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Biomedical subjects

E R Froesch

Publications and source records attributed to E R Froesch.

At least 163 records · Page 9Linked to original sources
PubMed1981

Effect of trypsin treatment of rat adipocytes on biological effects and binding of insulin and insulin-like growth factors: further evidence for the action of insulin-like growth factors through the insulin receptor.

Trypsin-treatment of isolated rat adipocytes abolishes the metabolic effects not only of insulin, but also of the insulin-like growth factors: in trypsin-treated cells, concentrations of these hormones that are otherwise maximally effective no longer stimulate 3-O-methylglucose transport and lipogenesis or inhibit epinephrine induced lipolysis. Concomitantly, the trypsin-treated adipocytes no longer display specific insulin binding. In contrast, the characteristics of the binding of the insulin-like growth factors are not grossly affected by prior trypsinization of the adipocytes. These findings add further support to the concept that the insulin-like growth factors act on glucose metabolism and antilipolysis via the insulin receptor of the adipocyte.

3-O-Methylglucose↗
PubMed1981

Radioimmunological determination of insulinlike growth factors I and II in normal subjects and in patients with growth disorders and extrapancreatic tumor hypoglycemia.

Serum levels of immunoreactive insulinlike growth factors (IGF) I and II were determined by a modified IGF I and a new IGF II radioimmunoassay in normal children and adults, and in patients with acromegaly, isolated growth hormone deficiency, and extrapancreatic tumor hypoglycemia. Serum samples were gel filtered by a simple routine procedure at acidic pH to dissociate and separate IGF from the IGF carrier protein. Mean immunoreactive IGF I levels (+/- SD; corrected for crossreactivity of IGF II) were 193 +/- 58 ng/ml in normal adult subjects, 712 +/- 245 ng/ml in acromegalic patients and 24 +/- 14 ng/ml in patients with isolated growth hormone deficiency. The lack of growth hormone alone, irrespective of an otherwise normal hormonal status, appears to be responsible for the drastic decrease of IGF I levels. Oversecretion of growth hormone does not increase the levels of immunoreactive IGF II: mean levels (+/- SD; corrected for crossreactivity of IGF I) in normal and acromegalic subjects are virtually identical (647 +/- 126 and 641 +/- 189 ng/ml, respectively). Apparently, normal growth hormone levels stimulate IGF II production already maximally. However in growth hormone deficiency immunoreactive IGF II is significantly decreased (252 +/- 99 ng/ml). Thus, IGF II, like IGF I, is growth hormone dependent. But in contrast to IGF I, the growth hormone dependence of IGF II seems to become apparent only at subnormal growth hormone levels. In normal children IGF I is age dependent: it is low in newborn cord sera (51 +/- 20 ng/ml) and gradually rises into the adult range with increasing age. At the onset of and during puberty mean IGF I levels lie above prepubertal values. In contrast, IGF II levels in normal children are independent of age and pubertal stage beyond the first year of life, whereas newborns have significantly lower IGF II values. Hypoglycemia resulting from extrapancreatic tumors is not associated with increased immunoreactive IGF I or II levels. IGF I is decreased in most of the sera (mean level +/- SD:56 +/- 39 ng/ml) whereas IGF II lies in the normal range (556 +/- 195 ng/ml).

Acromegaly↗
PubMed1981

In vivo control of insulin-sensitive phosphodiesterase in rat adipocytes by growth hormone and its parallelism to glucose transport.

As shown previously in adipocytes of hypophysectomized (hypox) rats, 3-O-methyl-glucose transport is already maximal in the basal state and insensitive to insulin. It is normalized by prolonged administration of GH to hypox rats. This study shows glucose transport in the presence and absence of phosphodiesterase (PDE) inhibitors in the fat cells of normal and hypox rats. Enhanced glucose transport in insulin-stimulated normal fat cells as well as enhanced glucose transport in adipocytes of hypox rats is inhibited by PDE inhibitors. The low Km phosphodiesterase activity, which is known to be acutely stimulated by insulin in normal adipocytes, is found to be increased in the fat cells of hypox rats, and further stimulation by insulin is not possible. Normalization occurs after GH administration for 4 days. Then, the low Km PDE activity is again low and stimulated in the presence of insulin. The similarity between the behavior of the activity of the glucose carrier system and that of the low Km PDE suggests that both may be dependent on a GH-induced membrane factor which would be acutely inhibited by insulin.

1-Methyl-3-isobutylxanthine↗
PubMed1981

Congenital familial thyroid aplasia.

A family with 4 siblings, 3 of which have hypothyroidism due to thyroid aplasia is described. A review of the literature revealed 10 families with familial occurrence of this disorder without other malformations. Therefore, thyroid aplasia or dysplasia should no longer be called "sporadic cretinism" since autosomal recessive inheritance of this disorder appears to occur rather frequently.

Adult↗
PubMed1981

Insulin hypoglycaemia in normal and adrenalectomized subjects: comparison of metabolic parameters and endocrine counter regulation.

Insulin tolerance tests were carried out in normal subjects and in adrenalectomized (ADX) patients in order to better understand the importance of counter regulatory hormones for the recovery from hypoglycaemia. Compared to normal subjects recovery of plasma glucose and of free fatty acid levels in adrenalectomized patients is retarded. The levels of glucagon are significantly higher in ADX patients during rest than in normal subjects. As expected, epinephrine and norepinephrine levels did not increase in ADX patients and, accordingly, blood pressure did not change. Growth hormone levels were the same in both groups of subjects. Interestingly, there was no clear-cut difference with regard to subjective symptoms of hypoglycaemia. It would appear that epinephrine is important for the rapid initial recovery from hypoglycaemia, whereas other hormones play a more important role later on.

Adrenalectomy↗
PubMed1981

Eleven cases of hereditary fructose intolerance in one Swiss family with a pair of monozygotic and of dizygotic twins.

A large pedigree of one Swiss family with 11 cases of hereditary fructose intolerance (HFI) is presented, among them a pair of monozygotic twins with HFI and a pair of dizygotic twins one of whom had the disorder. The clinical course of undiagnosed babies with HFI at home is described. The case histories point out the importance of the mother's awareness of the situation since in none of the 11 cases the corrected diagnosis of HFI was made by a physician.

Carbohydrate Metabolism, Inborn Errors↗
PubMed1980

[Improvement in the treatment of diabetes by means of a portable insulin-infusion apparatus. Preliminary results in 4 unstable juvenile diabetics].

Four type 1 diabetics, 10 to 21 years after onset of diabetes and with no detectable levels of plasma C-peptide, were kept on intravenous insulin for 4 months by a portable open-loop insulin infusion system (Siemens, Germany). Using this system, a constant basal rate of insulin was continuously infused into the superior vena cava. During meals additional insulin was delivered for one hour. The patients went home after a few days on the ward, during which time the doses of insulin (basal and extra rates) were established. All four patients maintained the same diet, went to work and continued their personal habits as before. Blood sugar (Glucoquant) and glucosuria (Clinitest) were regularly controlled before, during and after this period. During long-term ambulatory treatment with the insulin pump improved metabolic control was achieved, as shown by lower mean blood glucose values, decreased urinary glucose excretion and by lowering of hemoglobin AIc. All four patients felt well and the number of complications, all technical, was relatively small.

Adult↗
PubMed1980

Interactions of insulin-like growth factors I and II and multiplication-stimulating activity with receptors and serum carrier proteins.

Insulin-like growth factors (IGFs) I and II, purified from human plasma, and multiplication-stimulating activity (MSA), purified from media conditioned by the BRL 3A rat liver cell line, are polypeptides with similar biological and biochemical properties. We have compared the interaction of 125I-labeled and unlabeled MSA, IGF-I, and IGF-II with four intact cell or cell membrane preparations previously shown to possess MSA receptors: rat liver plasma membranes, chick embryo fibroblasts, human fibroblasts, and BRL 3A2 cells. In each case, specific binding of 125I-labeled IGF-I and IGF-II was demonstrated. With each 125I-labeled peptide, significant inhibition of binding and parallel dose-response curves were observed with unlabeled IGF-I, IGF-II, and MSA. Striking differences were noted, however, in the relative potencies of the unlabeled peptides as competitive inhibitors of binding. We conclude that the different specificities of binding inhibition reflect a significant heterogeneity among IGF receptors. A similar heterogeneity appears to occur among somatomedin carrier proteins in rat and human sera.

Animals↗
PubMed1980

Familial Cushing's syndrome with primary adrenocortical microadenomatosis (primary adrenocortical nodular dysplasia).

Cushing's syndrome was found in 2 of 4 siblings all of which also had other malformations. After bilateral adrenalectomy no hyperpigmentation was noted. Morphologically the adrenals of both siblings with Cushing's syndrome showed the typical lesions of the so-called microadenomatosis or primary adrenocortical nodular dysplasia with foci of eosinophilic giant cells. This is a new form of Cushing's syndrome due to an inborn error of the adrenals and no hypothalamic-pituitary dysfunction.

17-Hydroxycorticosteroids↗
PubMed1979

[Progress and developments in insulin therapy].

BANTING and BEST revolutionized diabetes therapy with the discovery of insulin 57 years ago. Since then, progress in this area has been slow despite tremendous reseach efforts. The subcutaneous injection of a depot insulin does not provide optimal control of blood sugar. True progress has been brought about by intravenous insulin administration for the management of diabetic coma. The authors do not recommend ultra low dose therapy. The prognosis of diabetic coma is much better than 20 years ago, in particular because of much improved and continuous supervision of the circulation (CVP, ECG, K+ etc.). Pancreas and islet transplantation fail in man due to immunological rejection. The "artificial pancreas" with a glucose sensor is useful for research purposes, and for controlling blood sugar for a few days at most. The implantable glucose sensor is not yet in sight. The authors have treated diabetics successfully with a programmable flexible open loop infusion program. The basal insulin infusion rate can be varied from 0.25 to 2 U/h, and rectangular one hour extra insulin infusions between 2 and 10 U/h are superimposed by pushing a button on the steering unit. The pump automatically switches back to the basal rate after one hour. No hypoglycemic reactions have been observed in patients on ths program on the ward or at home. At present, technical problems with the catheter remain to be solved before this simple therapeutic approach can be applied routinely.

Adolescent↗
PubMed1979

Receptor binding and effects of insulin and NSILA-S on glucose transport and metabolism in adipocytes from hypophysectomized rats.

Isolated fat cells from normal and hypophysectomized rats have been compared with respect to: 1) binding of insulin and NSILA-S, and 2) effects of these two hormones on glucose transport and metabolism. Although both insulin and NSILA levels were decreased in the serum of hypophysectomized rats, insulin binding was decreased to about 63% of normal, whereas NSILA-S binding remained unchanged. Basal lipogenesis was similar in adipocytes of normal and hypophysectomized rats, but was not stimulated by either insulin or NSILA-S. Similarly, neither of the two hormones stimulated the net gas exchange of "intact" fat pads from hypophysectomized rats. In striking contrast to these findings, 3-O-methylglucose transport in unstimulated fat cells of hypophysectomized rats proceeded at a maximal rate which was not further enhanced by insulin or NSILA-S. These results suggest that the lack of one or several hormones of the pituitary causes one or several enzyme deficiencies responsible for the limited rate of lipogenesis, which otherwise would proceed at a very rapid rate because of unrestrained glucose transport.

Adipose Tissue↗
PubMed1979

Transport and metabolism of fructose in fat cells of normal and hypophysectomized rats.

We have shown earlier that the glucose carrier of fat cells of hypophysectomized rats operates at maximal speed in the basal state and that these cells are insensitive to insulin. Here we characterize fructose transport and metabolism in adipocytes of normal and hypophysectomized rats. 3-O-methylglucose inhibits insulin-stimulated incorporation of [U-14C]fructose into fat cells and has no significant effect on basal fructose metabolism. In contrast, 2-deoxyglucose inhibits both basal and insulin-stimulated fructose incorporation. Insulin enhances fructose incorporation in normal adipocytes only in the absence of 3-O-methylglucose. In hypophysectomized rats, incorporation of glucose and of fructose is decreased and insensitive to insulin. In contrast to the glucose carrier, the specific fructose carrier appears to be insensitive to insulin and to continue to operate with unchanged characteristics after hypophysectomy. Thus, hypophysectomy leads to a specific alteration of the insulin-sensitive glucose carrier, whereas the insulin-insensitive fructose carrier remains unaltered.

Adipose Tissue↗