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At least 1,297 records · Page 72Linked to original sources
PubMed1989

A 13C-n.m.r. investigation of the metabolism of amino acids in renal proximal convoluted tubules of normal and streptozotocin-treated rats and rabbits.

13C-n.m.r. spectroscopy was used to determine the metabolic fate of alanine and aspartate in rat and rabbit kidney proximal tubules. The main purpose of the present study was to investigate the effect of streptozotocin-induced diabetes on the influx of 13C label from [3-13C]alanine into the tricarboxylic acid cycle and through the fructose-1,6-bisphosphatase pathway. This influx was calculated from the relative enrichment of 13C in the various glutamate and glutamine carbon atoms. The relative proportion of 13C label which entered the tricarboxylic acid cycle via pyruvate carboxylase relative to the proportion that entered via pyruvate dehydrogenase was 1.92 +/- 0.02 in fed control rats and 2.27 +/- 0.04 in streptozotocin-treated rats. However, streptozotocin-induced diabetes did not significantly affect this ratio in rabbit proximal convoluted tubular cells. Only in rat proximal convoluted tubular cells did we observe an increase in flux through the fructose-1,6-bisphosphatase pathway by streptozotocin treatment compared with fed controls. The data suggest that streptozotocin-induced diabetes in rats causes the same metabolic changes as does chronic acidosis.

Amino Acids↗
PubMed2006

Severe acidosis in patients taking metformin--rapid reversal and survival despite high APACHE score.

BACKGROUND: Metformin has been shown to reduce complications and mortality from Type 2 diabetes mellitus, and is increasingly used to treat this condition. This agent is, however, associated with a rare but serious risk of lactic acidosis. CASE REPORT: We present cases of 10 patients with Type 2 diabetes mellitus who developed acute renal failure and severe lactic acidosis. Despite the severity of their illness, all patients but one survived. CONCLUSIONS: The increasing prevalence of Type 2 diabetes and its treatment with metformin might result in more cases of lactic acidosis. However our case report demonstrates that early and aggressive treatment with haemofiltration can improve outcomes even in the presence of severe acidosis.

APACHE↗
PubMed1983

Alcoholic ketoacidosis: clinical and laboratory presentation, pathophysiology and treatment.

Alcoholic ketoacidosis is a common condition which occurs predominantly in chronic alcoholics. The usual picture is an interval of increased ethanol intake followed by one or more days of abdominal pain, vomiting, dehydration and a marked decrease in caloric intake. Acidosis is frequently as severe as in diabetic ketoacidosis, but the serum Acetest measurement of ketones may be negative or only slightly positive because of the predominance of beta-hydroxybutyrate compared with acetoacetate. Treatment with intravenous glucose and saline are the essentials of management. Insulin, bicarbonate and phosphate are usually not needed. The major cause of morbidity and mortality is not the acidosis but rather failure to adequately treat concurrent medical or surgical conditions.

Acidosis↗
PubMed1978

Hypothermia: a complication of diabetic ketoacidosis.

During 1969-77, 20 episodes of severe hypothermia occurred in 19 diabetic patients in Nottingham. Thirteen were associated with ketotic hyperosmolar coma, two with lactic acidosis, and one with hypoglycaemia, while in four there was no loss of diabetic control. Ketoacidosis accounted for 11.8% of all admissions for severe accidental hypothermia and was a commoner cause than hypothyroidism (8%). Patients with ketoacidosis were younger and developed hypothermia as often during the summer as during the winter. The metabolic disturbance was characteristic, with severe acidosis (mean pH 7.04), a high blood glucose concentration (mean 56.6 mmol/l; 1020 mg/100 ml), and high plasma osmolality (mean 379.7 mmol (mosmol)/kg). Eight of the 13 episodes proved fatal. Hypothermia may aggravate ketoacidosis and complicate treatment and should be sought in all patients with severe diabetic coma.

Adult↗
PubMed2004

Screening and management of patients with early chronic kidney disease.

Diabetic nephropathy has become the most prevalent cause of end-stage renal disease (ESRD) in many countries. ESRD patients with diabetes have a particularly poor prognosis compared with patients without diabetes. The course of diabetic nephropathy can be modified with early management of the condition and it is important that diabetes patients are screened regularly for early signs of kidney damage. Blood pressure control and use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers have been shown to slow the progression of chronic kidney disease. Patients with diabetes are at considerable risk of cardiovascular complications, and modifiable cardiovascular risk factors, such as anaemia and dyslipidaemia, should be treated at an early stage. Correction of anaemia with recombinant human erythropoietin is associated with improvements in quality of life, functional status, and cardiovascular morbidity and mortality, and may slow the progression of renal disease. Abnormalities in calcium and phosphate metabolism and acidosis may also occur in patients with diabetes and nephropathy and these should be monitored regularly. It is important that patients with kidney disease are detected promptly to allow intervention to slow renal disease progression and to treat modifiable cardiovascular risk factors. Improved collaboration between diabetologists and nephrologists will also ensure that patients receive optimal care.

Diabetes Mellitus, Type 2↗
PubMed1994

Hypermagnesiuria in children with newly diagnosed insulin-dependent diabetes mellitus.

In newly diagnosed insulin-dependent diabetes mellitus, the mechanisms underlying the concomitant occurrence of magnesium deficiency and normal blood magnesium concentration are unknown. The renal handling of magnesium was, therefore, studied in 37 children with newly diagnosed insulin-dependent diabetes mellitus and in 13 controls. Circulating magnesium levels were similar in patients and controls (0.86 vs. 0.84 mmol/l). However, the urinary excretion of magnesium was significantly higher in patients (90.6 vs. 32.2 mumol/l GFR). In the patients a significant positive correlation was found between excretion of magnesium and glycosuria or blood hydrogen ion activity. It is concluded that osmotic diuresis and acidosis increase magnesium excretion in newly diagnosed diabetes mellitus.

Child↗
PubMed1996

Adult-onset MELAS. Evidence for involvement of neurons as well as cerebral vasculature in strokelike episodes.

BACKGROUND: We report a 46-year-old woman with implications regarding pathogenesis of strokelike episodes in MELAS (mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes). She had a 10-month history of episodic seizures, strokes, cognitive decline, vomiting, and ileus. She also had sensorineural hearing loss, insulin-dependent diabetes mellitus of several years' duration, and persistent lactic acidosis. Family history was pertinent for a similar syndrome in her deceased mother (onset in her sixties), for hearing loss and diabetes mellitus in two brothers, and for hearing loss in her only child, a son. CASE DESCRIPTION: Serial MRIs of the brain revealed severe but evanescent cerebral cortical abnormalities. A left temporal brain biopsy was performed to exclude encephalitis. Light microscopy revealed a diffuse fibrillary gliosis with abundant reactive gemistocytes, focal evidence of ischemic neuronal injury, and edema. Electron microscopy revealed bizarre enlarged mitochondria and changes consistent with cellular edema. Succinate dehydrogenase staining was strongly reactive within cerebral blood vessels and within neurons. A point mutation was subsequently found at nt 3243 of the mitochondrial tRNA(Leu(UUR) gene in peripheral leukocytes and in brain, confirming the clinical diagnosis of MELAS. Quantitation revealed that 82% of brain mitochondria carried the disease mutation, indicating that most, if not all, tissues were affected. CONCLUSIONS: Our findings suggest that strokelike episodes in MELAS result from defects in neuronal metabolism, as well as in cerebral vasculature.

Age of Onset↗
PubMed1981

Radiation-induced acute necrosis of the pancreatic islet and the diabetic syndrome in th golden hamster (Mesocricetus auratus).

Exposure of golden hamsters to 35 000 rad of X-rays induced acute and specific necrosis of the cells of thd isles of Longerham of the pancreas within 4 hours whereas no other tissue revealed any drastic changes which would lead to a critical illness until 36 hours. Animals began to show the characteristic signs of diabetes, that is, hyperglycaemia, hyperkaliemia, ketonemia, and acidosis at 12 hours and these continued until death, 56+/- 8 hours later. These were accompanied by the disappearance of beta-cell granules and a decrease of plasma insulin. Treatment of irradiated animals with injections of insulin resulted in a reduction in high blood glucose and the prolongation of survival time up to 5 days, which is comparable to this radiation-induced diabetic syndrome resulted from acute necrosis of the cell of the islets of Langerhans, a previously unreported lethal effect of radiation in golden hamsters.

Animals↗