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At least 1,063 records · Page 59Linked to original sources

PubMed1996

Vasoactive intestinal peptide and impotence in experimental diabetes mellitus.

OBJECTIVE: To determine whether a defect in vasoactive intestinal peptide (VIP)-mediated vasodilatation underlies diabetic impotence. MATERIALS AND METHODS: Rats treated with streptozotocin for 8 weeks developed diabetes, as shown by hyperglycaemia and glycosuria, and had significant impairment of sexual function, as determined by tests of sexual behavior. The VIP content of the penis and major pelvic ganglion, the VIP release by the penis in vitro and the responsiveness of the vasculature of the penis in vivo to intracavernous VIP injection were determined. RESULTS: In diabetic rats, the VIP content of the major pelvic ganglion and penis was markedly increased, while the acetylcholine content of the penis was normal. The amount of VIP released in vitro by high potassium concentration or veratridine was similar for penile tissue slices of normal and diabetic rats. Intracavernous injection of VIP induced erection in the control rats but not in diabetic rats, whereas intracavernous injection of the adenylate-cyclase activator forskolin produced erection in both control and diabetic rats. CONCLUSION: Because VIP induces vasodilatation by activating adenylate cyclase, and forskolin produced erection in the diabetic rats, the failure of VIP to produce erection in these rats is unlikely to be due to a defect in the second-messenger mechanism or in the properties of vascular smooth muscle. Thus, a defect at the level of the VIP receptor or of the associated G-protein possibly explains the failure of intracavernous VIP to produce erection in the diabetic rats. Hence, an abnormality in VIP is a component of sexual dysfunction in the diabetic rat and the defect is at the level of the VIP receptor or associated G-protein.

Acetylcholine↗

PubMed2002

Long-term caffeine consumption exacerbates renal failure in obese, diabetic, ZSF1 (fa-fa(cp)) rats.

BACKGROUND: Our preliminary studies indicate that chronic caffeine consumption has adverse renal effects in nephropathy associated with high blood pressure and insulin resistance. The purpose of this study was to investigate the effects of early (beginning at 8 weeks of age) and long-term (30 weeks) caffeine treatment (0.1% solution) on renal function and structure in obese, diabetic ZSF1 rats. METHODS: Metabolic and renal function measurements were performed at six-week intervals and in a subset of animals (N = 6 per group) heart rate (HR) and mean arterial blood pressure (MABP) were monitored by a radiotelemetric technique. At the end of the study acute, measurements of renal hemodynamics and excretory function were conducted in anesthetized animals. RESULTS: Caffeine produced a very mild increase (4 to 5%) of MABP and HR, but greatly augmented proteinuria (P < 0.001), reduced creatinine clearance (P < 0.05) and had a mixed effect on metabolic status in obese ZSF1 rats. Caffeine significantly reduced body weight, glycosuria, fasting glucose and insulin levels and improved glucose tolerance, had no effect on elevated plasma triglycerides levels and significantly increased plasma cholesterol level (P < 0.001). Acute measurements of renal function revealed increased renal vascular resistance (95.1 +/- 11 vs. 50.7 +/- 2.4 mm Hg/mL/min/g kidney, P < 0.01) and decreased inulin clearance (0.37 +/- 0.11 vs. 0.97 +/- 0.13 mL/min/g kidney, P < 0.002) in caffeine-treated versus control animals, respectively. Caffeine potentiated the development of more severe tubulointerstitial changes (P < 0.05) and increased focal glomerulosclerosis (14.7 +/- 1.7 vs. 6.5 +/- 0.9%, caffeine vs. control, P < 0.002). CONCLUSION: The present study provides the first evidence that caffeine (despite improving insulin sensitivity) exacerbates renal failure in obese, diabetic ZSF1 rats. Further mechanistic studies of adverse renal effects of caffeine in chronic renal failure associated with metabolic syndrome are warranted.

Animals↗

PubMed2002

Aristolochic acid-induced Fanconi's syndrome and nephropathy presenting as hypokalemic paralysis.

Hypokalemic paralysis rarely is seen as the presenting feature in patients with Fanconi's syndrome. We describe a 60-year-old man who presented with the inability to ambulate on awakening in the morning. The pertinent history revealed he had consumed Chinese herbs for leg edema for 5 months. Physical examination was unremarkable except for extracellular fluid volume depletion and total paralysis of both lower extremities. Laboratory investigation showed hypokalemia (1.8 mEq/L), hyperchloremic metabolic acidosis (Cl-, 111 mEq/L, and HCO3-, 14.0 mEq/L), hypophosphatemia (0.9 mg/dL) with hyperphosphaturia, hypouricemia (1.3 mg/dL) with hyperuricosuria, and glycosuria, consistent with Fanconi's syndrome. Mild renal insufficiency (serum creatinine, 1.7 mg/dL) also was noticed. Blood and urine screens for heavy metals, autoantibodies, and monoclonal gammopathy were negative. A renal biopsy specimen revealed typical findings of aristolochic acid-associated nephropathy. Aristolochic acids were detected in the consumed Chinese herbs. This case highlights that consumption of Chinese herbs containing aristolochic acids may cause Fanconi's syndrome and should be considered as a cause of hypokalemic paralysis.

Acute Kidney Injury↗

PubMed2006

A rare case of combined syndrome of inappropriate antidiuretic hormone secretion and Fanconi syndrome in an elderly woman.

An 83-year-old Japanese woman was admitted to our hospital with severe hyponatremia (sodium, 108 mEq/L [108 mmol/L]), hypokalemia, hypochloridemia, hypocalcemia, hypophosphatemia, and hypouricemia. Despite low plasma osmolarity (232 mOsm/kg [232 mmol/kg]), urine osmolarity (320 mOsm/kg) was greater than that of plasma, and she had increased urinary sodium excretion (88 mEq/L [88 mmol/L]) and an unsuppressed high plasma level of antidiuretic hormone (ADH; 5.5 pg/mL [5.1 pmol/L]). These findings indicated that she had syndrome of inappropriate ADH secretion (SIADH). In addition, she had a generalized reabsorption defect of the proximal tubules, including decreased tubular reabsorption of phosphate, increased fractional excretion of uric acid, glycosuria despite a normal blood glucose level, and panaminoaciduria. Thus, combined SIADH and Fanconi syndrome was diagnosed. The cause was thought to be the antidepressant paroxetine, which is a selective serotonin reuptake inhibitor (SSRI). Several of the abnormal values resolved within 1 week after discontinuation of this drug. Although the precise mechanism responsible was not elucidated, we report an extremely rare case of combined SIADH and Fanconi syndrome, probably caused by short-term SSRI therapy.

Aged↗

PubMed2000

Misleading results of ethanol analysis in urine specimens from rape victims suffering from diabetes.

We report appreciably high concentrations of ethanol (82 and 102 mg/dL) in specimens of urine collected from two victims of date rape. Both girls (aged 15 and 18 years) suffered from diabetes mellitus, but adamantly denied drinking any alcohol before or after the incident. The presence of glycosuria and high risk of fungal infections in female diabetics suggests that ethanol was produced in vitro by fermentation after voiding. Making a routine test for sugar in the urine and ensuring that the sampling tubes contain sufficient sodium or potassium fluoride to inhibit glycolysis are recommended practices. A specific marker for post-sampling synthesis of ethanol might also be used such as the 5HTOL/5HIAA ratio.

Journal Article↗

PubMed1975

Islet transplantation in experimental diabetes in the rat. III. Studies in allogeneic streptozotocin-treated rats.

Diabetes of various degrees of severity was induced experimentally in rats by different doses of streptozotocin. These animals served as recipients for isolated islets of Langerhans from allogeneic donors. The islets were transplanted to different regions in the organism by paravascular or intravascular injection. As in pancreatectomized rats, the endocrine effect of the islets was only transient and consisted of disappearance of glycosuria, normalization of blood glucose and amelioration of intravenous glucose tolerance tests. When the islets were injected intravascularly (lung, liver) the influence of the transplanted islets was observable over a longer period than after subcutaneous or another paravascular transplantation. As in pancreatectomized animals, the period of survival was markedly prolonged in rats which had received a transplant compared to those which had not. The islets responded to glucose stimulation in vivo with insulin secretion similar to that of control rats, while only a very slight elevation of the low basis levels in streptozotocin-treated rats was observed.

Animals↗

PubMed1995

Perioperative management of the diabetic patient.

Patients with diabetes mellitus are at a higher risk to undergo surgical intervention compared with the non-diabetic population, and additionally, they have an increased perioperative morbidity and mortality. Insulin deficiency and insulin resistance are aggravated by surgery and anaesthesia. The consequences of hyperglycemia are glycosuria, volume depletion from osmotic diuresis, impairment of wound healing and leucocyte function and exacerbation of ischemic brain damage. Depending on the extent of hypoinsulinemia, lipolysis and ketogenesis are enhanced which may result in metabolic acidosis with subsequent electrolyte disturbances. Protein catabolism is increased because of increased breakdown and decreased synthesis. Insulin administration reverts or overcomes most of these disturbances. The preoperative assessment includes the diagnoses of the long-term complications to judge the intraoperative risks. Long-acting insulins, such as ultralente of animal origin should be stopped preoperatively and substituted by protamine and lente insulins. In type-2-diabetic patients, long-acting sulfonylurea drugs such as chlorpropamide should be stopped and substituted by short-acting agents. Metformin must always be stopped. Type-2-diabetic patients with marked hyperglycemia under oral treatment should be switched to insulin before operation. The insulin requirements in diabetic patients during surgery vary from 0.25-0.40 U per gram glucose in normal weight patients, 0.4-0.8 U per gram glucose in case of obesity, liver disease, steroid therapy or sepsis, to 0.8-1.2 U per gram glucose in patients undergoing cardiopulmonary bypass surgery. Therefore, the appropriate dose has to be determined individually. The regimen nowadays preferred by most authors is based on variable rate insulin infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗

PubMed2006

[Development of body weight during antidiabetic treatment].

Antidiabetic treatment of persons with type I or 2 diabetes mellitus is usually accompanied by body-weight gain. This is because any improvement in metabolism is associated with a decrease in glycosuria: Long-persisting loss of calories via urine is decreased. Furthermore, insulin has an antilipolytic effect simulates lipogenesis and promotes fluid retention. Hypoglycemia always necessitates additional intake of carbohydrates and thus also favors weight gain. During antidiabetic treatment with metformin the increase in body weight is significantly less than during treatment with sulphonylurea compounds or insulin. For this reason metformin is the drug of choice in the antidiabetic treatment of overweight diabetics. It is also superior to all other drugs when given together with insulin. The best results of insulin treatment with regard to weight control are obtained with basal insulin combined with metformin rather than insulin alone, prandial insulin substitution or intensified insulin treatment. If the aim is weight reduction, the pharmacokinetics of short-acting insulin analogs makes adaptation of insulin dose to reduced food intake easier than normal insulin. More attention than has previously been the case should be paid from the start to measures that prevent weight gain when planning antidiabetic treatment: prevention of weight gain is easier to achieve than weight reduction.

Diabetes Mellitus, Type 2↗

PubMed1988

Enhanced apomorphine-induced hypothermia in alloxan-treated rats.

Previous studies have indicated that drug-induced experimental diabetes is associated with increased receptor binding in the rat brain. The purpose of this study was to determine whether the dopamine receptor agonist apomorphine (APO) might produce an accentuated hypothermic response in rats rendered diabetic by alloxan (ALX) treatment. In a previous study, however, the only controls used were ALX-treated rats that failed to develop glycosuria. Therefore, in this study, APO (0.5 mg/kg IP) was administered to ALX-diabetic and non-diabetic as well as saline-treated control rats to ascertain whether the APO responsiveness of ALX-non-diabetic rats was comparable to that of saline control animals. ALX-diabetic rats experienced significantly greater hypothermic response to APO than did the saline control animals. Although ALX-non-diabetic rats were similar to the saline control animals in body weight and blood glucose levels, they too were hyperresponsive to APO. These findings indicate that pancreatic injury from ALX, while not always sufficiently severe to produce overt diabetes, does appear to induce an hyperresponsiveness to APO-induced hypothermia in a manner similar to that observed in severely diabetic animals.

Alloxan↗

PubMed1983

Hyperosmolar non-ketotic diabetic coma in the nonhuman primate: a first report.

Diabetes mellitus was diagnosed in an aged bonnet macaque (Macaca radiata). Six months later the monkey was found comatose. Laboratory findings of extreme hyperglycemia, hyperosmolality, and glycosuria without ketonuria were consistent with a diagnosis of hyperosmolar, non-ketotic diabetic coma (NKC). Further laboratory studies disclosed very low levels of immunoreactive insulin and depressed free fatty acid values. Growth hormone and cortisol levels were within normal limits.

Animals↗

PubMed1981

Renal tubular function and urinary acidification capacity in early juvenile diabetes.

Renal elimination of uric acid, calcium, phosphorus, sodium, potassium, chloride and magnesium and urinary acidification capacity were determined in ten insulin-dependent diabetics and in ten matched control subjects. The diabetics showed excessive excretion of uric acid, sodium, potassium, chloride and ammonia. Sodium, chloride and ammonia excretion fractions was also increased with respect to controls. The enhanced excretion of these substances in diabetics failed to relate to glomerular filtration rate, glycosuria or insulin requirements. These findings might be explained on the basis of glomerular filtration rate elevation, tubular response to this increment, and the underlying metabolic disturbances of diabetes.

Adolescent↗

PubMed1995

Protective effect of gamma-hydroxybutyrate and nicotinamide on low-dose streptozotocin-induced diabetes in mice.

The purpose of this study was to investigate the effect of a treatment by gamma-hydroxybutyrate (GHB) and nicotinamide (NA) on low-dose streptozotocin (STZ)-induced diabetes in mice. Mean plasma glucose level was significantly elevated in mice given STZ by day 12 after the first STZ injection compared to controls (15.0 +/- 4.7 vs 8.0 +/- 1.6 mmol/l, p < 0.001) and 100% of the animals were severely diabetic by day 18. Plasma glucose levels remained in the normal range and no diabetic values were found in mice treated with combined treatment by GHB and NA for 25 days. However, hyperglycemia and glycosuria appeared within one week after discontinuation of the treatment. Treatment by either GHB or NA alone had only a slight and transient effect in preventing hyperglycemia. In vitro experiment on isolated pancreatic islets demonstrated that STZ-induced loss of insulin response to glucose was also counteracted by incubation with GHB and NA (Peak insulin response to 16.4 mM glucose: 0.69 +/- 0.31 vs 3.03 +/- 0.67 microU/islet/min), but not by GHB or NA alone. These results indicate that GHB and NA have complementary effects in preventing STZ-induced beta cell damage both in vivo and in vitro. This should be taken into account for future preventive strategies in human insulin-dependent diabetes mellitus.

Animals↗

PubMed1980

Streptozotocin-induced liver damage in mice.

Diabetes incidence and liver damage was studied and identified in C3H-s mice 21 days after Streptozotocin (SZ) administration (250 mg/kg/i.v.) at 04 hs (4 a.m.) and 16 hs (4 p.m.). Metabolic disturbances were assessed by daily control of glycosuria and serum glucose determined at the end of the experiment. Liver damage was controlled by light and electron microscopy. Both effects showed a circadian variation, with significant greatest values in the 16-h-injected group. Liver damage appeared whether the animals became diabetic or not, consisting in degranulation of the rough-surfaced endoplasmic reticulum, mitochondrial swelling with loss of cristae and edema of the ground substance, with flocculent amorphous precipitate. In some hepatocytes, a dilated cisternae of the endoplasmic reticulum was seen. It was concluded that: a) beta-cell and hepatocytes have a synchronic circadian sensitivity to SZ; b) liver damage was present whether the animals became diabetic or not, suggesting the presence of a different threshold for SZ effect in hepatocytes. These results might be taken into account when planning SZ use, either for experimental or clinical purposes.

Animals↗

PubMed1979

Reduction to normal of plasma glucose in juvenile diabetes by subcutaneous administration of insulin with a portable infusion pump.

To improve plasma glucose control, we administered insulin via the subcutaneous route in seven ambulatory patients with juvenile diabetes (12 to 17 years of age), using a portable infusion pump at a basal rate with pulse-dose increments before meals. After two to four days, the mean plasma glucose (+/- 1 S.E.) of 94 +/- 5 mg per deciliter was markedly lower than when insulin was given by conventional methods in the patients' usual dose (243 +/- 28, P less than 0.01) or in a total dose equivalent to that administered with the pump (150 +/- 15, P less than 0.01). Maximal fluctuations in plasma glucose were also 50 to 150 mg per deciliter below those observed with conventional treatment (P less than 0.001). Glycosuria was eliminated in six of seven patients during pump treatment. None of the subjects had hypoglycemia. These results demonstrate that plasma glucose can be lowered to normal in ambulatory patients with brittle juvenile diabetes using a portable, subcutaneous insulin infusion system for two to four days. The feasibility and value of the long-term application of this technic need exploration.

Adolescent↗

PubMed1981

Effects of cysteamine therapy in nephropathic cystinosis.

We studied the effects of cysteamine in five children with nephropathic cystinosis who were treated for up to 30 months. Cysteamine caused a decline in leukocyte cystine levels to the range seen in clinically unaffected heterozygotes; both plasma and urinary cystine diminished by more than half. Therapy had no effect on progressively declining creatinine clearance in three patients, but improvement occurred in the other two. Phosphaturia, glycosuria, aminociduria, and organic aciduria did not improve in any of the patients. Both blood lactate and the lactate pyruvate ratio were diminished. Growth velocity, which was abnormal in four of the five children, did not improve. No major side effects were noted. Therapy with cysteamine caused a consistent, dose-related decline in levels of cystine in leukocytes and in extracellular fluid, caused no improvement so far in renal tubular function or growth velocity, and improved creatinine clearance in some patients.

Amino Acids↗

PubMed2003

High blood glucose and osmolality, but not high urinary glucose and osmolality, affect neuronal nitric oxide synthase expression in diabetic rat kidney.

We recently demonstrated that neuronal nitric oxide synthase (nNOS) messenger RNA (mRNA) is markedly increased in the kidneys of diabetic rats and water-deprived rats. It can be inferred that high plasma glucose and osmolality and high renal tubular glucose and osmolality are somehow involving in renal NOS synthesis in diabetic rats. Phlorizin, a competitive inhibitor of glucose transport in the proximal tubule, causes renal glycosuria in nondiabetic rats and reverses hyperglycemia in diabetic rats. To further investigate whether high plasma glucose and osmolality or high renal tubular glucose and osmolality influence renal NOS synthesis in diabetic rats, we measured nNOS mRNA levels in phlorizin-treated normal and diabetic rats. Neuronal NOS mRNA expression in the kidneys was not significantly different between normal rats and phlorizin-treated normal rats with high urinary glucose and osmolality. The phlorizin-treated diabetic rats showed a significant decrease in the ratio of nNOS to beta-actin mRNA compared with diabetic rats. On linear-regression analysis, plasma glucose was strongly positively correlated with nNOS mRNA expression in the cortex, outer medulla, and inner medulla (r(2) =.378, r(2) =.680, and r(2) =.445, respectively) of rat kidneys. Neither urine glucose concentration nor urine osmolality was correlated with nNOS mRNA expression in rat kidneys. In conclusion, our results indicate that nNOS mRNA expression in the kidneys of diabetic rats is directly affected by high blood glucose/osmolality but not by high urinary glucose or osmolality.

Actins↗

PubMed1987

Treatment of type 1 diabetes mellitus in non-obese diabetic mice by transplantation of allogeneic bone marrow and pancreatic tissue.

Non-obese diabetic (NOD) mice provide a model for type 1 diabetes mellitus. We previously showed that allogeneic bone marrow transplantation (ABMT) can prevent and treat insulitis and overt diabetes in NOD mice. However, ABMT alone could not be used to treat overt diabetes in NOD mice whose islets had been completely destroyed. To provide insulin-producing cells, pancreatic tissue from newborn mice was grafted under the renal capsules in combination with ABMT. The aims of concomitant ABMT are as follows. (i) It induces immunological tolerance to the donor-type major histocompatibility complex determinants and permits the host to accept subsequent pancreatic allografts from the bone marrow donor. (ii) ABMT replaces abnormal stem cells with normal stem cells. After transplantation of bone marrow plus newborn pancreas, NOD mice showed reduction of the glycosuria and a normal response in the glucose-tolerance test. Immunohistological study revealed the presence of clustered insulin-containing beta cells in the grafted pancreatic transplants. ABMT may become a viable treatment of established type 1 diabetes mellitus in humans.

Animals↗

PubMed1997

Phenotypic alterations in insulin-deficient mutant mice.

Two mouse insulin genes, Ins1 and Ins2, were disrupted and lacZ was inserted at the Ins2 locus by gene targeting. Double nullizygous insulin-deficient pups were growth-retarded. They did not show any glycosuria at birth but soon after suckling developed diabetes mellitus with ketoacidosis and liver steatosis and died within 48 h. Interestingly, insulin deficiency did not preclude pancreas organogenesis and the appearance of the various cell types of the endocrine pancreas. The presence of lacZ expressing beta cells and glucagon-positive alpha cells was demonstrated by cytochemistry and immunocytochemistry. Reverse transcription-coupled PCR analysis showed that somatostatin and pancreatic polypeptide mRNAs were present, although at reduced levels, accounting for the presence also of delta and pancreatic polypeptide cells, respectively. Morphometric analysis revealed enlarged islets of Langherans in the pancreas from insulin-deficient pups, suggesting that insulin might function as a negative regulator of islet cell growth. Whether insulin controls the growth of specific islet cell types and the molecular basis for this action remain to be elucidated.

Animals↗