Biomedical subjects
M Berger
Publications and source records attributed to M Berger.
[Therapy of insulin-dependent diabetes mellitus. Regular metabolic control and insulin dose adaptation by the patient].
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[Stabilisation of patients with insulin-depending diabetes mellitus].
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[Paper basket letters for physicians].
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[Massive obesity with disturbance of glucose tolerance (author's transl)].
A long-term study of 63 extremely obese persons with disturbed glucose tolerance showed a further deterioration of glucose tolerance over 10 years. In 9 out of 23 patients manifest diabetes mellitus developed despite partial weight reduction (greater than or equal to 10% of the initial weight excess). Out of 14 patients who did not lose weight during this time even 11 developed manifestations of diabetes. All patients who were in different weight groups at the 5- and 10-year follow-up showed a deterioration in glucose tolerance after 10 years. In the individual groups there were only minimal differences in other characteristics apart from the different weight behaviour.
[The course of diabetes and clinical findings in glucagonoma].
A 66-year-old male patient with non-insulin-dependent diabetes of probably 20 years' duration presented with necrolytic migratory erythema, stomatitis, anemia and weight loss. Plasma-glucagon concentration measured with Unger's antibody 30-K was 8500 pg/ml, representing a hundredfold elevation. Two thirds consisted of high molecular glucagon fractions (10 000--40 000 Dalton). This may be an important index for detection of glucagonoma with endocrine activity. After excision of the glucagonoma the clinical syndrome was reversed and the patient recovered completely. Histological and histochemical investigation confirmed that the tumor was a glucagonoma. Despite complete removal of the tumor and a normal plasma glucagon concentration, the diabetes remained unchanged. Excessive hyperglucagonemia does not appear to play a primary role in the pathogenesis of this patient's diabetes.
[Radicular and pseudoradicular symptoms of the middle and lower cervical vertebral column (author's transl)].
The differential diagnostic classification of the "shoulder-hand-syndrome" according to etiology and pathophysiological principles is of major importance. The radicular syndrome, subsumed as the shoulder-hand syndrome following a local lesion, must be exactly defined. The pseudoradicular syndrome, which frequently appears clinically in the cervical region under the guise of middle and lower cervical syndrome, has its cause in disturbed function of the vertebral joints. But it can also arise as a mixed syndrome, radicular and pseudoradicular, through a substantial root lesion. The diagnosis of a referred pain in a "shoulder-hand syndrome" can lead to the discovery of internal organic lesions or lesions of the locomotor apparatus of the extremities.
Inhibition of degradation of insulin by ophthalamic acid and by a bovine pancreatic proteinase inhibitor.
We have previously observed that, on subcutaneous administration, a significant proportion of insulin is degraded at the site of injection. The present paper reports that the degradative activity of slices of rat adipose tissue can be inhibited in vitro by ophthalmic acid, a natural analogue of glutathione, and by bovine pancreatic proteinase inhibitor, whereas it is increased by the addition of reduced glutathione.
[Adren beta receptor blocking agents].
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[Fractional distribution of anti-glucagon immunoreactivity (GIR) and amino acid concentration in the plasma in duodenopancreatectomized patients; preliminary report].
Glucagon immunoreactivity (IRG) was measured in plasma of 8 duodenopancreatectomized patients with antiserum 30-K. Arginine infusions failed to raise plasma IRG, whereas in control subjects IRG rose 3-fold. Column chromatography revealed that the basal IRG measured in these plasmas was not due to glucagon (molecular weight 3485) but to other plasma factors, mainly of high molecular weight. This suggests that diabetes mellitus does not require the presence of glucagon to produce the clinical picture, as suggested by other authors. Plasma levels of the amino acids alanine, serine, ornithine, and arginine were significantly (p less than 0.05) elevated, the former two being gluconeogenic substrates and the latter two constituents of the urea cycle. This amino acid abnormality may be a consequence of glucagon deficiency.
Glucose metabolism in perfused skeletal muscle. Demonstration of insulin resistance in the obese Zucker rat.
1. The effect of insulin (0.5, 10 and 50 munits/ml of perfusate) on glucose uptake and disposal in skeletal muscle was studied in the isolated perfused hindquarter of obese (fa/fa) and lean (Fa/Fa) Zucker rats and Osborne-Mendel rats. 2. A concentration of 0.5 munit of insulin/ml induced a significant increase in glucose uptake (approx. 2.5 mumol/min per 30 g of muscle) in lean Zucker rats and in Osborne-Mendel rats, and 10 munits of insulin/ml caused a further increase to approx. 6 mumol/min per 30 g of muscle; but 50 munits of insulin/ml had no additional stimulatory effect. In contrast, in obese Zucker rats only 10 and 50 munits of insulin/ml had a stimulatory effect on glucose uptake, the magnitude of which was decreased by 50-70% when compared with either lean control group. Since under no experimental condition tested was an accumulation of free glucose in muscle-cell water observed, the data suggest an impairment of insulin-stimulated glucose transport across the muscle-cell membrane in obese Zucker rats. 3. The intracellular disposal of glucose in skeletal muscle of obese Zucker rats was also insulin-insensitive: even at insulin concentrations that clearly stimulated glucose uptake, no effect of insulin on lactate oxidation (nor an inhibitory effect on alanine release) was observed; [14C]glucose incorporation into skeletal-muscle lipids was stimulated by 50 munits of insulin/ml, but the rate was still only 10% of that observed in lean Zucker rats. 4. The data indicate that the skeletal muscle of obese Zucker rats is insulin-resistant with respect to both glucose-transport mechanisms and intracellular pathways of glucose metabolism, such as lactate oxidation. The excessive degree of insulin-insensitivity in skeletal muscle of obese Zucker rats may represent a causal factor in the development of the glucose intolerance in this species.
Effect of physical training on glucose tolerance and on glucose metabolism of skeletal muscle in anaesthetized normal rats.
The effect of physical training on glucose tolerance in vivo and skeletal muscle glucose metabolism in vitro was investigated in normal rats. Treadmill running for 10 days up to 240 min/day led to a decrease of basal and glucose-stimulated plasma insulin levels without major alterations of the IV glucose tolerance (1 g/kg body weight). Swim training of two weeks' duration, i.e. exercise up to 2 X 75 min/day, which did not induce significant changes in body composition, skeletal muscle glycogen levels or citrate synthase activity, resulted in a significant improvement of IV glucose tolerance and substantial reductions of basal and glucose-stimulated plasma insulin levels. Associated with this apparent improvement of insulin sensitivity in vivo, significant increases of the insulin-stimulated glucose uptake (+ 55%) and lactate oxidation + 78%) in vitro were found on perfusion of the isolated hindquarter of swim-trained animals. It is suggested that mild physical training can improve glucose tolerance and insulin sensitivity in normal rats, at least in part, due to an increase of insulin sensitivity of skeletal muscle glucose metabolism.
Absorption kinetics of subcutaneously injected insulin. Evidence for degradation at the injection site.
The absorption of subcutaneously injected insulin was examined by injecting semisynthetic [3H] insulin in anaesthetized pigs and subsequently analysing the tissue excised from the injection site. Contrary to previously accepted views, a significant proportion of insulin was degraded at the injection site. The disappearance of intact [3H] insulin from the injection site followed a monoexponential function with a half-time of 59 min.
Preparation of rhenium-186 labelled EHDP and its possible use in the treatment of osseous neoplasms.
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Distribution and metabolism of intravenously injected tritiated insulin in rats.
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Percentage binding of testosterone and dihydrotestosterone and unbound testosterone and dihydrotestosterone in rabbit maternal and fetal plasma during sexual organogenesis.
The percentages of bound testosterone (17 beta-hydroxy-4-androsten-3-one; T) and dihydrotestosterone (17 beta-hydroxy-5 alpha-androstan-3-one; DHT) and their unbound concentrations were determined in pregnant rabbits and their fetuses from the 18th day of gestation to birth. T and DHT were also measured in fetal testes. In the testis, the total T/total DHT ratio, very high at 22 days (73.7 +/- 15.2), decreased until birth (6.7 +/- 0.8). In male fetuses the concentrations of total and unbound circulating T and DHT were always low and did not show any peak during sexual organogenesis. The percent binding of T (from 73.0 +/- 0.5 to 77.6 +/- 0.6) and DHT (from 76.5 to 83.7 +/- 1.1) in fetuses were similar in both sexes and significantly lower than those measured in mothers (T: from 87.2 +/- 0.6 to 91.6 +/- 0.9; DHT: from 87.3 +/- 0.9 to 93.8 +/- 0.9).
Antibodies that bind biotin and inhibit biotin-containing enzymes.
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Urinary kallikrein excretion in idiopathic nephrotic syndrome.
The plasma kallikrein-kinin system, a potent vasodilator, has been implicated in causing the protein loss of the idiopathic nephrotic syndrome. However, the kidney possesses a kallikrein-kinin system separate from the plasma system. Thus, urinary kallikrein may reflect more accurately intrarenal events. Using a radiochemical esterolytic assay we measured the urinary kallikrein excretion in a patient with a minimal lesion nephrotic syndrome during relapse. Protein excretion was initially elevated (8.1 plus or minus 2.0 gm. per 24 hours) as was urinary kallikrein excretion (96.4 plus or minus 46.6 EU per 24 hours). After initiation of steroid therapy protein and kallikrein excretion decreased significantly (p less than 0.05). During the entire study kallikrein excretion was significantly correlated with protein excretion (r equals 0.89, p less than 0.01). It is tempting to speculate that activation of the intrarenal kallikrein-kinin system participates in the protein loss characteristic of the nephrotic syndrome.