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PubMed2000

Transgenic reexpression of GLUT1 or GLUT2 in pancreatic beta cells rescues GLUT2-null mice from early death and restores normal glucose-stimulated insulin secretion.

GLUT2-null mice are hyperglycemic, hypoinsulinemic, hyperglucagonemic, and glycosuric and die within the first 3 weeks of life. Their endocrine pancreas shows a loss of first phase glucose-stimulated insulin secretion (GSIS) and inverse alpha to beta cell ratio. Here we show that reexpression by transgenesis of either GLUT1 or GLUT2 in the pancreatic beta cells of these mice allowed mouse survival and breeding. The rescued mice had normal-fed glycemia but fasted hypoglycemia, glycosuria, and an elevated glucagon to insulin ratio. Glucose tolerance was, however, normal. In vivo, insulin secretion assessed following hyperglycemic clamps was normal. In vitro, islet perifusion studies revealed that first phase of insulin secretion was restored as well by GLUT1 or GLUT2, and this was accompanied by normalization of the glucose utilization rate. The ratio of pancreatic insulin to glucagon and volume densities of alpha to beta cells were, however, not corrected. These data demonstrate that 1) reexpression of GLUT1 or GLUT2 in beta cells is sufficient to rescue GLUT2-null mice from lethality, 2) GLUT1 as well as GLUT2 can restore normal GSIS, 3) restoration of GSIS does not correct the abnormal composition of the endocrine pancreas. Thus, normal GSIS does not depend on transporter affinity but on the rate of uptake at stimulatory glucose concentrations.

Animals↗

PubMed1998

Effect of breakfast fat content on glucose tolerance and risk factors of atherosclerosis and thrombosis.

Twenty-four middle-aged healthy men were given a low-fat high-carbohydrate (5.5 g fat; L), or a moderately-fatty, (25.7 g fat; M) breakfast of similar energy contents for 28 d. Other meals were under less control. An oral glucose tolerance test (OGTT) was given at 09.00 hours on day 1 before treatment allocation and at 13.30 hours on day 29. There were no significant treatment differences in fasting serum values, either on day 1 or at the termination of treatments on day 29. The following was observed on day 29: (1) the M breakfast led to higher OGTT C-peptide responses and higher areas under the curves (AUC) of OGTT serum glucose and insulin responses compared with the OGTT responses to the L breakfast (P < 0.05); (2) treatment M failed to prevent OGTT glycosuria, eliminated with treatment L; (3) serum non-esterified fatty acid (NEFA) AUC was 59% lower with treatment L than with treatment M, between 09.00 and 13.20 hours (P < 0.0001), and lower with treatment L than with treatment M during the OGTT (P = 0.005); (4) serum triacylglycerol (TAG) concentrations were similar for both treatments, especially during the morning, but their origins were different during the afternoon OGTT when the Svedberg flotation unit 20-400 lipid fraction was higher with treatment L than with treatment M (P = 0.016); plasma apolipoprotein B-48 level with treatment M was not significantly greater than that with treatment L (P = 0.086); (5) plasma tissue plasminogen-activator activity increased after breakfast with treatment L (P = 0.0008), but not with treatment M (P = 0.80). Waist:hip circumference was positively correlated with serum insulin and glucose AUC and with fasting LDL-cholesterol. Waist:hip circumference and serum TAG and insulin AUC were correlated with factors of thrombus formation; and the OGTT NEFA and glucose AUC were correlated. A small difference in fat intake at breakfast has a large influence on circulating diurnal NEFA concentration, which it is concluded influences adversely glucose tolerance up to 6 h later.

Adult↗

PubMed1979

The dietary management of diabetes in adults.

The ultimate object of all types of dietary management before the introduction of insulin was to prevent emaciation and death: the consequences of metabolic derangements due to lack of insulin. Now, while dietary therapy continues to be important in minimizing the requirement for endogenous insulin or in balancing administered insulin, the major objects are changing to prevention of large vessel and microvascular disease. The next decade will probably see a more widespread introduction of diets containing a lower proportion of energy derived from fat. The increased carbohydrate intake will almost inevitably result in increased dietary fibre intake. Whether David Jenkins' Lente carbohydrate foods (those containing viscous unabsorbable polysaccharides) will prove to be of lasting value is not yet known. Since galactomannans occur in legumes perhaps we should consider the possibility of diets containing large proportions of legumes: a twentieth century 'Legume cure'? If this should prove of value it would not have excited ancient Indian physicians who wrote (in the Caraka-Samita) of their use of legumes in the treatment of glycosuria, at least as early as the first century AD, before Aretaeus had applied the term diabetes.

Adult↗

PubMed1976

Combating diabetic ketoacidosis and other hyperglycemic-ketoacidotic syndromes.

Diabetic ketoacidosis is an acute medical emergency that requires immediate diagnosis and treatment. Diagnosis may be established rapidly by measurement of urinary glucose and ketones, arterial blood pH and blood gases, and serum ketones. Rapid infusion of large volumes of fluids and electrolytes, together with continuous infusion of low doses of insulin, provides effective restoration of fluid and electrolyte balance and correction of metabolic derangements. Hyperosmolar nonketotic coma is characterized by marked hyperglycemia in the absence of ketoacidosis and occurs usually in patients with mild adult-onset diabetes. Symptoms develop more slowly than in diabetic ketoacidosis. Treatment is the same for both conditions. In alcoholic ketoacidosis, hyperketonemia is present without hyperglycemia. The syndrome differs from diabetic ketoacidosis in that blood glucose levels are lower and glycosuria is absent. Treatment consists of intravenous administration of dextrose in water and, if necessary, of sodium bicarbonate. Insulin administration usually is not necessary.

Alcoholism↗

PubMed2004

Tubulopathy consecutive to tenofovir-containing antiretroviral therapy in two patients infected with human immunodeficiency virus-1.

Tenofovir disopril fumarate, a new nucleotide analogue against human immunodeficiency virus-1 (HIV-1), can induce hypophosphataemia, the mechanism of which is unclear. Moreover, a renal tubulopathy can occur in long-term treated patients, as observed in 2 HIV-1-infected patients after 12 months of tenofovir therapy, with polyuria-polydipsia, proteinuria, glycosuria and amino-aciduria, which resolved after discontinuation of tenofovir. The risk of renal tubulopathy symptoms in patients on long-term tenofovir therapy should be noted.

Adenine↗

PubMed2006

Preliminary data on monosymptomatic nocturnal enuresis in children and adolescents with type 1 diabetes.

OBJECTIVE: To evaluate the prevalence of monosymptomatic nocturnal enuresis (MNE) in a group of children and adolescents prior to the onset of type 1 diabetes (Dt1). MATERIAL AND METHODS: We considered 88 patients with Dt1 with a mean age of 15.2 years over a period of 3 years. All patients were investigated by means of a questionnaire about the occurrence of MNE prior to the onset of Dt1. Each patient had normal urinalysis results, with no glycosuria, a normal urinary flow rate and no day-time symptoms such as urge incontinence or urgency. RESULTS: We found that 24/88 patients (27.2%) were bedwetters before the onset of Dt1. After beginning insulin treatment, 7/24 bedwetters (29.2%) kept presenting MNE. In total, 7 of the initial 88 patients (7.9%) displayed persistent features of MNE. CONCLUSIONS: The occurrence of MNE may overlap with symptoms of Dt1 but requires specific medical attention as a separate entity due to its possible persistence even when Dt1 has been controlled by insulin treatment.

Adolescent↗

PubMed2005

Chemometric analysis of biofluids following toxicant induced hepatotoxicity: a metabonomic approach to distinguish the effects of 1-naphthylisothiocyanate from its products.

Metabonomics using high-resolution 1H-NMR spectroscopy of biofluids and pattern recognition is highly successful at distinguishing both organ- and sub-organ-specific toxicity. In the current study, this technique was investigated to distinguish the different biological effects caused by 1-naphthylisothiocyanate (ANIT)-induced hepatotoxicity in the rat from that induced by exposure to 1-naphthylisocyanate (NI) and 1-naphthylamine (NA), two products of the metabolism of ANIT. While all three toxicants produced perturbations in similar urinary metabolites, principal components analysis of the temporal progression identified that the rapid initial glycosuria associated with ANIT toxicity was also present with NI but not NA dosing. However, longer-term perturbations in the urinary excretion of succinate, lactate and acetate were common to all three toxicants. The metabolic effects of the three compounds were also followed in blood plasma and liver tissue. Of the three toxicants, the most marked perturbations were induced by ANIT exposure, then NI, thereby indicating the effects of ANIT, NI and NA toxicity were distinct, with ANIT being the most, and NA the least, toxic of the three compounds. This indicates that metabonomics may be useful for following severity and mechanisms of toxicity in a series of related compounds during drug development.

1-Naphthylamine↗

PubMed1986

A crossover trial of high and low sucrose-carbohydrate diets in type II diabetics with hypertriglyceridemia.

Earlier work shows that hyperlipemic type II diabetics tolerate wide ranges of sucrose and carbohydrate intake without effects on glycemic control, but a rise of fasting serum triglycerides sometimes occurs. To address further the issue of individual susceptibility to carbohydrate, the current study was designed to use each patient as his own control when given diets widely varying in sucrose content. After a stabilization period in the hospital on a normal sucrose content diet, each subject was given either a very low sucrose (less than 3 gm/day)-low carbohydrate (38 +/- 2%) diet or a high sucrose (220 gm)-high carbohydrate (63 +/- 3%) diet for 4 weeks. On a separate admission the opposite diet was assessed, again after an initial normal sucrose content diet. No consistent differences occurred in serum glucose levels or in 24-hr urinary glycosuria. High sucrose-carbohydrate intake raised fasting hypertriglyceridemia after 2 weeks but less thereafter. Severe sucrose-carbohydrate restriction did not significantly decrease fasting serum triglycerides; postprandial triglycerides changed in a trend opposite to fasting levels. No differences occurred in fasting serum insulin or serum cholesterol levels, but postprandial insulin levels were higher in high sucrose-carbohydrate diets. A diet with low sucrose and low total carbohydrate appears to offer no improvement in glycemic control over at least 70-fold higher dietary sucrose levels. However, high sucrose and carbohydrate diets increase fasting triglyceride levels in hypertriglyceridemic type II diabetics.

Adult↗

PubMed1994

Vitamin C: an aldose reductase inhibitor that normalizes erythrocyte sorbitol in insulin-dependent diabetes mellitus.

OBJECTIVE: Diabetic hyperglycemia promotes sorbitol production from glucose via aldose reductase. Since the intracellular accumulation of sorbitol, or its sequelae, are postulated to contribute to the progression of chronic diabetic complications, aldose reductase inhibitors (ARI) offer therapeutic promise. Others have shown that vitamin C at pharmacologic doses decreases erythrocyte (RBC) sorbitol. We examined whether smaller, physiologic doses of vitamin C were also effective in individuals with insulin-dependent diabetes mellitus (IDDM) and whether vitamin C was an ARI in vitro. METHODS: Vitamin C supplements (100 or 600 mg) were taken daily for 58 days by young adults with IDDM and nondiabetic adults in an otherwise free-living design. Diabetic control was monitored by fasting plasma glucose, glycosylated hemoglobin, and glycosuria and was moderate to poor throughout the study. RBC sorbitol was measured at baseline and again at 30 and 58 days. Three-day dietary records and 24-hour urine collections were performed for each sampling day. RESULTS: RBC sorbitol levels were significantly elevated in IDDMs, on average doubled, despite their more than adequate dietary intakes of vitamin C and normal plasma concentrations. Vitamin C supplementation at either dose normalized the RBC sorbitol in IDDMs within 30 days. This correction of sorbitol accumulation was independent of changes in diabetic control. Furthermore, our in vitro studies show that ascorbic acid inhibited aldose reductase activity. CONCLUSIONS: Vitamin C supplementation is effective in reducing sorbitol accumulation in the erythrocytes of diabetics. Given its tissue distribution and low toxicity, we suggest a superiority for vitamin C over pharmaceutic ARIs.

Adult↗

PubMed1996

Vitamin and mineral deficiencies which may predispose to glucose intolerance of pregnancy.

There is an increased requirement for nutrients in normal pregnancy, not only due to increased demand, but also increased loss. There is also an increased insulin-resistant state during pregnancy mediated by the placental anti-insulin hormones estrogen, progesterone, human somatomammotropin; the pituitary hormone prolactin; and the adrenal hormone, cortisol. If the maternal pancreas cannot increase production of insulin of sustain normoglycemia despite these anti-insulin hormones, gestational diabetes occurs. Gestational diabetes is associated with excessive nutrient losses due to glycosuria. Specific nutrient deficiencies of chromium, magnesium, potassium and pyridoxine may potentiate the tendency towards hyperglycemia in gestational diabetic women because each of these four deficiencies causes impairment of pancreatic insulin production. This review describes the pathophysiology of the hyperglycemia and the nutrient loss in gestational diabetes and further postulates the mechanism whereby vitamin/mineral supplementation may be useful to prevent or ameliorate pregnancy-related glucose intolerance.

Chromium↗

PubMed1978

The nephron in transport of sodium, amino acids, and glucose.

The ability of the kidney to maintain overall control of sodium and fluid balance appears greater than the sum of its parts, yet microperfusion and dissection studies that have assigned particular transport processes to individual segments of the nephron are helping to clarify a number of clinical states. Among those that can be so localized are certain congenital disorders accompanied by glycosuria and aminoaciduria.

Adenosine Triphosphate↗

PubMed1997

Requirement of Fas for the development of autoimmune diabetes in nonobese diabetic mice.

Insulin-dependent diabetes mellitus (IDDM) is assumed to be a T cell-mediated autoimmune disease. To investigate the role of Fas-mediated cytotoxicity in pancreatic beta cell destruction, we established nonobese diabetic (NOD)-lymphoproliferation (lpr)/lpr mice lacking Fas. Out of three genotypes, female NOD-+/+ and NOD-+/lpr developed spontaneous diabetes by the age of 10 mo with the incidence of 68 and 62%, respectively. In contrast, NOD-lpr/lpr did not develop diabetes or insulitis. To further explore the role of Fas, adoptive transfer experiments were performed. When splenocytes were transferred from diabetic NOD, male NOD-+/+ and NOD-+/lpr developed diabetes with the incidence of 89 and 83%, respectively, whereas NOD-lpr/lpr did not show glycosuria by 12 wk after transfer. Severe mononuclear cell infiltration was revealed in islets of NOD-+/+ and NOD-+/lpr, whereas islet morphology remained intact in NOD-lpr/lpr. These results suggest that Fas-mediated cytotoxicity is required to initiate beta cell autoimmunity in NOD mice. Fas-Fas ligand system might be critical for autoimmune beta cell destruction leading to IDDM.

Adoptive Transfer↗

PubMed2003

Polychromatic LED therapy in burn healing of non-diabetic and diabetic rats.

OBJECTIVE: We determined the effect of polychromatic light-emitting diodes (LED) in burn healing of non-diabetic and streptozotocin-induced diabetic rats. BACKGROUND DATA: LEDs were used as the light source for phototherapy. MATERIALS AND METHODS: The polychromatic LED is a cluster of 25 diodes emitting photons at wavelengths of 510-543, 594-599, 626-639, 640-670, and 842-879 nm with 272-mW output power. Age-matched, male Sprague-Dawley rats (n = 30) were used. Streptozotocin (70 mg/kg) was used for diabetes induction. Rat weight, hyperglycemia, and glycosuria were monitored for the first 3 days and weekly thereafter. Rats were anesthetized and shaved after 1 week of diabetes. Burn areas of 1.5 +/-.03 cm2 were created using a metal rod pre-heated up to 600 degrees C that was applied for 2 sec. Diabetic and non-diabetic rats were randomized into the following treatment groups: control, 5, 10, 20, and 30 J/cm2. Light treatment commenced after burn infliction and was repeated three times per week. Burn areas were measured daily. RESULTS: Burn healing was impaired significantly during diabetes by -46.17%. Polychromatic LED treatment using 5, 10, 20, and 30 J/cm2 incident doses influenced healing by 6.85%, 4.93%, -4.18%, and -5.42% in the non-diabetic rats; and 73.87%, 76.77%, 60.92%, and 48.77% in the diabetic rats, relative to their controls, respectively. CONCLUSION: The effect of polychromatic LED in non-diabetic rats was insignificant; however, it simulated the trend of stimulation and inhibition seen using low-level lasers. Significant stimulation observed in the diabetic rats demonstrated the usefulness of polychromatic LED in diabetic burn healing.

Animals↗

PubMed2001

Effects of plasmid DNA injection on cyclophosphamide-accelerated diabetes in NOD mice.

Type 1 diabetes results in most cases from the destruction of insulin-secreting beta cells by the immune system. Several immunization methods based on administration of autoantigenic polypeptides such as insulin and glutamic acid decarboxylase (GAD) have been used to prevent autoimmune diabetes in the non-obese diabetic (NOD) mouse. In the work presented here, a gene-based approach was taken for a similar purpose. A plasmid carrying different cDNAs was used to investigate the effects of injecting naked DNA on cyclophosphamide-accelerated diabetes in female NOD mice. Four-week-old animals received intramuscular injections of plasmid DNA encoding either intracellular GAD, a secreted form of GAD, or a secreted form of a soft coral luciferase. Monitoring of glycosuria and hyperglycemia indicated that injection of plasmid DNA encoding secreted GAD and secreted luciferase could prevent and delay diabetes, respectively. In contrast, injection of DNA encoding intracellular GAD did not suppress the disease significantly. Analysis of anti-GAD IgG(1) antibody titers in animal sera indicated that diabetes prevention after injection of GAD-encoding DNA was possibly associated with increased Th2-type activity. These results suggest that cellular localization of GAD is a factor to consider in the design of GAD-based genetic vaccines for the prevention of autoimmune diabetes.

Animals↗

PubMed2006

Diabetic ketoacidosis in an undiagnosed diabetic precipitated by high altitude pulmonary edema.

A unique case of HAPE precipitating diabetic ketoacidosis in a previously undiagnosed Type 2 diabetic is reported. A 39-year-old male, previously well, was admitted at a hospital situated at a height of 3500 m with complaints of increasing breathlessness on effort, cough, and fever of short duration, 5 days after high altitude reascent. Examination at admission revealed a febrile (38 degrees C) patient with tachycardia (104/min), SaO2 was 82% (on supplemental oxygen), chest examination revealed bilateral crackles in all lung fields, and chest radiograph demonstrated bilateral fluffy heterogeneous opacities in all zones. He was diagnosed as suffering from high altitude pulmonary edema. The patient did not show adequate improvement despite conventional treatment for HAPE with supplemental oxygen and rest. Investigations revealed leucocytosis, and urinalysis revealed glycosuria and ketonuria. Subsequent arterial blood gas analysis revealed that acidemia and serum glucose levels were raised. He was thereafter managed as for HAPE and DKA and recovered in 2 weeks. The patient has been on regular follow-up with satisfactory glycemic control with oral hypoglycemic agents.

Acute Disease↗

PubMed1984

Fanconi's syndrome associated with carburetor fluid intoxication.

A patient who ingested carburetor fluid developed methanol intoxication followed by hypouricemia, hypophosphatemia, glycosuria, and hyperchloremic metabolic acidosis. Renal clearances of phosphate, uric acid, glucose, and bicarbonate were found to be elevated indicating the presence of Fanconi's syndrome. The authors postulate that the Fanconi's syndrome observed in our patient was the result of the organic solvents present in the mixture.

Acidosis↗

PubMed2004

Effect of dexamethasone on perioperative renal function impairment during cardiac surgery with cardiopulmonary bypass.

BACKGROUND: In cardiac surgery with cardiopulmonary bypass (CPB), corticosteroids are administered to attenuate the physiological changes caused by the systemic inflammatory response. The effects of corticosteroids on CPB-associated renal damage have not been documented. The purpose of this study was to evaluate the effects of dexamethasone on perioperative renal dysfunction in patients undergoing cardiac surgery with CPB. METHODS: Renal damage was prospectively studied in 20 patients without concomitant morbidity undergoing coronary artery surgery with CPB. Patients were randomized in a double-blind fashion to receive dexamethasone or placebo. Markers of glomerular function (creatinine clearance) and damage (microalbuminuria), and markers of tubular function (fractional excretion of sodium and free water clearance) and damage (N-acetyl-beta-D glucosaminidase (NAG)) were evaluated in addition to plasma and urinary glucose levels. Plasma and urinary specimens were obtained at the following time periods: (1) baseline, during the 12 h before surgery; (2) skin incision before heparinization; (3) from heparinization until the end of CPB; (4) during the 2 h following weaning from CPB; (5) in the intensive care unit from 2 to 6 h after weaning of CBP; (6) and from 36 to 60 h after weaning of CPB. RESULTS: CPB was associated with an increase in markers in the placebo group, which returned to baseline during the second postoperative day, demonstrating a transient impairment of glomerular and tubular renal function. Similar patterns were observed in patients treated with dexamethasone. While postoperative glycosuria was significantly higher in the dexamethasone-treated group, no other differences between groups were observed. CONCLUSION: Dexamethasone administration before CPB has no protective effect on perioperative renal dysfunction in low-risk cardiac surgical patients.

Aged↗

PubMed2000

The quality of risk factor screening during antenatal consultations in Niger.

A decade after the first International Conference on Safe Motherhood, maternal mortality remains very high in most West African countries, even in capital cities. The detection of high risk pregnancies, known as the risk approach, during antenatal consultations has been the basis of most maternal and child health programmes over the last decade. The effectiveness of antenatal care as a tool to prevent or predict obstetric complications is being questioned more and more. In addition to the scarcity of reliable data about the predictivity of most risk factors, the quality of the screening must be questioned. The goal of this study was to assess the frequency of risk factors among a sample of pregnant women attending antenatal care in Niger and to assess the quality of the screening of those risk factors. Overall, 330 pregnant women were enrolled in the study. Each woman was examined twice: the first time by a midwife, the second time by one of the authors but without knowledge of the results of the first consultation. Fifty-five percent of pregnant women had at least one risk factor, 31% had more than one. Ninety-one percent of the risk factors were detected at interview. The following risk factors were not systematically searched for by midwives: height (48.5%), blood pressure (43.6%), glycosuria (40.6%), vaginal bleeding (38.2%), oedema (37.3%), parity (17%), age (16%), previous caesarean section (15.2%), previous stillbirth (15.2%) and previous miscarriages (14.8%). This study has shown that, in Niger, the quality of screening for risk factors during antenatal consultation is poor. In the urban settings where this study took place, lack of personnel, lack of equipment, lack of time and poor compliance by women cannot be made responsible for this situation. While screening of these risk factors continues as policy, the quality of screening must be dramatically improved.

Adolescent↗