlation between PPK concentration and PTT (R(S)=-0.43, p <0.001) and positive correlation between PPK concentration and FET (R(S)=+0.59, p <0.00001) in the entire study group. CONCLUSIONS: The occurrence of diabetic retinopathy is connected with higher levels of plasma prekallikrein.

Adult↗
PubMed2006

A novel method to quantify in vivo transferrin glycation: applications in diabetes mellitus.

BACKGROUND: In vitro glycation of transferrin leads to increased oxidative stress by impairing iron-binding antioxidant capacity. The aim of this study is to develop a method to evaluate in vivo transferrin glycation in diabetes. METHODS: We adapted the nitroblue tetrazolium assay to measure in micro-well plates the fructosamine content of transferrin isolated from serum by immunocomplexation. RESULTS: Introduction of the immunocomplexation step did not affect the analytical performance of the fructosamine measurement and analytical variability was lower than 7%. The diabetic group (n=107) had significantly higher transferrin glycation (1.39+/-1.12 versus 0.79+/-1.09 micromol fructosamine/g transferrin in the non-diabetic group, n=91, p<0.0005) and this was most pronounced in type 1 diabetes (1.95+/-1.02 versus 1.06+/-1.04 micromol fructosamine/g transferrin in type 2, p<0.0005). Transferrin glycation was associated with parameters of glycaemic control but did not correlate with serum iron or total iron-binding capacity. Total iron-binding capacity was lower in type 1 diabetes (63+/-9 versus 69+/-12 micromol/l in type 2, p<0.05) and was mainly determined by transferrin concentration. CONCLUSIONS: These results indicate that the adapted nitroblue tetrazolium assay combined with immunocomplexation of serum transferrin is suitable to detect differences in in vivo transferrin glycation between non-diabetic, type 1 and type 2 diabetic subjects.

Diabetes Mellitus↗
PubMed2004

Protective effect of Montilla-Moriles appellation red wine on oxidative stress induced by streptozotocin in the rat.

This study evaluated the protective effect of Montilla-Moriles appellation red wine (Cordoba, Spain) on oxidative stress, course and intensity of symptoms in experimental diabetes induced by the injection of streptozotocin in male Wistar rats. The rats were injected with a single dose of streptozotocin (60 mg/kg i.p.) and given water and red wine separately. After 4 weeks of treatment, blood samples were obtained to determine sugar and fructosamine concentrations in blood plasma, serum insulin concentration, and percentage of glycosylated hemoglobin in blood. The kidney, liver, and pancreas were removed to determine lipid peroxidation levels, reduced glutathione content, and antioxidative enzyme activity. A significant increase of glucose concentration in urine was found in the rats after injecting the streptozotocin. The administration of red wine before streptozotocin elevated reduced glutathione content and antioxidative enzyme activity, while lowering the lipid peroxidation level. Moreover, the red wine induced decreased levels of glycemia, plasma fructosamine and percentage of glycosylated hemoglobin, while increasing levels of insulin. These data suggest that red wine has a protective effect against oxidative stress and diabetes induced by streptozotocin.

Animals↗
PubMed1996

Clinical usefulness of serum 1,5-anhydroglucitol in monitoring glycaemic control.

BACKGROUND: To evaluate prospectively the clinical value of measuring serum concentrations of 1,5-anhydroglucitol (1,5AG) in monitoring glycaemia in patients with newly diagnosed non-insulin-dependent diabetes mellitus (NIDDM), we measured serum 1,5AG in 56 such patients. METHODS: 28 patients (group A) were started on, and continuously received, an oral hypoglycaemic agent for at least 6 weeks. The other 28 patients (group B) were given such agents for 4 weeks, and then stopped taking them for at least 2 weeks. All patients were then followed for an additional 10 weeks. Serum 1,5AG, fructosamine, glycated haemoglobin (HbA1c), and self-monitoring of blood glucose were monitored every 14 days for 16 weeks. FINDINGS: When sudden worsening of glycaemia occurred within 2 weeks, entailing withdrawal of oral treatment, 1,5AG accurately detected the slight change in glycaemia whereas HbA1c and fructosamine both failed to detect it. Although the change was detected by measurement of fasting plasma glucose (FPG) concentrations, FPG was less sensitive than 1,5AG. In patients with "near-normoglycaemia" (HbA1c about 6.5%) in the preceding 8 weeks, those who showed a lower concentration of 1,5AG (<10.0 micrograms/mL) manifested a higher mean daily plasma glucose concentration even though HbA1c measurement suggested good control of glycaemia. Results of 1,5AG were correlated more strongly with the FPG (r=0.790) and mean daily plasma glucose (r=-0.835) estimated on the same day than those estimaoffted in the preceding 2, 4 and 8 weeks, and with a fall in the Spearman correlation coefficient at any preceding time interval. INTERPRETATION: Because 1,5AG accurately detected a slight change in glycaemia without delay, it is suitable for use in monitoring for strict control of glycaemia, an important clinical goal.

Biomarkers↗
PubMed1999

Glycation of plasma low density lipoproteins increases interaction with arterial proteoglycans.

The increased susceptibility to atherosclerosis of diabetic individuals, may result from diabetes-associated modification in plasma low density lipoproteins (LDL) which enhance their interaction with arterial extracellular matrix proteoglycans. Using a nonhuman primate model for human diabetes, studies were conducted to examine diabetes-induced changes in LDL. Plasma LDL were isolated from control (n = 4) and streptozotocin-induced diabetic (n = 3) cynomolgus macaques by differential ultracentrifugation. An in vitro binding assay was used to measure LDL interaction with arterial proteoglycans. Significantly more diabetic LDL bound to proteoglycans than control LDL (12.9+/-0.7 microg LDL cholesterol/microg proteoglycan versus 8.9+/-0.5 microg LDL cholesterol/microg proteoglycan (mean +/- S.E.M.), P < 0.005). Glycation of LDL, determined by fructosamine content, was significantly enhanced in diabetic versus control animals (37+/-3.1 versus 20+/-1.5 micromol/l (mean +/- S.E.M.) P < 0.005). The correlation coefficient between fructosamine content of LDL and its binding to arterial proteoglycans was 0.95. No LDL compositional variables other than glycation correlated with proteoglycan binding. Removal of the glycated portion of LDL from diabetic animals returned LDL proteoglycan binding to normal. These data demonstrate that the diabetes induced glycation of LDL increases its proteoglycan binding properties: thus, a critical mechanism in atherosclerosis, enhanced LDL interaction with arterial proteoglycans, may be accelerated by the diabetic state.

Animals↗
PubMed2006

Lymphocyte ecto-5'-nucleotidase in obese type 2 diabetic patients treated with gliclazide.

OBJECTIVE: Lymphocyte 5'-nucleotidase is sensitive to superoxide anion, and is an indicator of oxidative stress in humans. The aim of this study was to assess the effect of the sulfonylurea drugs gliclazide and glibenclamide on lymphocyte ecto-5'-nucleotidase of type 2 diabetic patients. METHODS: Thirty obese type 2 diabetic patients were treated for three months after randomisation either with gliclazide or glibenclamide. Basic laboratory parameters (glycaemia, fructosamine, C-peptide), plasma malondialdehyde levels (MDA) as well as lymphocyte 5'-nucleotidase activity were determined, for all patients and 16 healthy controls, before and after the treatment. RESULTS: 5'-nucleotidase activity in diabetic patients before treatment with gliclazide was 1.61 +/- 0.16 nmol/min/10(6) lymphocytes, and was significantly (P < 0.01) increased compared with the level in healthy controls. After three months of gliclazide treatment, ecto-5'-nucleotidase activity fell significantly by 47.39% and 36% in unstimulated Con A- and PMA-stimulated lymphocytes, respectively. Glibenclamide treatment had no effect on ecto-5'-nucleo-tidase of type 2 diabetic patients. Glycoregulation was improved, as plasma fructosamine decreased from 53.4 to 42.1 and from 50.5 to 43.4 U/g proteins after gliclazide and glibenclamide treatment, respectively. Plasma MDA levels markedly decreased after gliclazide but not glibenclamide treatment. CONCLUSION: These results show that gliclazide treatment inhibits the activity of lymphocyte ecto-5'-nucleotidase and presumably de-creases the concentration of adenosine at the cell surface. A decrease in 5'-nucleotidase activity and attenuation of adenosine production may be a factor in the protection of tissue injury in type 2 diabetic patients.

5'-Nucleotidase↗
PubMed2004

Arabinoxylan fibre improves metabolic control in people with Type II diabetes.

OBJECTIVE: To determine whether diet supplementation with arabinoxylan-rich (AX)-fibre from wheat improves glycaemic control in Type II diabetes. DESIGN: Randomized, crossover intervention trial. SETTING: Monash Medical Centre. SUBJECTS: A total of 15 subjects with Type II diabetes. INTERVENTIONS: Over two 5-week periods, subjects supplemented their usual diet with control bread and muffins (50% whole wheat, 50% white flour) (control diet) or with AX-bread and muffins (50% whole wheat, 36% white flour, 14% AX fibre) (AX diet). Subjects completed a 7-day food diary. At 0 and 5 weeks, venous blood was collected for determination of fasting and 2 h glucose, insulin, fructosamine and blood lipids. Blood pressure, body weight and body fat were also determined. A 24 h faecal sample, from 12 subjects, was weighed and analysed for faecal polysaccharide as a marker for dietary compliance. RESULTS: Control and AX diets were similar except the AX diet supplied an additional 15.1 (12.0-18.5) (mean (95% confidence intervals)) g/day dietary fibre (P=0.000). Consumption of the AX diet increased faecal output by 61.5 (0.2-122.8) g/day (P=0.05) on a wet weight basis and significantly lowered fasting and 2 h plasma glucose, 2 h insulin and serum fructosamine (P=0.002, 0.000, 0.015, and 0.02, respectively). Blood lipids, body weight, fat mass and blood pressure remained unchanged. CONCLUSION: A supplement of 15 g/day of AX-rich fibre can significantly improve glycaemic control in people with Type II diabetes.

Blood Glucose↗
PubMed2002

Assessment of nerve fiber layer in diabetic patients with scanning laser polarimetry.

OBJECTIVES: To evaluate the effects of diabetes mellitus, diabetic retinopathy and degree of blood glucose (BG) regulation on retinal nerve fiber layer (RNFL) thickness by using a scanning laser polarimeter (NFA-GDx). METHODS: We prospectively assessed RNFL thickness in four groups of patients, who were all age matched. Diabetic patients without diabetic retinopathy were grouped according to their BG regulation level into two, as: BG-regulated group (BG <140 mg/dl, HbA1c <8%, fructosamine <285 micromol/l, TG <200 mg/dl, n = 50), and BG-non-regulated group (BG = 140-250 mg/dl, HbA1c >8%, fructosamine >285 micromol/l, TG >200 mg/dl, n = 44). A group of patients with nonproliferative diabetic retinopathy (NPDR) formed the 3rd group (n = 41). The 4th group consisted of healthy subjects and acted as a control group (n = 50). Symmetry, superior maximum, ellipse modulation and the average thickness variables of NFA-GDx were used for the assessment. ANOVA test was used for the statistical analysis of variables between groups. RESULTS: The mean superior maximum and ellipse modulation values were statistically significantly lower than the control group in BG-non-regulated and NPDR groups (P < 0.05). The average thickness value was also statistically significantly lower than the control group in NPDR group. These values in the BG-regulated group were not statistically significantly different from the control group (P > 0.05). CONCLUSIONS: This is the first clinical study demonstrating the effects of diabetic glucose regulation level on RNFL by using NFA-GDx. RNFL thickness was seen to decrease with development of diabetic retinopathy and with impairment of metabolic regulation. This issue should be taken into account while assessing RNFL in diabetic glaucomatous patients.

Adult↗
PubMed2003

Enzymatic deglycation--a new paradigm or an epiphenomenon?

Following the discovery of FN3K (fructosamine 3-kinase), and more recently of FN3KRP (FN3K-related protein), research in our laboratory has been focused on testing the enzymatic deglycation hypothesis and investigating the roles of FN3K and FN3KRP. Thus far, using human erythrocytes as a model system, we have obtained the following evidence of enzymatic deglycation: (a) production of GHb (glycated haemoglobin) by D-glucose in intact erythrocytes is 5-fold lower than in haemolysates; (b) glycation of GHb by D-glucose in intact erythrocytes is 5-fold lower than that by L-glucose; (c) inhibition of ATP production in erythrocytes leads to an acceleration in the rate of GHb production by D-glucose; and (d) inhibition of FN3K in erythrocytes by a competitive inhibitor increases the accumulation of GHb. In spite of these data supporting the enzymatic deglycation hypothesis, some outstanding issues remain. These include, among others, the fact that while the apparent deglycation mechanism does not operate on L-glucose, semi-purified FN3K appears to be able to use both D- and L-fructosamines as substrates. Moreover, analysis of the fructoselysine 3-phosphate content of haemoglobin from diabetic subjects suggests that, in addition to FN3K, another deglycating mechanism may be operative in human erythrocytes. Elucidation of these issues is a challenge in the evolving field of deglycation research. Most important, however, is the question of whether enzymatic deglycation is truly an important defence mechanism or merely an epiphenomenon.

Adenosine Triphosphate↗
PubMed2000

Tumour necrosis factor-alpha plasma level in patients with type 1 diabetes mellitus and its association with glycaemic control and cardiovascular risk factors.

OBJECTIVES: Diabetic patients reveal a significant increase in their cardiovascular risk. Beside glycaemic control and management of established risk factors, determination of cytokines, like serum levels of tumour necrosis factor-alpha (TNF-alpha), might offer a tool to determine patients at high risk. The cytokine TNF-alpha reveals a complex relationship with diabetes. It is involved in beta-cell damage leading to type 1 diabetes, causes insulin resistance associated with obesity and is of influence in the formation of atherosclerotic vascular lesions. We were interested in the possible association of this cytokine with metabolic control and cardiovascular risk factors in patients with type 1 diabetes. DESIGN AND SUBJECTS: TNF-alpha plasma levels were determined in 44 outdoor patients (15 women, 29 men) with type 1 diabetes mellitus (mean duration 11.2 +/- 8.7 years) and in 24 healthy controls by use of a solid phase enzyme amplified sensitivity immunoassay (TNF-alpha ELISA, Biosource Fleurus, Belgium). None of our study participants suffered from inflammatory or other concurrent diseases. Relationships between variables were evaluated by non-parametric Spearman correlation coefficients. RESULTS: TNF-alpha plasma levels were significantly higher in diabetic patients (19.3 +/- 7.5 pg mL-1) than in non-diabetic subjects (11.1 +/- 5.8 pg mL-1; P < 0. 023), and revealed a significant positive correlation with glycated haemoglobin (HbA1c) (r = 0.43; P < 0.004) and fructosamine (r = 0. 31; P < 0.049) values, and a negative correlation with HDL cholesterol (r = -0.36; P < 0.018) and apoAI-levels (r = -0.37; P < 0.015). These relationships could be observed in patients with a duration of diabetes for more than 5 years, as well as in patients with a shorter duration of diabetes. In the male group, TNF-alpha plasma levels revealed a significant positive correlation with plasma levels of thiobarbituric acid reacting substances (r = 0.61; P < 0.001). Plasma levels of thiobarbituric acid reacting substances showed a positive correlation with the duration of diabetes (r = 0. 58; P < 0.008), as well as with the serum levels of the vascular adhesion molecules intercellular adhesion molecule (ICAM) (r = 0.34; P < 0.051) and vascular cell adhesion molecule (VCAM) (r = 0.30; P < 0.052). CONCLUSIONS: Our data indicate that TNF-alpha plasma levels are increased in type 1 diabetes mellitus and reveal a significant association with metabolic long-term control parameters, HbA1c and fructosamine for glycaemic control, and HDL cholesterol for triglyceride metabolism, as well with lipid peroxidation.

Adult↗
PubMed1999

Glycaemic control, muscle glycogen and exercise performance in IDDM athletes on diets of varying carbohydrate content.

The aim of this study was to examine the effects of a high carbohydrate diet on glycaemic control, resting muscle glycogen levels and exercise performance in athletes with insulin dependent diabetes (IDDM). Seven trained (mean +/- S.D., VO2max 50.3 +/- 7.4 ml/kg/min) IDDM males consumed a high carbohydrate diet (HCD) or a normal mixed diet (NMD) for 3 week periods in a randomised crossover trial with a one week wash-out. Carbohydrate provided 59% or 50% of total energy intake, respectively, on the two diets. Fasting plasma lipids, mean blood glucose (over 96 h), fructosamine and muscle glycogen were measured and insulin use recorded. Exercise performance was evaluated by a 15 min time trial following a 50 min pre-loading block. Statistical significance was assessed using two tailed paired Student t-tests. Mean blood glucose was 10% higher on HCD than NMD (p = 0.005), fructosamine levels were 375 +/- 54 and 353 +/- 51 (mol/L on HCD and NMD, resp., p = 0.04) and daily insulin requirements were 15% higher on HCD than NMD (p = 0.02). Fasting blood lipids were similar on the two diets. Muscle glycogen was significantly lower on HCD than NMD (88.2 +/- 19.2 and 95.6 +/- 14.6 mmol/kg ww, respectively, p = 0.02). Exercise completed during the time trial was 6% less on HCD than on NMD (p = 0.007). An increased carbohydrate intake for three weeks, in IDDM athletes, is associated with a deterioration in glycaemic control, increased insulin requirements, decreased muscle glycogen and reduced exercise performance. These data do not support recommendations for IDDM athletes to consume a high carbohydrate diet, at least not when glycaemic control worsens upon following this advice, as was observed in this short-term study.

Adolescent↗
PubMed1996

Purification and characterization of a membrane-bound deglycating enzyme (1-deoxyfructosyl alkyl amino acid oxidase, EC 1.5.3) from a Pseudomonas sp. soil strain.

Searching for novel approaches for uncoupling glycation from hyperglycemia as a cause of diabetic complications, a Pseudomonas sp. soil strain containing a membrane-bound enzyme that deglycates amino acids under release of free fructosamine was isolated (Gerhardinger, C., Marion, S. M., Rovner, A., Glomb, M., and Monnier, V. M. (1995) J. Biol. Chem. 270, 218-224). This enzymatic activity was found to be very sensitive to inactivation by most detergents. From the plasma membrane ( approximately 3 mg/ml protein concentration), the enzyme could be solubilized in active form using 10 mM 3-[(3-chlolamidopropyl) dimethylammonio]-2-hydroxy-1-propanesulfonate aided by 2 M NaCl and 10% glycerol (27% optimal solubilization yield). The supernatant from a 55% saturation (NH4)2SO4 cut was fractionated onto a phenyl-Superose HR 5/5 column and enzymatic activity was eluted with a inverse gradient of (NH4)2SO4. Following removal of (NH4)2SO4 with PD-10 columns and fractionation with a Mono Q HR 5/5 column, a sharp peak of enzyme activity was eluted. Analysis on sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed a major band at 106 kDa and, on isoelectrofocusing gel, a pI of 5.1. The activity was completely inhibited by CN- and N3-, suggestive of copper as a likely cofactor. Identification of the protein was confirmed by affinity labeling with 14CN- and isoelectrofocusing. The "amadoriase" activity was also inhibited by Hg2+, Ag2+, Cu2+, and Zn2+ and had Km and Vmax values of 0.14 mM and 0.48 unit/ml (16 units/mg of protein), respectively, for epsilon-(1-deoxyfructosyl) aminocaproate. Significant activity was noted toward many glycated amino acids (highest with epsilon-fructosyl lysine) but not with glycated proteins. The sequence of the first 16 NH2-terminal amino acids and a search in various data bases revealed that this amadoriase enzyme is a novel protein. Based on its properties, this deglycating enzyme, which degrades Amadori products oxidatively into free fructosamine, is classified as fructosyl aminocaproate:oxygen oxidoreductase (EC 1.5.3).

Amino Acid Oxidoreductases↗
PubMed2004

The effects of diet, sulfonylurea, and Repaglinide therapy on clinical and metabolic parameters in type 2 diabetic patients during Ramadan.

BACKGROUND AND AIM: Diabetes and its treatment can cause problems for the Muslim population. The aim of this study was to evaluate the effect of different therapy models on clinical and metabolic status in type 2 diabetic patients during Ramadan. MATERIAL AND METHODS: Fifty-two type 2 diabetic patients were included to this study. Twelve of patients were on diabetic diet only before and during Ramadan (Group 1). Forty of patients had had sulfonylurea (Glimepiride 23 patients, gliclazide 17 patients) before Ramadan. Thirteen of these patients were on a single dose sulfonylurea (Glimepiride 8 patients, gliclazide 5 patients) (Group 2) and 27 were on Repaglinide 2 x 2 mg (Group 3) during Ramadan. Beta-hydroxybutyric acid, glucose, fructosamine, HbA1c, lipid levels and body weight were measured before and after Ramadan. RESULTS: Body weight, fasting plasma glucose, fructosamine, HbA1c, total cholesterol were not changed in groups during the study. Triglyceride level decreased after Ramadan in groups 2 (p = 0.002) and 3 (p = 0.024). HDL-cholesterol level increased in group 3 (p = 0.022). Fasting capillary beta-hydroxybutyric acid level increased in group 1 (p = 0.034) and didn't change in groups 2 and 3 during the Ramadan. Only one hypoglycemic event occurred at day 6 of Ramadan in patients in group 2 (the patient was on 3 mg glimepiride). CONCLUSION: Our results conclude that Ramadan fasting affects metabolic parameters in type 2 diabetes and hypoglycemia should be kept in mind especially in patients using sulfonylurea treatment. Ramadan fasting is not advised for type 2 diabetics while taking medical therapy. If the patient wants Ramadan fasting, these patients using Repaglinide can reduce the frequency of hypoglycemia.

3-Hydroxybutyric Acid↗
PubMed2003

Effects of short-term transdermal hormone replacement therapy on glycaemic control, lipid metabolism, C-reactive protein and proteinuria in postmenopausal women with type 2 diabetes or hypertension.

BACKGROUND: The study was carried out to evaluate the effects of short-term transdermal hormone replacement therapy (HRT) on glycaemic control, lipid metabolism, C-reactive protein (CRP) and proteinuria in high-risk postmenopausal women. METHODS: A total of 20 well-controlled type 2 diabetic, hypertensive and 21 well-controlled glucose-tolerant, hypertensive postmenopausal women were prospectively enrolled. After 12 weeks of transdermal HRT, the changes in serum lipid sub-fractions, fasting glucose, fructosamine, glycated haemoglobin (HbA(1c)), CRP, creatinine, 24 h urine protein levels, creatinine clearance and blood pressure were evaluated. RESULTS: After 12 weeks of treatment, serum total-cholesterol and low-density cholesterols (LDL-cholesterol) appeared slightly reduced and serum triglyceride slightly elevated, although non-significantly so in both groups. The increase in HDL-cholesterol (P < 0.05) and reduction in very low density (VLDL)-cholesterol (P < 0.05) levels were significant in hypertensive patients. Elevation in the Apolipoprotein A1 (P < 0.05) and reduction in the Apolipoprotein B (P < 0.05) levels were statistically significant in all patients. HRT was associated with significant decreases in serum fasting glucose (P < 0.05) and fructosamine (P < 0.05) levels in diabetic patients. Serum HbA(1c), CRP, creatinine, 24 h urine protein levels, creatinine clearance and systolic and diastolic blood pressure did not change significantly in either group. CONCLUSIONS: There were no detrimental effects of transdermal HRT on lipid profile, glucose metabolism, CRP and urine protein levels in our well-controlled diabetic or hypertensive patients. A decision regarding HRT use should be taken on a case-by-case basis.

Administration, Cutaneous↗