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  • Articles: DFG German National Licenses  (4)
  • adverse effects  (2)
  • glucose fatty acid cycle  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Multiple defects of both hepatic and peripheral intracellular glucose processing contribute to the hyperglycaemia of NIDDM (1995)
    Springer
    Diabetologia 38 (1995), S. 326-336 
    Details
    ISSN: 1432-0428
    Keywords: Key words Hepatic glucose production ; glucose fatty acid cycle ; Cori cycle ; muscle glucose metabolism ; glycogen synthase.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Non-insulin-dependent diabetic (NIDDM) patients were studied during a modified euglycaemic state when fasting hyperglycaemia was normalized by a prior (–210 to –150 min) – and later withdrawn (–150–0 min) – intravenous insulin infusion. Glucose metabolism was assessed in NIDDM patients (n = 10) and matched control subjects (n = 10) using tritiated glucose turnover rates, indirect calorimetry and skeletal muscle glycogen synthase activity determinations. Total and non-oxidative exogenous glycolytic flux rates were measured using appearance rates of tritiated water. A + 180 min euglycaemic hyperinsulinaemic (40 mU · m–2· min–1) clamp was performed to determine the insulin responsiveness of the various metabolic pathways. Plasma glucose concentration increased spontaneously during baseline measurements in the NIDDM patients (-120 to 0 min: 4.8 ± 0.3 to 7.0 ± 0.3 mmol/l; p 〈 0.01), and was primarily due to an elevated rate of hepatic glucose production (3.16 ± 0.13 vs 2.51 ± 0.16 mg · kg FFM–1· min–1; p 〈 0.01). In the NIDDM subjects baseline glucose oxidation was decreased (0.92 ± 0.17 vs 1.33 ± 0.14 mg · kg FFM–1· min–1; p 〈 0.01) in the presence of a normal rate of total exogenous glycolytic flux and skeletal muscle glycogen synthase activity. The simultaneous finding of an increased lipid oxidation rate (1.95 ± 0.13 vs 1.61 ± 0.07 mg · kg FFM–1· min–1; p = 0.05) and increased plasma lactate concentrations (0.86 ± 0.05 vs 0.66 ± 0.03 mmol/l; p = 0.01) are consistent with a role for both the glucose-fatty acid cycle and the Cori cycle in the maintenance and development of fasting hyperglycaemia in NIDDM during decompensation. Insulin resistance was demonstrated during the hyperinsulinaemic clamp in the NIDDM patients with a decrease in the major peripheral pathways of intracellular glucose metabolism (oxidation, storage and muscle glycogen synthase activity), but not in the pathway of non-oxidative glycolytic flux which was not completely suppressed during insulin infusion in the NIDDM patients (0.55± 0.15 mg · kg FFM–1· min–1; p 〈 0.05 vs 0; control subjects: 0.17 ± 0.29; NS vs 0). Thus, these data also indicate that the defect(s) of peripheral (skeletal muscle) glucose processing in NIDDM goes beyond the site of glucose transport across the cell membrane. [Diabetologia (1995) 38: 326 –336]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400638
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Long-term therapy of arterial hypertension with nifedipine given alone or in combination with a beta-adrenoceptor blocking agent (1982)
    Springer
    European journal of clinical pharmacology 22 (1982), S. 101-103 
    Details
    ISSN: 1432-1041
    Keywords: hypertension ; nifedipine ; beta-adrenoceptor blockade ; long-term treatment ; adverse effects ; propranolol ; timolol ; metoprolol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The antihypertensive effect of nifedipine during long-term therapy was investigated in 5 patients receiving nifedipine as the sole drug and in 10 patients who had nifedipine in combination with a beta-adrenoceptor blocking drug. Nifedipine monotherapy was problematic because of side-effects and development of resistance to therapy after a few months. In patients who received the combined therapy significant and stable blood pressure reductions were maintained during the whole observation period (12–33 months). However, the occurrence of peripheral oedema in 4 of the patients necessitated the addition of a thiazide diuretic. It is concluded that nifedipine is not a first choice drug for the long-term treatment of arterial hypertension. When given in addition to a beta-blocker it is well tolerated and powerful but fluid retention may occur and if not counteracted by a diuretic it will limit the antihypertensive potential of the drug.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00542452
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Effect of bepridil on metabolic control and insulin secretion in diabetics (1988)
    Springer
    European journal of clinical pharmacology 34 (1988), S. 221-226 
    Details
    ISSN: 1432-1041
    Keywords: bepridil ; diabetes mellitus ; Type I ; Type II ; insulin secretion ; C-peptide ; adverse effects ; diabetic control
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary In a double-blind cross-over study bepridil 900 mg followed by 300 mg daily for 11 days was given to 37 insulin (Type I) or non-insulin (Type II)-dependent diabetic patients. It did not modify the metabolic control of the patients as levels of glucose in blood and urine, doses of insulin and oral hypoglycaemic drugs, energy intake, and the number of hypoglycaemic attacks during therapy were unchanged. The serum concentration of C-peptide was not modified in either type of diabetic patient, and serum insulin in the Type I but not in the Type II patients was slightly higher during active drug treatment. No adverse organotoxic or arrhythmogenic effects or changes in possible atherogenic lipid fractions in serum could be demonstrated during bepridil therapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00540947
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Multiple defects of both hepatic and peripheral intracellular glucose processing contribute to the hyperglycaemia of NIDDM (1995)
    Springer
    Diabetologia 38 (1995), S. 326-336 
    Details
    ISSN: 1432-0428
    Keywords: Hepatic glucose production ; glucose fatty acid cycle ; Cori cycle ; muscle glucose metabolism ; glycogen synthase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Non-insulin-dependent diabetic (NIDDM) patients were studied during a modified euglycaemic state when fasting hyperglycaemia was normalized by a prior (−210 to −150 min) — and later withdrawn (−150–0 min) — intravenous insulin infusion. Glucose metabolism was assessed in NIDDM patients (n=10) and matched control subjects (n=10) using tritiated glucose turnover rates, indirect calorimetry and skeletal muscle glycogen synthase activity determinations. Total and non-oxidative exogenous glycolytic flux rates were measured using appearance rates of tritiated water. A+180 min euglycaemic hyperinsulinaemic (40 mU·m−2·min−1) clamp was performed to determine the insulin responsiveness of the various metabolic pathways. Plasma glucose concentration increased spontaneously during baseline measurements in the NIDDM patients (−120 to 0 min: 4.8±0.3 to 7.0±0.3 mmol/l; p〈0.01), and was primarily due to an elevated rate of hepatic glucose production (3.16±0.13 vs 2.51±0.16 mg·kg FFM−1·min−1; p〈0.01). In the NIDDM subjects baseline glucose oxidation was decreased (0.92±0.17 vs 1.33±0.14 mg·kg FFM−1·min−1; p〈0.01) in the presence of a normal rate of total exogenous glycolytic flux and skeletal muscle glycogen synthase activity. The simultaneous finding of an increased lipid oxidation rate (1.95±0.13 vs 1.61±0.07 mg·kg FFM−1·min−1; p=0.05) and increased plasma lactate concentrations (0.86±0.05 vs 0.66±0.03 mmol/l; p=0.01) are consistent with a role for both the glucose-fatty acid cycle and the Cori cycle in the maintenance and development of fasting hyperglycaemia in NIDDM during decompensation. Insulin resistance was demonstrated during the hyperinsulinaemic clamp in the NIDDM patients with a decrease in the major peripheral pathways of intracellular glucose metabolism (oxidation, storage and muscle glycogen synthase activity), but not in the pathway of non-oxidative glycolytic flux which was not completely suppressed during insulin infusion in the NIDDM patients (0.55±0.15 mg·kg FFM−1·min−1; p〈0.05 vs 0; control subjects: 0.17±0.29; NS vs 0). Thus, these data also indicate that the defect(s) of peripheral (skeletal muscle) glucose processing in NIDDM goes beyond the site of glucose transport across the cell membrane.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400638
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
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