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At least 973 records · Page 54Linked to original sources

PubMed1982

The relationship of serum uric acid to hypertension and ischemic heart disease in Hisayama population, Japan.

The association of serum uric acid (SUA) with hypertension, ischemic ECG change, diabetes mellitus, and drinking and smoking habits was studied by multivariate analysis among 1871 residents aged 40 and over in Hisayama, Japan. Blood pressure level and history of hypertension did not correlate with an increased level of SUA when other factors such as serum creatinine, obesity, beta-lipoprotein and leucineaminopeptidase were taken into account. Antihypertensive medication was a significant factor influencing SUA. The association of SUA with Minnesota code 4.1-3 (S-T depression) was insignificant in men and significant in women when other factors influencing SUA were taken into account. Glycosuria was negatively correlated with SUA, while alcohol ingestion has positive correlation. There was no correlation between the amount of tobacco smoked and the level of SUA.

Alcohol Drinking↗

PubMed1994

Dorsal root ganglia microenvironment of female BB Wistar diabetic rats with mild neuropathy.

Abnormalities in the microenvironment of dorsal root ganglia (DRG) might play a role in the pathogenesis of sensory abnormalities in human diabetic neuropathy. We examined aspects of DRG microenvironment by measuring local blood flow and oxygen tension in the L4 dorsal root ganglia of female BB Wistar (BBW) diabetic rats with mild neuropathy. The findings were compared with concurrent measurements of local sciatic endoneurial blood flow and oxygen tension. Diabetic rats were treated with insulin and underwent electrophysiological, blood flow and oxygen tension measurements at either 7-11 or 17-23 weeks after the development of glycosuria. Nondiabetic female BB Wistar rats from the same colony served as controls. At both ages, BBW diabetic rats had significant abnormalities in sensory, but not motor conduction compared to nondiabetic controls. Sciatic endoneurial blood flow in the diabetic rats of both ages was similar to control values, but the older (17-23 week diabetic) BBW diabetic rats had a selective reduction in DRG blood flow. Sciatic endoneurial oxygen tensions were not significantly altered in the diabetic rats. DRG oxygen tension appeared lowered in younger (7-11 week diabetic) but not older (17-23 week diabetic) BBW rats. Our findings indicate that there are important changes in the DRG microenvironment of diabetic rats with selective sensory neuropathy.

Animals↗

PubMed1988

The effects of subtotal pancreatectomy on renal growth in streptozotocin diabetic rats.

Increases in kidney size and function are characteristic features of the early stages of Type I diabetes mellitus, and may contribute to the pathogenesis of diabetic nephropathy. Other studies have shown that the relative circulating concentrations of insulin and glucagon may be regulatory to renal growth and function. In order to elucidate the role of pancreatic glucagon in diabetic renal growth, subtotal pancreatectomy was performed prior to administration of streptozotocin to rats. Glycosuria and kidney weight were significantly reduced by subtotal pancreatectomy, although creatinine clearance and blood glucose levels were not different from diabetic controls. These data suggest that hyperglucagonemia may be an important mediator of renal growth in insulinopenic diabetes mellitus.

Animals↗

PubMed1996

Glycosylated hemoglobin and fructosamines: does their determination really reflect the glycemic control in diabetic patients?

The present experiment was designed to determine whether scavenging capacity of serum, in addition to glucose level, influences hemoglobin and serum protein glycosylation in non-insulin dependent diabetic patients. For this purpose forty-seven patients homogeneous for age, disease duration, therapy and glyco-metabolic control were selected. Fasting and post-prandial glycemia and insulinemia as well as glycosuria were weekly analysed during the sixty days preceding glycosylated hemoglobin (HbA1c), fructosamines and serum scavenging capacity determination. This last parameter has been evaluated by a method based on the property of beta-phycoerythrin (beta-PE) to loss its fluorescence when damaged by oxygen radicals, that were produced by Cu++ and H2O2. The oxygen radical absorbance capacity (ORACOH) of serum was assayed as the ability of serum to delay the loss of beta-PE fluorescence. As expected, a statistically significant positive correlation was found comparing both fructosamines and HbA1c levels with mean fasting glycemia measured over twenty and sixty days, respectively. The key result of this study is represented by the finding that both HbAlc and fructosamines levels show a statistically significant negative correlation with ORACOH values. This correlation can explain a large percent of the data dispersion occurring when ORACOH is not taken into account. In order to better describe the role of ORACOH, patients were separated into two sub-groups with an ORACOH lower (L-ORACOH) and greater (H-ORACOH) than 100 U/ml. Examining the correlation between mean fasting glycemia and the two glycosylated proteins considered in these two sub-groups, curves with different slopes were obtained, supporting that the rate of glycosylation of both proteins was higher in L-ORACOH patients as compared to those with H-ORACOH. Present data suggest that for a proper interpretation of the HbA1c and fructosamines data in diabetic patients, the scavenging capacity level of serum should be taken into account.

Aged↗

PubMed1976

Renal excretion of uric acid during prolonged fasting.

Serum and urine uric acid were evaluated during prolonged therapeutic fasting in 15 obese patients. With increasing ketonemia the serum uric acid rose from a control value of 5.9 +/- 0.4 to 12.5 +/- 1.0 mg/100 ml at 7 days and then decreased progressively to 7.7 +/- 1.3 mg/100 ml by 28 days despite sustained ketonemia. The uric acid clearance were 5.5 +/- 0.9, 1.8 +/- 0.2, and 4.4 +/- 1.5 ml/min at days 0, 7, and 25 of fasting. At the same times the creatinine clearances were 114 +/- 11, 80 +/- 6, and 64 +/- 6.3 ml/min. There was no evidence of a renal tubular abnormality as assessed by glycosuria, bicarbonaturia, or increased phosphaturia. Urate binding to plasma proteins remained unchanged. Acute studies of the renal handling of uric acid revealed a uricosuric response to the administration of sodium lactate or sodium bicarbonate by intravenous infusion and low-dose acetylsalicylic acid orally. This renal tubular response departs significantly from that observed during the overnight fasted state and could not be accounted for by extracellular fluid volume expansion or the induced acid-base changes.

Adolescent↗

PubMed1978

Role of glucagon in the pathogenesis of diabetes: the status of the controversy.

The current controversy concerning the role of glucagon in the pathogenesis of diabetes is reviewed. The traditional "unihormonal abnormality concept," namely, that all of the metabolic derangements of diabetes are the direct consequence of deficient insulin secretion or activity, and the newer so-called bihormonal abnormality hypothesis, proposing that the fullblown diabetic syndrome requires, in addition to the insulin abnormality, a relative glucagon excess, are scrutinized. The relationship of insulin deficiency to the A-cell malfunction of diabetes, the conflicting evidence concerning the essential role of glucagon in mediating the marked overproduction of glucose and ketones in severe insulin deficiency and the contribution of glucagon to the endogenous hyperglycemia of diabetics without insulin deficiency are examined. Finally, the possibility that therapeutic suppression of diabetic hyperglucagonemia may make possible better control of hyperglycemia than is presently attainable by conventional therapeutic methods is considered. It is concluded that (1) although insulin lowers glucagon levels, restoration to normal of the A-cell dysfunction of diabetes requires that plasma insulin levels vary appropriately with glycemic change; (2) that glucagon mediates the severe endogenous hyperglycemia and hyperketonemia observed in the absence of insulin; (3) that in diabetics in whom insulin is present but relatively fixed an increase in glucagon causes hyperglycemia and glycosuria; and (4) that glucagon suppression could be a potentially useful adjunct to conventional antihyperglycemic treatment of diabetics.

Alanine↗

PubMed1980

Muscle protein catabolism in diabetes: 3-methylhistidine excretion in the spontaneously diabetic "BB" rat.

The muscle protein lost in uncontrolled diabetes may be due to decreased synthesis, increased catabolism, or to any combination of alteration in these rates that results in net loss. Differing methods of examining these rates in vivo and in vitro have given conflicting results. We assessed the rate of catabolism of proteins containing 3-methylhistidine (3-MH) by measurement of its urinary excretion in spontaneously diabetic "BB" Wistar rats. Prior to overt diabetes, rates of excretion were appropriate to the age of the rats (1.46 +/- 0.15 mumole/day), with 34%-47% as the nonacetylated form. Accompanying diabetes there was an increase in urine urea nitrogen of two to threefold over 4-14 days, and an increase in ammonium nitrogen of sixfold. 3-MH excretion doubled by 4 days, and 81%-96% was excreted as the nonacetylated form. Subcutaneous insulin in doses sufficient to improve glycosuria and hyperglycemia was associated with normalized total 3-MH excretion (N-acetyl 3-MH plus 3-MH) but a greater proportion than normal appeared in the nonacetylated form. These results suggest that muscle protein catabolism increased with insulin deficiency and that this defect can be corrected by therapy. Both untreated and treated diabetic rats appear to have a limited capacity for acetylation of 3-MH prior to its excretion.

Acetylation↗

PubMed1980

In vitro culture--a method of pancreatic islet preservation for transplantation.

Pancreatic islets from adult rats, accumulated daily for a period of 2 wk, were cultured in artificial capillary culture units that were perfused with nutrient medium. Viability and functional capacity of these islets in this in vitro culture system has been shown to be maintained. The therapeutic efficiency of cultured islets was comparable to freshly isolated islets when assessed by transplantation into streptozotocin-induced diabetic rats. Intraportal implantation of either freshly isolated or cultured islets into isogeneic diabetic rats resulted in normal weight gain as well as complete reversal of hyperglycemia, glycosuria, and polyuria in the diabetic rat recipient. The normoglycemic state was sustained for more than 12 mo. Plasma glucose clearance rate (KG) were significantly lower in both the transplanted fresh or cultured islet groups than in the normal controls; however, the cultured islets were not less effective than the fresh islets. The results of the present study indicate the feasibility of accumulation of large numbers of islets in the in vitro culture system without any loss of therapeutic efficiency when implanted in vivo. Further improvement of this in vitro culture system can thus be applied in islet preservation for islet transplantation.

Animals↗

PubMed1991

Improvement of glucose-primed intravenous glucose tolerance and correction of acute insulin decrement by glipizide in type II diabetes.

Improved glucose disposal after repeated intravenous (IV) glucose loads, known as the Staub effect, is absent in both type I and type II diabetes. Acute decrements of insulin secretion (AID) are observed following the early phase of insulin release on IV glucose stimulation in non-insulin-dependent diabetes mellitus (NIDDM). The AID cannot be corrected by acute infusions of glyburide or glipizide, or phentolamine, or by glycemic control after 2 weeks of intensive insulin treatments. Fifteen male subjects had 3 hourly successive IV glucose tolerance tests before and after 6 months of glipizide, at a final maintenance dose of 30 +/- 3 mg/d. Before treatment, AID, defined as the difference of the lowest of post IV glucose 7- or 10-minute samples from the preceding baseline insulin levels, was detected in the three loads: -6.4 +/- 1.9 microU/mL in the first, and then more consistently in the second and third loads, -11 +/- 2 microU/mL, and -17 +/- 9 microU/mL, respectively. There was a stepwise increase in insulin sums after each load. After glipizide therapy, the AIDS following all three IV glucose loads were no longer demonstrable; both insulin values, as well as insulin sums, were significantly elevated after all three glucose loads. While in the untreated state, the Staub effect was absent: serum glucose disappearances (K), corrected for glycosuria, were K1 = 0.52 +/- 0.02, K2 = 0.50 +/- 0.04, and K3 = 0.52 +/- 0.03.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗

PubMed1992

Correlation between residual beta-cell function and age at onset of spontaneous diabetes in Long Evans Tokushima lean rats.

We studied the natural course of disease in spontaneously diabetic rats, Long Evans Tokushima Lean (LETL) rats, to determine whether it showed similar pathogenetic heterogeneity to that of patients with insulin-dependent diabetes mellitus (IDDM) with regard to the relationships between age at onset, rapidity of disease progress, and degree of beta-cell function at the time of its manifestation. Type 1 diabetes developed in 35 rats (6.3%) between 40 and 140 days of age. Eight rats that became diabetic at age 69 days or less were more severely ketotic at the time of first detection of glycosuria and showed more rapid deterioration than seven rats that became diabetic later after birth (mean plasma 3-hydroxybutyrate levels, 4,707 +/- 1,215 pmol/L v 1,390 +/- 859 pmol/L; mean +/- SEM, P < .01). The mean plasma levels and pancreatic content of immunoreactive insulin (IRI) of the early onset rats, 47 +/- 13 pmol/L and 19 +/- 12 pmol/g tissue weight, were significantly lower (P < .01) than the corresponding values of the late-onset rats, 262 +/- 52 pmol/L and 348 +/- 87 pmol/g tissue weight, respectively. Both values were markedly lower than the mean values of 25 nondiabetic LETL rats, 976 +/- 122 pmol/L and 3,488 +/- 628 pmol/g tissue weight. Plasma immunoreactive glucagon (IRG) levels were significantly increased in the diabetic groups (early onset, 57 +/- 13 pmol/L; late-onset, 51 +/- 12 pmol/L; nondiabetic, 18 +/- 1 pmol/L; P < .01). These changes in pancreatic hormone levels of the early onset and late-onset rats were compatible with the histological features of their pancreatic islets.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1993

Insulin and satiety from feeding in pancreatic-normal and diabetic rats.

Insulin's role in food ingestion and satiety was investigated in streptozotocin-diabetic and pancreatic-normal rats. Markedly diabetic rats (60-65 mg/kg b.wt. streptozotocin with mean glycemia of 380 mg/dl) were observed for daily food/water intake and body weight changes and meal pattern in a standard operant chamber. Diabetic animals showed an immediate hypophagia (days 1-4) by decreasing meal size (MS). As animals lost weight, a significant hyperphagia appeared, accomplished by an elevation in MS. Treatment with insulin infused via osmotic minipump at a stable rate (6.0 U/24 h) reduced polyuria and glycemia, eliminated glycosuria, and restored weight gain. MS did not, however, return to baseline immediately. In a second experiment with milder diabetes (20-22 mg/rat streptozotocin, which produced glycemia ranging from 148 to 304 mg/dl), significant hyperphagia appeared, again attributable to an increase in MS. Minipumps infusing 2.4-4.0 U insulin/24 h reversed this hyperphagia. In pancreatic-normal rats, pumps infusing insulin at 1.2 or 2.4 U/24 h produced a modest hypophagia accomplished by a primary decrease in nocturnal intake (11% suppression in dark feeding). Subdiaphragmatically vagotomized rats showed an attenuation of this suppression (no significant effects on food or water intake produced by insulin infused). Insulin appears to participate in satiety by limiting MS, without significantly shortening latency to take the next meal.

Animals↗

PubMed1994

Food intake in diabetic rats: relationship to metabolic effects of insulin treatment.

Hyperphagic streptozotocin-diabetic rats were given week-long treatment with 0 (vehicle), 3, or 6 U/rat/day of regular insulin via a SC osmotic pump. Insulin reduced urinary glucose excretion and plasma glucose and increased body weight in a dose-related manner starting on the first day of treatment. Insulin treatment also increased carcass weight, carcass fat, and liver glycogen within 3 days. Food intake did not decrease until the fifth day of insulin treatment, and this change was unrelated to the amount of insulin administered. These results show that the effects of insulin on food intake and metabolism of diabetic rats can be dissociated with respect to both time course and dose of insulin. The findings indicate that hypoinsulinemia, glycosuria, body weight loss, and depletion of body fat and liver glycogen are symptoms of diabetes, not causes of diabetic hyperphagia.

Animals↗

PubMed1984

Subchronic oral toxicology of 4-fluoro-3-nitroaniline in the rat.

4-Fluoro-3-nitroaniline (4-F-3-NA), an intermediate used in the production of commercial hair dyes, was administered daily for 90 days via po intubation to Charles River CD rats at doses of 40, 120, or 360 mg/kg to determine its subchronic toxicology. All animals receiving 360 mg/kg died prior to termination of the study. The principal effect to rats of 4-F-3-NA exposure was alteration of the hematopoietic system characteristic of hemolytic anemia. Hematocrit, hemoglobin concentration, and erythrocyte count were decreased and reticulocytes increased in a dose-related pattern in both male and female animals. Histopathological change consistent with hemolytic anemia was observed in the bone marrow (erythroid hyperplasia), kidneys (deposition of biliverdin and pigment-laden macrophages in the tubules), liver (pigmented Kupffer cells), and spleen (increased hematopoiesis) in males and females. Heinz bodies and an increase in methemoglobinemia were not observed in this study. In the testes, aspermia and testicular degeneration were seen in isolated tubules, but these changes were significant only at the high dose. Additional pathologic changes noted at the high dose included colloid depletion and follicular cell hypertrophy of the thyroid gland, hypertrophy of the zone fasciculata in the adrenal glands, and lymphoid cell depletion in mesenteric lymph nodes. The calcification of the myocardium and coronary arteries was considered metastatic in nature, secondary to kidney damage. Serum ALT and BUN were elevated in males and AP was elevated in females from the high dose group. Glycosuria, bilirubinuria, and urobilinogenuria were also increased in both sexes at this dose.

Administration, Oral↗

PubMed1987

Comparative acute toxicity of chlorocitrate and fluorocitrate in dogs.

The high-dose effects of chlorocitrate [(-)-threo-chlorocitric acid] were compared in vivo to another halogenated citrate analog, and a well-known inhibitor of the tricarboxylic acid (TCA) cycle, fluorocitrate. The compounds were given iv to two dogs per sex per group, and a control group received an equimolar amount of citric acid. Chlorocitrate (100 mg/kg) showed TCA cycle inhibition as did fluorocitrate (8 mg/kg) in that both caused depletion of ATP and accumulation of citrate in the liver. Chlorocitrate was a significantly weaker inhibitor of citrate metabolism than fluorocitrate as evidenced by a substantially lower accumulation of serum citrate despite a much higher dose. Both halocitrates produced a similar diabetes-like syndrome (hyperglycemia, glycosuria) mediated by a significant hyperglucagonemia and slight hypoinsulinemia. Chlorocitrate was more potent in this effect and a much greater buildup of plasma lactate ensued (18- versus 3.7-fold increase), enough to explain lethality observed in earlier studies. In contrast, fluorocitrate produced a severe life-threatening hypocalcemia (-30%), and hypercalcuria was observed. This effect on calcium distribution was only minimal with chlorocitrate. Both halocitrates had a similar depressive effect on circulation as evidenced by hypothermia, bradycardia, and elongation of the QT-interval. These changes were considered to be the result of lactic acidosis and the ongoing ion imbalance since heart ATP levels were not depleted.

Adenosine Triphosphate↗

PubMed1990

Alteration of renal amino acid transport system in cadmium-intoxicated rats.

Effects of cadmium intoxication on renal transport systems for various amino acids were studied. Subcutaneous injections of CdCl2, at a dose of 2 mg Cd/kg.day for 2 weeks, resulted in polyuria, proteinuria, glycosuria, phosphaturia, and aminoaciduria, as observed in chronic cadmium-intoxicated humans and experimental animals. The nature of aminoaciduria was nonspecific, including iminoacid as well as almost all species of neutral, acidic, and basic amino acids. In renal cortical brush border membrane vesicles isolated from cadmium-intoxicated rats, Na(+)-dependent transport of L-proline, L-alanine, and L-lysine was markedly attenuated, whereas the amino acid transport in the basolateral membrane vesicle was not significantly affected. Similar results were obtained in the normal membrane vesicles directly exposed to inorganic cadmium. These results indicate that cadmium intoxication impairs various Na(+)-amino acid cotransport systems in the renal brush border membrane, which leads to panaminoaciduria.

Amino Acids↗

PubMed1987

Experimental diabetes in the rat: alterations in the vesical function.

Vesical function has been studied in vivo in alloxan-diabetic rats. Rhythmic contractions evoked as a micturition reflex by a controlled distension of the bladder were recorded in urethane-anesthetized animals. These rhythmic contractions are essentially induced by the parasympathetic and inhibited by the sympathetic outflow. The study has been performed on male Sprague-Dawley rats. They were treated at the age of two months with vehicle (control group) or alloxan (100 mg/kg s.c.). Such treatment caused hyperglycemia (greater than 250 mg/dl) and glycosuria in most of the animals. In control animals, analyzed between 5 and 8 months of age, the contractions evoked by vesical distension appeared at a threshold volume between 0.5 and 1 ml, and they had a regular rate. In a first series of experiments, diabetic animals 3 months after treatment showed the evoked response at an average threshold volume of about 1.7 ml. while in animals with 6 months of experimental diabetes the average threshold volume was about 3.2 ml. The rate of contractions in diabetic animals became more and more irregular as the duration of diabetes increased. These marked functional alterations were associated with the evidence of bladder enlargement. In a second series of experiments, bovine brain gangliosides (10 mg/kg i.p./day) or saline were given to diabetic rats between the 30th and the 90th day after alloxan. Ganglioside administration significantly reduced bladder enlargement and the threshold volume for micturition reflex and improved the rate of bladder contractions. It is suggested that alterations of the autonomic nervous system can be expressed as functional vesical dysfunction in experimental diabetes.

Animals↗

PubMed1989

Glucose tolerance during pregnancy in Asian women.

The present study was aimed at examining differences in gestational diabetes mellitus (GDM) between two ethnic populations (immigrant Asians and indigenous White Caucasians) residing in Leicester, U.K. The study was divided into two parts: to determine the prevalence of GDM and to determine the level at which glycaemia may impose a risk to the mother and the foetus. Of a total of 12,005 pregnancies (4561 Asian and 7444 White Caucasian), over a 3-year period, 314 (6.8%) Asian and 504 (6.7%) White Caucasian were given a 75-g oral glucose tolerance test (OGTT) at 28-32 weeks for indications of 'large for date' pregnancies, hydramnios, glycosuria, a history of previous abortions, stillbirths, congenital abnormalities or glucose intolerance, and family history of diabetes. Abnormal glucose tolerance (AGT) was taken as a 2-h venous plasma glucose greater than or equal to 7.8 mmol/l which reverted to normal when formally tested during the puerperium (WHO criteria, 1985). AGT was found in 1.38% Asian and 0.87% White Caucasian pregnancies (P less than 0.01). This was further divided into impaired glucose tolerance (IGT) (2-h value 7.8-11.1 mmol/l) and gestational diabetes mellitus (GDM) (2-h value greater than or equal to 11.1 mmol/l). IGT was found in 1.2% Asian and 0.84% White Caucasian pregnancies (P less than 0.01), and GDM in 0.18% and 0.02% respectively (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Antibodies to GAD in Japanese diabetic patients: a multicenter study.

We determined the prevalence of antibodies to glutamic acid decarboxylase (anti-GAD) in Japanese diabetic patients. Anti-GAD were detected by RIP Anti-GAD Hoechst, which is a new sensitive radioimmunoassay (RIA) kit using purified pig brain GAD as the antigen. One thousand nine hundred Japanese patients were collected by the Study Group for Antibodies to GAD. The prevalence of anti-GAD in the subjects of this study was: 35.4% (326/921) in all patients with IDDM, 50.3% (96/191) in patients with IDDM less than 1-year duration, 4.3% (29/680) in NIDDM, 37.9% (39/103) in slowly progressive IDDM, 10.5% (4/38) in gestational diabetes mellitus, 0% (0/27) in impaired glucose tolerance, 4.8% (6/124) in the school children with glycosuria, 2.1% (1/47) in the relatives of IDDM and 5.0% (1/20) in neurological diseases without diabetes. The prevalence in normal subjects was 2.2% (7/323). Anti-GAD are frequently detected by the RIA kit in patients with IDDM of short duration and this assay may be useful for population screening for IDDM and for better understanding of its pathogenesis.

Adolescent↗