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PubMed1993

Lipoprotein composition in the insulin-deficient non-acidotic phase of type I diabetic patients and early evolution after the start of insulin therapy.

Lipoproteins, including intermediate density lipoproteins and lipoprotein(a), and apolipoproteins A-I, B, C-II, C-III and E, were studied in 13 newly-diagnosed type I diabetic patients with severe insulinopenia without dehydration or acidosis. At baseline, the main finding was a significant increase in serum triglycerides due to raised triglyceride concentrations in all lipoproteins, particularly triglyceride-rich lipoproteins. Cholesterol concentrations were slightly increased in lipoproteins and led to a significant increase in serum cholesterol. Two days after the start of insulin therapy, lipoprotein profiles had normalized except for the LDL triglyceride contents, which remained significantly increased on the fifth day of treatment. No significant modifications were observed in lipoprotein(a), apolipoproteins A-I and E concentrations throughout the study. However, serum apolipoproteins B, C-II and C-III were increased at baseline and fell to normal levels 2 days after the start of insulin therapy. On the other hand, apolipoprotein C-II/C-III ratios in high and very low density lipoprotein, showed no significant differences at baseline compared with controls, suggesting that an apolipoprotein C-II deficiency or apolipoproteins Cs imbalance can be ruled out. In conclusion, significant lipoprotein abnormalities were observed in the insulin-deficient state of type I diabetes mellitus; insulin therapy normalizes the lipoprotein profile in two days, except for low density lipoprotein triglyceride contents which remain increased at the fifth day.

Adolescent↗
PubMed1988

Hyporeninemic hypoaldosteronism in diabetic patients with chronic renal failure.

Plasma renin activity, plasma aldosterone levels and renal tubular capacity to excrete hydrogen ions were studied in 13 patients suffering from diabetes mellitus with a creatinine clearance of less than 40 ml/min. The results were compared with those obtained in a control group, in a group of nondiabetic subjects with chronic renal failure (CRF) and in a group of diabetic patients without CRF. Twelve of the thirteen diabetic patients with CRF had data characteristic of hyporeninemic hypoaldosteronism associated with type IV renal tubular acidosis. On comparing the results with those of the other two groups of patients, it was observed that the manifestations of the latter two groups considered separately were different from those of the problem group, although in the diabetic patients with normal glomerular filtration rate (GFR) hyporeninism but not hypoaldosteronism was present accompanied by a lower net acid excretion (p less than 0.001) due to a lower excretion of NH4 (p less than 0.05) and titratable acid (p less than 0.001) when the patients were challenged with an NH4Cl overload. We believe that a conjunction of diabetes and renal failure is necessary for the diabetic patients with a decrease in GFR to show hyporeninemic hypoaldosteronism and type IV tubular acidosis.

Acidosis, Renal Tubular↗
PubMed2005

Effect of D-alpha-tocopherol on tubular nephron acidification by rats with induced diabetes mellitus.

The objective of the present study was to determine if treatment of diabetic rats with D-alpha-tocopherol could prevent the changes in glomerular and tubular function commonly observed in this disease. Sixty male Wistar rats divided into four groups were studied: control (C), control treated with D-alpha-tocopherol (C + T), diabetic (D), and diabetic treated with D-alpha-tocopherol (D + T). Treatment with D-alpha-tocopherol (40 mg/kg every other day, ip) was started three days after diabetes induction with streptozotocin (60 mg/kg, ip). Renal function studies and microperfusion measurements were performed 30 days after diabetes induction and the kidneys were removed for morphometric analyses. Data are reported as means +/- SEM. Glomerular filtration rate increased in D rats but decreased in D + T rats (C: 6.43 +/- 0.21; D: 7.74 +/- 0.45; D + T: 3.86 +/- 0.18 ml min-1 kg-1). Alterations of tubular acidification observed in bicarbonate absorption flux (JHCO3) and in acidification half-time (t/2) in group D were reversed in group D + T (JHCO3, C: 2.30 +/- 0.10; D: 3.28 +/- 0.22; D + T: 1.87 +/- 0.08 nmol cm-2 s-1; t/2, C: 4.75 +/- 0.20; D: 3.52 +/- 0.15; D + T: 5.92 +/- 0.19 s). Glomerular area was significantly increased in D, while D + T rats exhibited values similar to C, suggesting that the vitamin prevented the hypertrophic effect of hyperglycemia (C: 8334.21 +/- 112.05; D: 10,217.55 +/- 100.66; D + T: 8478.21 +/- 119.81 microm(2)). These results suggest that D-alpha-tocopherol is able to protect rats, at least in part, from the harmful effects of diabetes on renal function.

Acidosis, Renal Tubular↗
PubMed1990

Radical splenopancreatectomy with duodenal loop conservation in rats.

In an attempt to find a reproducible method of total splenopancreatectomy (TSP) with duodenal loop conservation in rats, we used the technique recently described by S. Houry and M. Huguier (Eur. Surg. Res. 15: 328, 1983) but were not able to induce a true diabetes. We therefore developed a more radical splenopancreatectomy (RSP) in rats and compared this technique with the TSP. RSP involves a more extensive dissection of the common bile duct, a short choledocoduodenal anastomosis, and total excision of the retroportal pancreatic lobules with the aid of a dissecting microscope. In rats who had undergone the TSP technique, blood glucose levels were maximal 8 hr after operation (270 +/- 16 mg/dl), and thereafter recovered baseline values. In contrast, after the RSP technique all the rats became diabetic as documented by persistent hyperglycemia (347 +/- 20 mg/dl at 8 hr, P = 0.01 compared to TSP; 500 +/- 20 mg/dl at 8 hr, P less than 0.0001). Eight hours after the operation, blood lipase levels increased more significantly after TSP than after RSP (847 +/- 247 IU/liter and 130 +/- 37 IU/liter, respectively, P = 0.01), and then decreased to 92 +/- 19 IU/liter at 24 hr in the TSP group and less than or equal to 30 IU/liter in the RSP group (P = 0.003), suggesting a more radical dissection of pancreatic tissue with the RSP technique. At sacrifice at 48 hr, no complications were found with either technique on macroscopic and microscopic examination, except for marked gastric distension with RSP. A third group of rats underwent RSP and were followed until natural death.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed2002

Acetazolamide-induced muscle weakness in hypokalemic periodic paralysis.

A 46-year-old man with hypokalemic periodic paralysis (HypoPP) and diabetes mellitus (DM) had worsened muscle weakness after acetazolamide (ACZ) treatment. During the paralytic episode, serum potassium levels were reduced, and serum chloride and insulin levels were increased. The data suggested proximal renal tubular acidosis due to ACZ. We determined arterial-venous concentrations of potassium, insulin and glucose across the forearm. Venous potassium levels were markedly reduced. ACZ is thought to potentiate potassium uptake into muscles. Hyperinsulinemia and DM could contribute to ACZ-induced exacerbation in our patient. We should pay more attention to ACZ-treated HypoPP patients with hyperinsulinemia and DM.

Acetazolamide↗
PubMed1981

Epidural anesthesia for cesarean section in diabetic parturients: maternal and neonatal acid-base status and bupivacaine concentration.

Acid-base status and blood levels of bupivacaine were determined in 16 diabetic parturients and their infants after epidural anesthesia for cesarean section. The newborn infants were divided into two groups based on umbilical artery pH at birth. Group A consisted of 10 infants who had a pH of less than 7.2 and group B consisted of six infants with a pH of greater than 7.2. Neonatal acidosis was related to both the severity of maternal diabetes and the presence of maternal hypotension after epidural anesthesia. In addition, the half-life to bupivacaine was prolonged in acidotic infants. The placental transfer of bupivacaine, as judged by umbilical vein/maternal vein ratios, was significantly greater in acidotic infants.

Acid-Base Equilibrium↗
PubMed1977

[Lactic acidosis after administration of guanidine derivatives (buformine, phenformine) (author's transl)].

Three patients are reported on, who at the time of admittance showed a decompensated metabolic acidosis, elevated concentrations of serum lactate and a reduced kidney funktion. All the patients had taken guanidine derivates (phenformine, buformine) because of diabetes mellitus. The serum biguanid concentrations, however, were elevated in only two cases. Therapy of the lactic acidosis has to be directed at the underlying disease. In biguanid incluced acidosis, haemodialysis with simultaneous administration of sodium bicarbonate is indicated.

Acidosis↗
PubMed1964

THE EFFECTS OF DEXTROTHYROXINE IN DIABETES.

Eighteen diabetic patients were treated with dextrothyroxine (from 2 mg to 8 mg daily) for varying periods up to six months. This produced a decided reduction of serum cholesterol levels. Statistically valid comparisons were made of their fasting blood sugar levels before and after two weeks of dextrothyroxine treatment. Administration of this drug was associated with a significant elevation of fasting blood sugar levels. Good diabetic control did not preclude this adverse effect. After more prolonged treatment with the drug, 8 of the 18 patients experienced progressive deterioration of their diabetic control, necessitating increased amounts of insulin or oral drugs. Despite close observation, one patient developed acidosis. When dextrothyroxine was discontinued, there was a significant drop in blood sugar levels in these patients. Two patients had hypoglycemic reaction. When the fasting blood sugar values of the 18 patients, studied while they were receiving significant doses of dextrothyroxine, are compared with a control series of blood sugar determinations obtained on these same patients before dextrothyroxine administration was begun, the diabetogenic effect of this drug is confirmed by the highly significant difference demonstrated. Four patients were given dextrothyroxine a second time, and again experienced deterioration of diabetic control.

Acidosis↗
PubMed1982

The effects of metabolic acidosis in vivo on insulin binding to isolated rat adipocytes.

Insulin resistance in vivo and impaired insulin binding to isolated adipocytes are characteristic of diabetic ketoacidosis in the rat. To determine the respective roles of diabetes and acidaemia in the genesis of the binding defect, insulin binding to adipocytes from alkali-treated ketoacidotic diabetic and ammonium chloride acidotic rats was studied. Reversal of the acidaemia of ketoacidotic rats by sodium bicarbonate infusion (pH 6.73 +/- 0.027 to 7.35 +/- 0.027, p less than 0.001, n = 12) increased adipocyte insulin binding (0.51 +/- 0.21% to 2 x 10(5) cells/ml, n = 6 untreated versus 1.10 +/- 0.27% to 2 x 10(5) cell, n = 6 treated, p less than 0.05). Scatchard analysis showed this to be due to an increase in insulin receptor concentration. Ammonium chloride infusion caused marked metabolic acidaemia (pH 6.72 +/- 0.04, n = 12) and insulin binding to adipocytes was markedly decreased (0.81 +/- 0.12% to 2 x 10(5) cells/ml n = 6 versus 2.40 +/- 0.22% to 2 x 10(5) cells/ml, n = 6 in controls p less than 0.02), due to a change in receptor concentration. The apparent affinity of the receptor was markedly decreased in diabetic animals compared with normal controls but was unchanged in ammonium chloride acidotic animals. Thus in diabetic ketoacidosis there is both decreased affinity and number of insulin receptors partially reversible by prolonged alkali infusion. Only changes in affinity appeared to be specific for the diabetic state.

Acidosis↗
PubMed1999

Metformin and contrast media--a dangerous combination?

Metformin is a biguanide used to treat type II diabetes mellitus. Since the recent introduction of this drug into the United States there has been considerable interest in metformin associated lactic acidosis (MALA) following intravenous contrast media. The Royal College of Radiologists published advice in November, 1996 (Advice to Members and Fellows with regard to metformin-induced lactic acidosis and X-ray contrast medium agents, RCR Publication) supporting the manufacturers' advice that metformin should not be used in the 48 h before or after intravenous (i.v.) contrast medium. We performed a systematic review of the literature and this has shown that almost all reported cases of MALA following i.v. contrast medium occurred where there was either pre-existing poor renal function or another contraindication to metformin usage. There has been only one reported case of lactic acidosis following the use of intravenous contrast medium in a patient with normal renal function. We suggest that the Royal College of Radiologists' advice should be modified and that it is safe to give i.v. contrast medium to patients on metformin with normal renal function.

Acidosis, Lactic↗
PubMed2001

Structure of rat BCKD kinase: nucleotide-induced domain communication in a mitochondrial protein kinase.

Mitochondrial protein kinases (mPKs) are molecular switches that down-regulate the oxidation of branched-chain alpha-ketoacids and pyruvate. Elevated levels of these metabolites are implicated in disease states such as insulin-resistant Type II diabetes, branched-chain ketoaciduria, and primary lactic acidosis. We report a three-dimensional structure of a member of the mPK family, rat branched-chain alpha-ketoacid dehydrogenase kinase (BCK). BCK features a characteristic nucleotide-binding domain and a four-helix bundle domain. These two domains are reminiscent of modules found in protein histidine kinases (PHKs), which are involved in two-component signal transduction systems. Unlike PHKs, BCK dimerizes through direct interaction of two opposing nucleotide-binding domains. Nucleotide binding to BCK is uniquely mediated by both potassium and magnesium. Binding of ATP induces disorder-order transitions in a loop region at the nucleotide-binding site. These structural changes lead to the formation of a quadruple aromatic stack in the interface between the nucleotide-binding domain and the four-helix bundle domain, where they induce a movement of the top portion of two helices. Phosphotransfer induces further ordering of the loop region, effectively trapping the reaction product ADP, which explains product inhibition in mPKs. The BCK structure is a prototype for all mPKs and will provide a framework for structure-assisted inhibitor design for this family of kinases.

Adenosine Diphosphate↗
PubMed1970

Hyperglobulinaemic renal tubular acidosis: a report of nine cases.

Of nine women with hyperglobulinaemic renal tubular acidosis four presented with acidosis and five had the "incomplete" form of the disorder. Seven patients had nephrogenic diabetes insipidus, but none had the Fanconi syndrome. Investigation showed abnormal immunoglobulins and autoantibodies in all nine patients. Diseases coexisting with renal tubular acidosis were Sjögren's syndrome, hyperglobulinaemic purpura, autoimmune liver and thyroid disease, diffuse pulmonary fibrosis, and a peripheral neuropathy. It is suggested that this type of renal tubular acidosis might be due to an autoimmune process.

Acidosis, Renal Tubular↗
PubMed1989

Diabetic ketoacidosis in Denmark: epidemiology, incidence rates, precipitating factors and mortality rates.

The epidemiology of uncontrolled diabetes mellitus was studied in an 11.2% sample of the Danish population (574,696 inhabitants) during a 24-month period. Some 175 admissions in ketoacidosis (heavy ketonuria and plasma bicarbonate below 21 mmol/l) were recorded. Based on prevalence rates from a socio-economically and ethnically comparable Danish county, the annual incidence rate was calculated to be 0.045 per diabetic. The incidence rate of moderate and severe episodes (bicarbonate less than 16 mmol/l) was 0.032 and of severe episodes only (bicarbonate less than 10 mmol/l) 0.017 per diabetic. The major risk group was female teenagers. The total annual frequency of recurrence was 8.7%: 48% of the male episodes were ketoacidosis (DKA) associated with onset of diabetes, against 30% of the female episodes (P = 0.02). All Danish diabetics were at the time of the survey (1978-79) treated with conventional insulin treatment. Annual incidence rate in these established diabetics was 0.028, i.e. three to five times less than reported during treatment with continuous subcutaneous insulin infusion. Mortality of DKA was low, 3.4%, and dependent upon age and precipitating factor but not upon the degree of acidosis. The overall annual mortality rate was 1.5 per 100 diabetics.

Adolescent↗
PubMed1989

[Diabetic ketoacidosis and hyperglycemic hyperosmolar nonacidotic syndrome in type I and II diabetics].

The author analyzes 46 hyperglycaemic comatose conditions in diabetics treated at the medical clinic of the Paediatric Faculty, Charles University Prague in 1978-1985. In the group older patients with type II diabetes predominated, where acute decompensation was frequently of the hyperosmolar type without acidosis and it was usually associated with a higher mortality. The cause of the metabolic breakdown was most frequently infection, in type II diabetes, however, an equally important part was played by acute cardiovascular disease. Insulin was administered in small doses by the i.v. route either as a continuous infusion or in fractionated doses. The results of both procedures were comparable only the insulin requirement in the fractionated doses was higher.

Adult↗
PubMed1986

Coronary vascular responses to hypoxia in the diabetic lamb: independence from adenosine and autonomic mechanisms.

We have previously found that the coronary dilator response to infused adenosine is attenuated in diabetic (alloxan) lambs. Adenosine responsiveness is restored by administration of insulin. The present studies tested the hypothesis that coronary flow changes with hypoxia, if mediated by adenosine, would also be modified. Studies were carried out in eight control and six diabetic lambs. The animals were anesthetized and prepared to maintain constant arterial pressure (reservoir), cardiac output (pump), and heart rate (paced). Atropine and practolol were given. Forced inspired oxygen was reduced in steps. Arterial and coronary sinus blood samples were analyzed for Po2, oxygen content, pH, hematocrit, and glucose. Myocardial oxygen delivery and uptake (MVO2) were calculated. Coronary flow increased identically in both control and diabetic animals as PaO2 was reduced below 60 Torr. Oxygen delivery and MVO2 fell equally in both groups. Acidosis potentiated hypoxic coronary flow changes. Alpha blockade (phentolamine) was without effect in control lambs but caused coronary flow to increase in diabetic lambs. Changes in coronary flow with hypoxia were unaffected, however. Insulin caused no change in the coronary dilator response to hypoxia in either control or diabetic lambs. It is concluded that coronary alpha tone is increased in diabetes but does not modify changes in coronary flow during hypoxia. As coronary flow responses to hypoxia were unaltered in diabetic lambs, and unaffected by insulin, adenosine may not be the primary mediator of coronary vascular dilatation. Potentiation of adenosine by tissue acidosis is apparently insufficient to explain these findings. The mechanism for coronary dilatation during hypoxia is unclear but may involve direct effects of reduced oxygenation of coronary vascular smooth muscle.

Acidosis↗