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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 94 (1972), S. 5518-5519 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Plasma amino acids ; liver gluconeogenesis ; glucose ; insulin ; glucagon ; cortisol ; fetus ; newborn ; rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The present study examines the role of insulin, glucagon and cortisol in the regulation of gluconeogenesis from lactate and amino acids in fetal and newborn rats. Injection of glucagon in the fullterm fetal rat caused a rise in glucose (and insulin) and a fall in blood levels of most individual amino acids, stimulated hepatic accumulation of 14C-amino isobutyric acid and 14C-cycloleucine and increased the conversion of 14C lactate, alanine and serine to glucose in vivo and in vitro (liver slices). Such changes were equivalent to the changes seen in 4 h old newborn rats. When glucagon was administered at birth, little difference was observed between control and treated animals in plasma amino acids and a smaller increment in conversion of 14C substrate to glucose occurred. By contrast, insulin injection at birth caused hypoglycemia, suppression of levels of certain amino acids and inhibition of conversion of 14C substrates into glucose. Glucose injection at birth caused elevated glycemia and plasma insulin and suppression of most amino acid levels and of conversion of 14C substrate into glucose. Cortisol injection at birth caused a marked, generalized hyperaminoacidemia, a stimulation of glucagon secretion and of conversion of 14C substrates into glucose. These observations support the thesis that glucagon plays a major role in the induction of hepatic gluconeogenesis and that insulin acts as an antagonist hormone.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 19 (1980), S. 521-528 
    ISSN: 1432-0428
    Keywords: Pregnant rat ; insulin resistance ; glucose tolerance ; glucose production ; glucose utilization ; glucose turnover ; insulin sensitivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The glucose disappearance rate measured after IV glucose injection (1 g/kg body wt) remained unchanged between 12 and 21 day of gestation in the rat. In contrast, insulin secretion in response to IV glucose was markedly increased on day 19 and 21 of pregnancy, suggesting resistance to endogenous insulin. Glucose kinetics (glucose production, utilization and clearance) in response to various doses of IV insulin have been studied in anaesthetised postabsorbtive 19 day pregnant and virgin rats using 6-3H glucose. With the supramaximal dose of insulin (4 U/kg body wt) no differences in glucose kinetics were found between pregnant and virgin rats. In contrast, with the two lower doses of insulin (0.15 and 0.05 U/kg body wt) glucose production was inhibited by 36±3% and 13±2% (Mean±SEM) respectively in virgin rats, but was not decreased in pregnant rats. When the effect of insulin on glucose clearance was expressed as % of the maximal effect obtained with 4 U/kg body weight, the rise in glucose clearance in response to the two lower doses of insulin (0.15 and 0.05 U/kg body wt) was lower in pregnant (57.5±6 and 27.4±4%) than in virgin rats (73.3±6 and 42.2±7%). These results suggest that a decreased sensitivity to insulin appears in late pregnancy in the rat and could involve both liver and skeletal muscle.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0428
    Keywords: Glucose infusion ; pregnant rats ; fetus ; plasma insulin ; fetal body weight ; lipid synthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Mild hyperglycaemia was induced in unrestrained pregnant rats from day 20.5 to day 23.5 of pregnancy, using a continuous glucose infusion. Control rats were infused with distilled water. In post-mature fetuses from glucose-infused rats, raised plasma glucose and insulin concentrations were related to increased body weight (6.03±0.07 g) and total carcass fat (2.02±0.04% of fresh weight) compared with control fetuses of the same age (5.35±0.07 and 1.5±0.04 g, respectively). Concurrently, the rate of lipogenesis in the carcass, estimated from the incorporation of tritium from tritiated water into fatty acids, was significantly increased in fetuses from glucose infused rats compared with control rats (6.00±0.34 versus 2.62±0.27 and 3H2O · h-1 · g tissue-1, respectively).
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0428
    Keywords: Metformin ; lactic acidosis ; acute renal failure ; blood alanine ; pyruvate ; 3-hydroxybutyrate ; acetoacetate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Lactic acidosis occourred in 6 metformin-treated diabetic patients. Five of them had received 1.6 to 2.4 g metformin per day over a period of weeks or years. Acute renal failure, induced by i. v. pyelography, arteriography, or severe dehydration, preceded lactic acidosis by a few days and apparently precipitated it. The sixth patient had normal renal function prior to taking a massive overdose of metformin in an attempt at suicide. The metabolic pattern was very similar to that observed in phenformin-induced lactic acidosis: severe metabolic acidosis (pH: 7.02±0.95; HCO 3 − : 6.3±0.9 mmol/l; PaCO2: 25±4 mmHg; PaO2: 110±19 mmHg); hyperlactataemia (18.4±3.3 mmol/l) and high lactate/pyruvate ratio (51±5); high blood alanine (2.82±1.10 mmol/l); high 3-hydroxybutyrate (15.8±3.3 mmol/l) and high 3-hydroxybutyrate/ acetoacetate ratio (26±10). Hypoglycaemia (25 to 60 mg per 100 ml) was observed in 4 patients, in spite of high glucagon (760±148 pg/ml) and low insulin (13±5μU/ml) levels. A guanidine substance was characterized in the plasma at concentrations 45 to 110 μg/ml; it was similar to metformin and distinct from creatinine, according to chromatographic and other criteria; its concentration in the plasma decreased during dialysis, and the same substance appeared in the dialysis effluent. The treatment included massive alkalinization (710 ±130 mmol/l i. v. for 48 h), plasma volume expanders (5630±1000 ml/48 h), forced-diuresis and/or dialysis, insulin (30±10 U/48 h) and glucose (300 ±50 g/48 h). — It is concluded that: 1. metformin, like other biguanides, can induce lactic acidosis; 2. acute renal failure is a prominent causal factor; 3. pharmacokinetics of metformin account for this fact since metformin cannot be inactivated by the liver (as distinct from phenformin) and is normally excreted by the kidney; 4. accumulation of biguanide is suggested by guanidine assay in the plasma; 5. metformin should not be prescribed in the presence of renal failure.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 14 (1978), S. 261-267 
    ISSN: 1432-0428
    Keywords: Lactic acidosis ; phenformin ; biguanides
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An experimental model of phenformininduced lactic acidosis was established in rats. Following a subtotal nephrectomy, renal failure developed (serum creatinine 4.5±0.1mg/100ml and 2.8±0.1 mg/100 ml on the 1st and 8th postoperative days respectively). Immediately after nephrectomy intra-peritoneal phenformin treatment, 16 mg/day, was commenced. Lactic acidosis developed progressively within 8 days, or earlier in the rats with the most severe renal insufficiency. The metabolic pattern was very similar to that observed in diabetic patients with a biguanide-induced lactic acidosis: on the 8th day, 2 h after the last phenformin injection, blood lactate was 10.8±1.0 mmol/1 (controls: 1.50±0.03); pyruvate was 0.56±0.06 mmol/1 (controls: 0.10±0.01) and blood pH: 7.00 ± 0.02 (vs 7.34±0.02); 3-hydroxybutyrate was 1.41±0.37 mmol/1 (vs 0.32 ±0.03); acetoacetate: 0.51±0.15 mmol/1 (vs 0.17 ±0.01), and free glycerol: 0.63 ±0.07 mmol/1 (vs 0.14 ±0.02). Increased concentrations of alanine (1.66±0.26 mmol/1, vs 0.48 ± 0.04 in controls) and low blood glucose levels (23± 8 mg/ 100 ml vs 70 ± 2, after a 12 hours fast) accompanied the lactic acidosis in spite of high glucagon levels (2030±170 pg/ml vs 108±10 in controls) and low insulin/glucagon molar ratio (0.19 vs 6.9 in controls). Normal rats, treated with phenformin at same doses, and nephrectomized rats injected with saline served as controls and remained free of lactic acidosis. Hydroxyphenformin (16 mg/day) injected in nephrectomized rats, was biologically inactive. Glucose production from14C-lactate was 425 ±85 μmol/100 g body wt/h, vs 1050 ± 90 in control animals. Blood lactate specific activity declined more slowly in the lactic acidotic rats than in controls, suggesting that a decrease in lactate utilization contributed to hyperlactataemia more than an increased lactate production.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0428
    Keywords: Colchicine ; vincristine ; puromycin ; cycloheximide ; cytochalasin B ; microfilaments ; microtubules ; glucagon ; A2 cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to document the cytophysiology of glucagon release by A2 cells, isolated perfused rat pancreases were stimulated by arginine after exposure to colchicine, vincristine, cytochalasin B, cycloheximide and puromycin. Colchicine, 10−4 mol/l, enhanced the early phase of glucagon release after a short exposure time (35 min). This potentiation vanished with longer exposure (45 to 100 min) and was replaced by a reduction in glucagon release, affecting both phases of secretion, but more the second phase than the first. When exposure time was kept constant (45 min) and the concentration of colchicine varied, a similar potentiating effect was observed for colchicine 10−7 mol/l (first phase) and 10−6 mol/l (both phases); an inhibitory influence was apparent with higher concentrations (10−5 to 10−3 mol/l) affecting mainly the second phase of release. Similar results were obtained with vincristine, 10−5 mol/l (infused for 35 to 100 min) and vincristine 10−8 to 10−4 mol/l, after a constant 45 min exposure. These findings are compatible with a participation of microtubules in the dynamics of glucagon release: a reduction of both phases of secretion being caused by an extended disruption in the microtubular apparatus, whereas more limited disturbance of this system is associated with facilitated glucagon release. Cytochalasin B, 10 μg/ml, potentiated the A2 cell response to arginine and the basal glucagon release in the presence of glucose 4.4 mmol/l. Puromycin 100 μg/ml and cycloheximide 0.5 mg/ml reduced selectively the second phase of glucagon release; cycloheximide, 1 mg/ml, completely inhibited the basal release, and the early and late phases of the arginine-stimulated release. These results suggest that emiocytosis in A2 cells is very similar to that in B cells. The specificity of antitubulins and other agents as dissecting tools for the secretory process depends upon the experimental conditions.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 15 (1978), S. 459-463 
    ISSN: 1432-0428
    Keywords: Newborn ; suckling ; dichloroacetate ; glucose ; gluconeogenic substrates ; gluconeogenesis ; glucose utilization ; ketone bodies ; insulin ; glucagon
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Subcutaneous injection of sodium dichloroacetate (1 mg/g body wt every 3 h) in suckling newborn rats caused in 6 h a fall of 2.5 mmol/l in blood glucose concentrations, and a rise of 2.4 mmol/ l in total blood ketone body levels, but no change in the high levels of plasma non esterified fatty acids. Glucose utilization, measured after intraperitoneal injection of D-glucose (2 mg/g body wt), was not increased in newborns injected with dichloroacetate. The hypoglycaemia resulted from a decrease in gluconeogenic rate, secondarily to a lowering effect of dichloroacetate on blood levels of lactate, pyruvate and alanine. The hypoglycaemia induced by dichloroacetate was completely reversed by injecting newborn rats with a mixture of gluconeogenic precursors (lactate, pyruvate and alanine). It is concluded that the high rate of gluconeogenesis observed in suckling newborn rats in sustained by an increased release of lactate and, to a much smaller extent of pyruvate and alanine, by peripheral tissues. This probably resulted from the low pyruvate dehydrogenase activity found in peripheral tissues of the newborn rat. The hyperketonaemia induced by dichloroacetate could result from an increased ketogenesis and/or a decreased ketone body utilization.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0428
    Keywords: Glucose infusion ; pregnant rats ; prolonged pregnancy ; fetus ; plasma insulin ; plasma glucagon ; liver phosphoenolpyruvate carboxykinase ; liver glycogen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Continuous glucose infusion was used to induce mild hyperglycaemia in unrestrained pregnant rats during the last three days of pregnancy. Control pregnant rats were infused with distilled water. Fetuses were studied after normal or prolonged pregnancy. Fetuses from glucose-infused rats, compared with controls, showed higher plasma glucose levels, increased plasma insulin and lower plasma glucagon concentrations. Pregnancy prolonged until day 23.5 resulted in a rise in the glucagon/insulin ratio from 6.5 to 67 in fetuses from control rats and from 1.3 to 13 in fetuses from glucose-infused rats. Concurrently in fetuses from control rats, liver phosphoenolpyruvate carboxykinase activity increased markedly and liver glycogen stores decreased sharply. In fetuses from glucose-infused rats, liver phosphoenolpyruvate carboxykinase activity rose and glycogen content decreased, but to a lesser extent. These results show that both the A and B cells of the rat fetal pancreas are sensitive to chronic glucose stimulation.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1420-9071
    Keywords: Human growth hormone (HGH) ; urine ; IRMA ; ultrasensitive assay
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary An immunoradiometric assay for human growth hormone (HGH) has been developed which has a detection limit of 1ng/l and can measure HGH in unextracted urine from normal children and adults. The assay is based on a two-step procedure, using a solid-phase goat-anti-HGH immunosorbent for immunoextraction and [125I]-labeled monoclonal HGH-antibody for detection and quantification. The assay is not affected by urea, NaCl or changes of pH from 5–8. The mean urine HGH concentration in normal children is 6.78±7.6 (SD) pg/ml, in patients with HGH-deficiency 1.3±0.9 pg/ml which increases to 11.7±13.4 pg/ml on the day of growth hormone injection.
    Type of Medium: Electronic Resource
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