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PubMed1996

Teratogenic effects of diabetes mellitus in the rat. Prevention by vitamin E.

We wanted to determine whether administration of vitamin E could reduce the production of free radicals which could play a role in the teratogenic effects of diabetes mellitus. Diabetes was induced in Wistar rats by the intravenous administration of streptozotocin. The animals were divided into six groups: one with no supplement (D) and two, supplemented during pregnancy either with oral vitamin E (150 mg/day) (D + E) or with a placebo (safflower oil) (D + O). Three other groups were kept under the same conditions, but were treated with insulin: D + I, D + I + E and D + I + O. There were three groups of matched controls: C, C + E and C + O. All animals were killed on day 11.5 of pregnancy. In C animals the percentages of reabsorptions and malformations were 1.3 and 2%, respectively, compared with 23.6, 24.3, 6.2 and 13.2%, respectively in D and D + I groups. The crown-rump length, number of somites, and protein and DNA content were higher in C animals than in the diabetic rats, independent of insulin treatment. When vitamin E was administered no changes in these parameters were observed in C and D + I animals; however, in the D mothers it reduced the rate of embryo malformations to 4.6% and increased the crown-rump length and the number of somites. However, vitamin E did not modify the protein and DNA content and the percentage of reabsorptions. In conclusion, administration of vitamin E to diabetic animals decreases the rate of embryo malformations and increases their size and maturation, supporting a role for free radicals in the teratogenic effects of diabetes.

3-Hydroxybutyric Acid↗
PubMed1992

Pulmonary complications of type 1 (insulin-dependent) diabetic patients.

We have investigated the influence of diabetes mellitus including the presence of late complications of the pulmonary system. To check this relationship 31 Type 1 (insulin-dependent) diabetic patients (mean age 30.6 +/- 5.32 years, mean duration of diabetes 12.9 +/- 5.05 years) were admitted into the trial and compared with 18 control subjects. Pulmonary function tests were measured including spirometric parameters, diffusing capacity, specific diffusing capacity and dynamic compliance measured at 20 and 60 breaths per min. No disturbance of the spirometric parameters was observed in the diabetic patients. Diffusing capacity in the diabetic patients with complications was significantly lower than in both the diabetic patients without complications and the control group (81.2 +/- 16.2%, 104 +/- 13.7%, 99.3 +/- 2.8%; p < 0.001, p < 0.005 respectively). Specific diffusing capacity was significantly lower in the diabetic patients than in the control subjects (80.3 +/- 13.1% vs 89.4 +/- 12.9%; p < 0.05). In the group with late complications specific diffusing capacity was lower than in the group without complications (69.7 +/- 9.17%; 87.2 +/- 10.7%, respectively; p < 0.001). Dynamic compliance at 20 breaths per min in diabetic patients was 84.06 +/- 17.08% vs 95.2 +/- 11.59% in the control subjects (p < 0.05). It was particularly low in the group with late complications 80.6 +/- 13.2% and patients with metabolic poor control, 80.3 +/- 12.02% (both p < 0.005 vs the control group). Dynamic compliance at 60 breaths per min was 60.1 +/- 15.0% as compared to 83.2 +/- 13.3% in the control group (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Alterations of biochemical and biomechanical properties of rat tail tendons caused by non-enzymatic glycation and their inhibition by dibasic amino acids arginine and lysine.

The influence of dibasic amino acids arginine and lysine on non-enzymatic glycation of tail tendon fibers from old (900-day-old) and young (61-day-old) rats was investigated in vitro. The biomechanical changes in tendon fibers of young rats after an incubation interval of 7 or 14 days in a glucose solution were abolished by the addition of arginine or lysine (molar ratio amino acid:glucose 1:10). Glucose incorporation into rat tail tendon fibers as well as Amadori product formation was decreased significantly in the presence of the amino acids. The inhibitory effect of arginine was further confirmed by measurement of the amount of ketoamine formed during the glycation reaction using soluble albumin as a protein target. The effective inhibition of non-enzymatic glycation by arginine or lysine suggests their potential use in vivo as a means of controlling protein over-glycation.

Aging↗
PubMed1991

Disturbed handling of ascorbic acid in diabetic patients with and without microangiopathy during high dose ascorbate supplementation.

Abnormalities of ascorbic acid metabolism have been reported in experimentally-induced diabetes and in diabetic patients. Ascorbate is a powerful antioxidant, a cofactor in collagen biosynthesis, and affects platelet activation, prostaglandin synthesis and the polyol pathway. This suggests a possible close interrelationship between ascorbic acid metabolism and pathways known to be influenced by diabetes. We determined serum ascorbic acid and its metabolite, dehydroascorbic acid, as indices of antioxidant status, and the ratio, dehydroascorbate/ascorbate, as an index of oxidative stress, in 20 matched diabetic patients with and 20 without microangiopathy and in 22 age-matched control subjects. Each study subject then took ascorbic acid, 1 g daily orally, for six weeks with repeat measurements taken at three and six weeks. At baseline, patients with microangiopathy had lower ascorbic acid concentrations than those without microangiopathy and control subjects (42.1 +/- 19.3 vs 55.6 +/- 20.0, p less than 0.01, vs 82.9 +/- 30.9 mumol/l, p less than 0.001) and elevated dehydroascorbate/ascorbate ratios (0.87 +/- 0.46 vs 0.61 +/- 0.26, p less than 0.01, vs 0.38 +/- 0.14, p less than 0.001). At three weeks, ascorbate concentrations rose in all groups (p less than 0.0001) and was maintained in control subjects (151.5 +/- 56.3 mumol/l), but fell in both diabetic groups by six weeks (p less than 0.01). Dehydroascorbate/ascorbate ratios fell in all groups at three weeks (p less than 0.0001) but rose again in the diabetic groups by six weeks (p less than 0.001) and was unchanged in the control subjects. Dehydroascorbate concentrations rose significantly from baseline in all groups by six weeks of ascorbic acid supplementation (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1996

Troglitazone, an insulin action enhancer, improves metabolic control in NIDDM patients. Troglitazone Study Group.

The effects of troglitazone, a novel thiazolidinedione, in non-insulin-dependent diabetic (NIDDM) patients were studied in a double-blind, parallel-group, placebo-controlled, dose-ranging trial. A total of 330 patients (63% male), mean age 57 years (range 39-72), with two fasting capillary blood glucose values > or = 7 and < or = 15 mmol/l (within 2.5 mmol/l of each other) were randomised to treatment with placebo or troglitazone at doses of 200, 400, 600 or 800 mg once daily, or 200 or 400 mg twice daily, for 12 weeks. Prior to the study, treatment had been with diet alone (38% patients) or with oral hypoglycaemic agents which were stopped 3-4 weeks before study treatment started. During treatment, HbA1c tended to rise in patients taking placebo (7.2-8.0%), but remained unchanged with all doses of troglitazone. After 12 weeks of treatment, HbA1c was significantly lower in the troglitazone-treated (mean 7.0-7.4%) compared to the placebo-treated (8.0%) patients (p = 0.055 to < 0.001), as was fasting serum glucose concentration (troglitazone, 9.3-11.0 mmol/l vs placebo, 12.9 mmol/l, p < 0.001). All doses of troglitazone were equally effective. Troglitazone also lowered fasting plasma insulin concentration, by 12-26% compared to placebo (p = 0.074 to < 0.001). Insulin sensitivity assessed by homeostasis model assessment (HOMA) was greater after 12 weeks of treatment in troglitazone-treated patients (troglitazone, 34.3-42.8% vs placebo, 29.9%, p < 0.05). In addition, serum triglyceride and non-esterified fatty acid concentrations were significantly lower and HDL cholesterol higher at troglitazone doses of 600 and 800 mg/day. LDL cholesterol increased at 400 and 600 mg doses only (from 4.3 and 3.9 mmol/l at baseline to 4.8 and 4.5 mmol/l, respectively at 12 weeks, p < 0.05), but not at doses of 800 mg once daily or 400 mg twice daily. LDL/HDL ratio did not change during treatment. All doses were well tolerated; incidence of adverse events in troglitazone-treated patients was no higher than in those treated with placebo. However, a tendency to reduced neutrophil counts was observed in patients taking the highest doses of troglitazone. We conclude that troglitazone is effective and well-tolerated and shows potential as a new therapeutic agent for the treatment of NIDDM.

Adult↗
PubMed1999

Amplitude loss of electrically and magnetically evoked sympathetic skin responses in early stages of type 1 (insulin-dependent) diabetes mellitus without signs of dysautonomia.

The sympathetic skin responses following both electrical nerve (eSSRs) and magnetic (mSSRs) brain stimulations have been investigated in 19 insulin-dependent diabetic patients with no evidence of a peripheral neuropathy or dysautonomia and compared to those obtained in 10 age-matched healthy subjects. SSR was recorded from the right hand and foot, controlateral to the stimulated side. The main findings were amplitude loss and disappearance of the eSSR in 12/19 (63.2%) and 11/19 (57.9%) patients, occurring more frequently than the mSSR; 7/19 (36.8%) and 5/19 (26.3%) were recorded from the hand and foot, respectively. The SSR to electrical stimulation was significantly reduced in the upper and lower extremities (p < 0.0001) compared to control results, whereas latencies were normal to both stimulation modalities. Only in two cases the responses were absent from the foot, one following electrical stimulation and the other after magnetic stimulation. No correlation was found between the SSR and metabolic indexes of diabetes mellitus or conduction velocity studies. On the basis of these data an early impairment of afferent pathways may be postulated.

Adult↗
PubMed1993

Renal function and insulin sensitivity during simvastatin treatment in type 2 (non-insulin-dependent) diabetic patients with microalbuminuria.

The effect of simvastatin (10-20 mg/day) on kidney function, urinary albumin excretion rate and insulin sensitivity was evaluated in 18 Type 2 (non-insulin-dependent) diabetic patients with microalbuminuria and moderate hypercholesterolaemia (total cholesterol > or = 5.5 mmol.l-1). In a double-blind, randomized and placebo-controlled design treatment with simvastatin (n = 8) for 36 weeks significantly reduced total cholesterol (6.7 +/- 0.3 vs 5.1 mmol.l-1 (p < 0.01)), LDL-cholesterol (4.4 +/- 0.3 vs 2.9 +/- 0.2 mmol.l-1 (p < 0.01)) and apolipoprotein B (1.05 +/- 0.04 vs 0.77 +/- 0.02 mmol.l-1 (p < 0.01)) levels as compared to placebo (n = 10). Both glomerular filtration rate (mean +/- SEM) (simvastatin: 96.6 +/- 8.0 vs 96.0 +/- 5.7 ml.min-1 x 1.73 m-2, placebo: 97.1 +/- 6.7 vs 88.8 +/- 6.0 ml.min-1 x 1.73 m-2)(NS) and urinary albumin excretion rate (geometric mean x/divided by antilog SEM) (simvastatin: 18.4 x/divided by 1.3 vs 16.2 x/divided by 1.2 microgram.min-1, placebo 33.1 x/divided by 1.3 vs 42.7 x/divided by 1.3 micrograms.min-1)(NS) were unchanged during the study. A euglycaemic hyperinsulinaemic clamp was performed at baseline and after 18 weeks in seven simvastatin- and nine placebo-treated patients. Isotopically determined basal and insulin-stimulated glucose disposal was similarly reduced before and during therapy in both the simvastatin (2.0 +/- 0.1 vs 1.9 +/- 0.1 (NS) and 3.1 +/- 0.6 vs 3.1 +/- 0.7 mg.kg-1 x min-1 (NS)) and the placebo group (1.9 +/- 0.1 vs 1.8 +/- 0.1 (NS) and 4.1 +/- 0.6 vs 3.8 +/- 0.2 mg.kg-1 x min-1 (NS)).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

Plasma and urine malondialdehyde levels in non-insulin-dependent diabetic patients with and without microalbuminuria.

Malondialdehyde, a marker of lipid peroxidation, was measured as thiobarbituric acid-reactive substance in 78 non-insulin-dependent diabetic patients and 28 healthy subjects. Patients were divided into groups and subgroups according to the presence of microalbuminuria and other complications. Plasma and urine malondialdehyde concentrations were significantly higher in patients with and without microalbuminuria than in controls. In contrast to urine malondialdehyde, plasma malondialdehyde levels were significantly higher in microalbuminuric diabetes than in the normolbuminuric diabetic group. There was no correlation between malondialdehyde concentration and glycemic control. This study confirmed the existence of lipid peroxidation disorders in diabetic patients.

Adult↗
PubMed1996

Differential expression of fructosyllysine-specific receptors on monocytes and macrophages and possible pathophysiological significance.

A differing individual expression of fructosyllysine-specific receptors has been found on the monocytes of 90 insulin-dependent diabetic patients and 101 healthy control subjects. The degree of receptor expression is neither age- nor sex-dependent; however, in the diabetic group it correlates significantly with the severity and age of onset of diabetic microangiopathy. To interpret the results of the human study, spontaneously diabetic and non-diabetic BB/OK rats were used to estimate tissue content of glucose-modified proteins and capillary basement membrane thickness in relation to the receptor expression on macrophages. In non-diabetic and diabetic rats no correlation was found between receptor expression and tissue content (i.e. artery, nerve) of fructosyllsine and fluorescent advanced glycation end products. However, animals which express the fructosyllysine receptor showed a greater increase in muscle capillary basement membrane thickness. There are indications that fructosyllysine receptor expression is positively associated with indices of diabetic complications such as microangiopathy and/or capillary basement membrane thickening.

Adult↗
PubMed1993

Metformin ameliorates diabetes but does not normalize the decreased GLUT 4 content in skeletal muscle of obese (fa/fa) Zucker rats.

We studied the expression of the glucose transporter GLUT 4 in the soleus and red gastrocnemius muscles from obese, diabetic (fa/fa) Zucker rats compared to their lean littermates (Fa/-), with and without treatment with the antidiabetic drug metformin. In the untreated groups of rats, the GLUT 4 content in a crude membrane fraction of both the soleus and the red gastrocnemius muscles were significantly lower in the obese (fa/fa) rats (3.46 +/- 0.28 vs. 6.04 +/- 0.41, p < 0.001 and 6.0 +/- 0.24 vs. 9.1 +/- 0.48, p < 0.0001, respectively). Differences in GLUT 4 expression in soleus muscle from the same rats were confirmed by quantitative immunofluorescence microscopy, and the results were significantly correlated with the results obtained from quantitative immunoblotting (rho = 0.70, p < 0.0005). The decreased expression of GLUT 4 in fa/fa rats could contribute to the well-established insulin resistance in skeletal muscle of these animals. After 4 weeks of treatment with metformin, weight gain was not affected in either the diabetic (fa/fa) rats or the lean (Fa/-) rats. Improvement of glucose homeostasis by metformin was not associated with normalization of the GLUT 4 expression in the skeletal muscles studied, indicating (1) that the decreased GLUT 4 expression is not directly related to hyperinsulinaemia and diabetes mellitus and (2) that metformin does not normalize the expression of GLUT 4 in skeletal muscle of the diabetic (fa/fa) Zucker rats.

Animals↗
PubMed2003

Voluntary exercise and mild food restriction effectively retard the collagen biomarker of aging.

BACKGROUND AND AIMS: Obesity and lack of physical exercise characterize increasing numbers of people in Western societies, resulting in increasing morbidity and mortality. Regular physical exercise, on the other hand, has been shown to be beneficial. Beneficial effects have also been shown in laboratory rodent studies--lifelong physical exercise increases the mean life span but not the maximum life span, while food restriction increases both life spans. We studied male Sprague-Dawley rats in order to further analyze these beneficial effects. METHODS: We compared voluntary running in wheels (RW) with food restriction to pair weight with RW (PW), and mild forced running in treadmill (TM)--all animals housed individually. Control groups were sedentary ad libitum-fed animals housed individually (S1) and four to a cage (S4). The collagen biomarker of aging was calculated as a composite parameter from thermal stability data for 5 (baseline), 15, 19 and 23 months of age. RESULTS: In RW and PW, the increase in the composite parameter was retarded to the same extent. The retardation in TM was less efficient. S4 had the highest value for the composite parameter, together with the highest body weight and fat content. In groupwise comparisons, the composite parameter tended to predict survival in the groups up to the age of 23 months. CONCLUSIONS: Voluntary running in wheels is more beneficial than mild-forced exercise on the treadmill. The composite parameter is a useful indicator of different interventions on aging rats.

Aging↗
PubMed1999

Comparison between continuous and intermittent physical exercise on aging rats: changes in patterns of spontaneous activity and connective tissue stability.

Life-long physical exercise increases the mean but not maximum life span of laboratory rodents. It further improves the performance in an open field setting, which suggests a delay of sensorimotor disturbances, and retards the aging increase of thermal stability of collagen. The purpose of the present study was to examine whether the amount or continuity of training is more important. We trained male Sprague-Dawley rats for 12 months from the age of 12 months in a treadmill: 1) continuously for 3 km/week (total distance covered: 144 km); 2) intermittently for 3 km/week for 8-week periods with 8-week resting periods in between (72 km), and 3) intermittently for 6 km/week for 8-week periods with 8-week resting periods in between (144 km). All training regimens prevented the increase in body weight seen in sedentary animals, although the intermittent training programs caused fluctuations with the training and resting periods. With respect to spontaneous movements in an open field setting, continuous training was most effective in counteracting age-related changes. Continuous training was also most effective for delaying age-related increase in thermal stability of collagen. We conclude that the continuity of training is more important than the amount and intensity of training.

Aging↗
PubMed2000

Rosiglitazone short-term monotherapy lowers fasting and post-prandial glucose in patients with type II diabetes.

AIMS/HYPOTHESIS: The short-term efficacy, safety and tolerability of rosiglitazone were compared with placebo in patients with Type II (non-insulin-dependent) diabetes mellitus in a dose-ranging study. METHODS: After a 2-week placebo run-in phase, 303 patients were randomly assigned to 8 weeks of treatment with twice-daily placebo or 2, 4 or 6 mg of rosiglitazone. RESULTS: All rosiglitazone doses significantly reduced fasting plasma glucose compared with baseline. All rosiglitazone treatment groups showed significantly reduced peak postprandial glucose concentrations compared with baseline (p < 0.001) and with placebo (p < 0.0001) and reduced postprandial glucose excursion, without an increase in the area under the postprandial insulin concentration-time curve. Rosiglitazone at 4 and 6 mg twice daily prevented the increase in HbA1c observed in the placebo group. C peptide and serum insulin concentrations were significantly reduced from baseline in all rosiglitazone treatment groups. In all rosiglitazone treatment groups, nonesterified fatty acids decreased significantly (p < 0.0001) and triglycerides did not change. Although total LDL and HDL cholesterol increased significantly in the rosiglitazone treatment groups, total cholesterol/HDL ratios did not change significantly. The proportion of patients with one or more adverse event was similar in all four treatment groups. No patient showed evidence of hepatotoxicity. CONCLUSION/INTERPRETATION: Rosiglitazone given twice daily significantly reduced fasting and postprandial glucose concentrations, C peptide, insulin and nonesterified fatty acids in Type II diabetic patients. The glucose-lowering effect of the 4-mg twice-daily dose of rosiglitazone was similar to that of 6-mg twice daily, suggesting that 4 mg twice daily should be the maximum clinical dose.

Aged↗
PubMed1994

Elevated GLUT 1 level in crude muscle membranes from diabetic Zucker rats despite a normal GLUT 1 level in perineurial sheaths.

Recently, we demonstrated that approximately 60% of GLUT 1 in a crude membrane fraction of rat skeletal muscle originates from perineurial sheaths. To study the in vivo regulation of GLUT 1 expression in different tissues in muscles, we measured the level of GLUT 1 in crude muscle membranes and in perineurial sheaths in diabetic (fa/fa) Zucker rats and lean controls, with and without metformin treatment. The GLUT 1 concentration in perineurial sheaths was identical in all four groups of rats, both when measured by quantitative immunofluorescence and by immunoblotting and densitometry. In a fraction of crude membranes of soleus muscles GLUT 1 expression was more than two-fold higher in (fa/fa) rats than in lean controls (p < 0.005). Metformin treatment significantly elevated GLUT 1 in control rats (p < 0.05) and tended to decrease GLUT 1 in diabetic rats (p < 0.075). The expressions of GLUT 1 and GLUT 4 in crude muscle membranes were inversely correlated (p < 0.01), and GLUT 1 expression correlated positively with fasting glucose (p < 0.05). In conclusion, GLUT 1 expression in perineurial sheaths is unaffected by alterations in glucose homeostasis and by the genes responsible for obesity and diabetes in the Zucker rat. GLUT 1 expression in a crude membrane fraction of soleus muscle is increased in the diabetic animals, likely due to an increased expression in muscle cells proper.

Animals↗
PubMed1997

Length of metabolic normalization after rat islet cell transplantation depends on endocrine cell composition of graft and on donor age.

In vitro studies have demonstrated that beta-cell functions are negatively influenced by age and positively by the presence of glucagon producing alpha cells. This study examines whether the function of beta-cell grafts varies with the age of the donor and with the presence of other endocrine islet cells. Islet beta and endocrine non-beta-cells were purified from 10- to 30-week-old Lewis rats, and reaggregated into pure beta and mixed endocrine cell aggregates. Grafts consisted of 1.2 to 1.7 million beta cells with or without 0.6-0.7 million alpha cells. Their intraportal transplantation in 10-week-old streptozotocin-diabetic rats corrected hyperglycaemia in all experimental groups, with normal glucose tolerance curves at post-transplantation week (PT wk) 4. Recipients of mixed endocrine cell grafts from 10-week-old donors maintained a glucose tolerant state until PT wk 20, but turned glucose intolerant thereafter; only 1 of 12 animals was overtly diabetic at PT wk 64. Recipients of pure beta-cell grafts from 10-week-old donors became glucose-intolerant from PT wk 4 on, with 5 of 11 cases developing overt diabetes before PT wk 64. When grafts were prepared from 30-week-old donors, metabolic deterioration started earlier, again with a more rapid loss for pure beta-cell grafts; at PT wk 64, virtually all recipients were overtly diabetic. It is concluded that delayed graft failure can be the consequence of an insufficient number of islet endocrine non-beta-cells as well as of a higher donor age. This observation can explain late failures in animal and human islet transplantation using marginally low beta-cell numbers. The interpretation of long-term studies on islet cell transplantation can benefit from the use of standardized grafts with well defined cellular composition.

Age Factors↗
PubMed1999

Advanced glycation end products-cytokine-nitric oxide sequence pathway in the development of diabetic nephropathy: aminoguanidine ameliorates the overexpression of tumour necrosis factor-alpha and inducible nitric oxide synthase in diabetic rat glomeruli.

AIMS/HYPOTHESIS: Advanced glycation end products are believed to contribute to diabetic microvascular complications by inducing glomerular damage but their role has not been fully clarified. In this study, we explain their central role in the induction of inducible nitric oxide synthase and production of nitric oxide (NO) in streptozotocin-induced diabetic rat glomeruli. METHODS: Localization of carboxymethyllysine, which is one of the chemical components of advanced glycation end products, glomerular expression of inducible nitric oxide synthase and urinary excretion and glomerular production of NO2-/NO3- were examined at 0, 26, 51, and 52 weeks after the induction of diabetes. Therapeutic effects of aminoguanidine were also examined. RESULTS: Carboxymethyllysine was detected in the mesangial area in glomeruli and it progressively accumulated during 52 weeks of observation. Immunohistochemistry and hybridization studies in situ showed that the number of inducible nitric oxide synthase-positive cells was notably increased in diabetic rat glomeruli at 52 weeks. Further, this augmented expression paralleled intraglomerular expression of TNF-alpha and NO2-/NO3- in diabetic rat glomeruli. Treatment with aminoguanidine reduced the expression of TNF-alpha, inducible nitric oxide synthase and intraglomerular NO2-/NO3- production. It also ameliorated proteinuria in diabetic rats. CONCLUSION/INTERPRETATION: This study showed that carboxymethyllysine possibly enhances the expression of inducible nitric oxide synthase by stimulating the expression of TNF-alpha in diabetic rat glomeruli. The carboxymethyllysine-cytokine-NO sequence pathway could be one of the major mechanisms in the development of diabetic nephropathy.

Animals↗