PubMed Health⌕ Search

Biomedical subjects

E R Froesch

Publications and source records attributed to E R Froesch.

At least 145 records · Page 8Linked to original sources
PubMed1983

Progesterone-controlled growth hormone overproduction and naturally occurring canine diabetes and acromegaly.

Female pet dogs exhibiting either glucose intolerance alone or glucose intolerance and acromegaly were investigated. Some dogs developed the disorder(s) during dioestrus and some animals developed the disorder(s) after they were given medroxyprogesterone acetate (MPA). Elevated fasting plasma glucose levels (12.3 +/- 1.9 mM, mean +/- SEM) were accompanied by fasting hyperinsulinaemia (144 +/- 21 microU/ml, mean +/- SEM) and drastic elevation of plasma growth hormone (GH) levels (112.6 +/- 45 ng/ml, mean +/- SEM). An iv glucose tolerance test (IVGTT) performed on all dogs revealed non-suppressibility of GH levels and glucose intolerance. Plasma concentrations of glucose, insulin and GH during IVGTT in affected dogs differed significantly from the concentrations measured in normal dogs during the same test. MPA withdrawal and/or ovariohysterectomy (OVx-HYx) in affected animals was followed by reversal of GH levels to normal and improved glucose tolerance. Acromegaly associated soft tissue changes were also reversible after MPA withdrawal and/or OVx-HYx when GH levels had dropped. In 5 dogs which had developed diabetes during dioestrus and in which a spontaneous decrease in plasma progesterone occurred during the investigation a concomittant decrease in GH levels was observed. Plasma GH measured at different stages of pregnancy in 45 dogs was found to be elevated in one animal only. The results show that the development of spontaneous diabetes/acromegaly occurring in some female dogs is related to progestagen (progesterone/MPA) exposure and that reversal of the signs is achieved by progesterone/MPA withdrawal. The results suggest that diabetes/acromegaly in the dogs studied was caused by progesterone/MPA-evoked GH elevation. Finally, the findings also suggest that the GH axis normally not appreciably responsive to progestagen exposure in some dogs becomes and/or is paradoxically controlled by physiologic levels of endogenous progesterone or low doses of MPA.

Acromegaly↗
PubMed1982

Parathormone promotes glycogen formation from [14C]glucose in cultured osteoblast-like cells.

Parathyroid hormone stimulates [U-14C]glucose incorporation into glycogen of cultured osteoblast-like calvaria cells. This effect is detectable only several hours after the addition of PTH and it is mimicked by dibutyryl cyclic AMP. In contrast to insulin (in pharmacological concentrations), PTH enhances glycogen formation only in calvaria cells, but not in fibroblasts. Insulin-like growth factor I in physiological concentrations promotes glycogen-synthesis shortly after addition.

Animals↗
PubMed1982

Insulin absorption from the abdomen and the thigh in healthy subjects during rest and exercise: blood glucose, plasma insulin, growth hormone, adrenaline and noradrenaline levels.

Insulin was absorbed faster from the abdomen than from the thigh under resting conditions and during exercise. Exercise enhanced the rate of insulin absorption marginally. The fall of blood glucose during rest and exercise was not significantly different after insulin injection into either site. The faster absorption of insulin from the abdomen during rest and exercise was reflected in a sharper rise of serum growth hormone levels and urinary adrenaline excretion. Therefore exercise should not be taken immediately after injection of a large dose of soluble insulin, particularly into the abdomen.

Abdomen↗
PubMed1982

Glucose transport in adipocytes and its control by growth hormone in vivo.

Previous results showed maximally enhanced basal glucose transport in adipocytes of hypophysectomized rats and restoration to normal after human growth hormone (hGH) administration. The data suggested a hGH-dependent "limiting factor" for glucose transport in the adipocyte membrane, which is acutely inhibited by insulin resulting in enhanced glucose transport. In this study the effect of hGH was investigated with respect to dose and time dependence. hGH was administered by continuous infusion from subcutaneously implanted Alzet minipumps. A significant decrease of basal glucose transport was obtained at the lowest hGH dose of 50 mU/day for 6 days. This effect of hGH was strictly correlated to the effects on growth (tibial epiphyseal width, DNA synthesis, body weight, serum level of insulin-like growth factor). The effect of hGH on basal glucose transport was already observed after 12 h of infusion, and it increased to a maximum after 3 days. The data support the concept that GH regulates the glucose transport system in adipose tissue in vivo.

3-O-Methylglucose↗
PubMed1982

Insulin-like growth factor in pregnancy: studies in a growth hormone-deficient dwarf.

Serum concentrations of insulin-like growth factors I and II (IGF I and IGF II) were measured before, during and after pregnancy in a GH-deficient dwarf. At no time during these periods did the patient secrete GH in response to an arginine infusion or insulin tolerance test. IGF I and IGF II concentrations before pregnancy were low and similar to those of patients deficient only in GH. During the 35th week of gestation, IGF I and IGF II serum concentrations were within the normal range (165 and 127 ng/ml for IGF I and 740 and 860 ng/ml for IGF II). Abnormally low values of IGF I and IGF II were again recorded 36 h postpartum and 35 days later. These data indicate that some material, probably of placental origin, stimulates the secretion of not only IGF I, but IGF II as well. Alternatively, the human placenta may produce IGF. Such secretion can occur without the prior maternal secretion of pituitary GH.

Arginine↗
PubMed1982

Is extrapancreatic tumor hypoglycemia associated with elevated levels of insulin-like growth factor II?

We have tried to answer the still controversial question of whether or not extrapancreatic tumor hypoglycemia is associated with elevated levels of insulin-like growth factor II (IGF II), keeping in mind that controversial results may be due to methodological differences. Serum levels of IGF II were determined by a rat liver membrane radioreceptor assay and by RIA. Serum samples were gel filtered at acidic pH, and some sera were also tested after acid-ethanol extraction as an alternative method for dissociating and separating IGF from the IGF carrier protein. Additionally, the radioreceptor assay was performed with a labeled partially purified IGF preparation [nonsuppressible insulin-like activity soluble in acid-ethanol (NSILA-s "70")] that was used by a group reporting elevated NSILA-s levels in about 40% of their patients with tumor hypoglycemia. Mean serum levels of receptor-reactive IGF II and immunoreactive IGF II (+/- SD) were 436 +/- 169 and 540 +/- 256 ng/ml in 22 patients with tumor hypoglycemia, as compared with 578 +/- 155 and 647 +/- 217 ng/ml in 28 normal adults. This pattern of slightly, but not significantly lower mean IGF II values in tumor hypoglycemia was unchanged when a less pure IGF preparation (NSILA-s 70) was used as a tracer or when the sera were extracted with acid-ethanol. Thus, hypoglycemia resulting from extrapancreatic tumors is not likely to be associated with increased receptorreactive or immunoreactive IGF II levels.

Adolescent↗
PubMed1982

Insulin-like growth factors in the fed and fasted states.

The effect of GH administration (5 mg twice daily for 5 days) on the serum concentration of insulin-like growth factors I and II (IGF I and IGF II) was compared in GH-deficient subjects during a period of fasting and a period of normal food intake. Before treatment with GH, the mean concentration of IGF I was 35.2 +/- 7.5 ng/ml. After 5 days of GH treatment in the fed state, IGF I increased nearly 10-fold to 317.4 +/- 55.9 ng/ml (P less than 0.001 vs. pretreatment value). During fasting, identical treatment of the group resulted in only a modest increase of IGF I to 81 +/- 23 ng/ml (P less than 0.001 vs. fed state response). The serum concentration of IGF II before therapy was reduced to only 174 +/- 37 ng/ml. With GH given in the fed state, IGF II increased to 793 +/- 171 ng/ml. These data suggest that IGF II, like IGF I, is GH dependent and, hence, a somatomedin. GH therapy in the fasted state increased IGF II to 437 +/- 70 ng/ml (P = 0.05 vs. fed state response). In a second study, six normal subjects were fasted for 72 h. The integrated serum IGF I concentration (24 samples/subject) decreased 42% by the third day of fasting; IGF II decreased 27% during the same period. The data from both studies are consistent with the conclusion that the metabolic milieu of fasting inhibits IGF secretion in man. IGF I appears to be affected more than IGF II.

Adult↗
PubMed1981

Dwarfism in the pygmy. An isolated deficiency of insulin-like growth factor I.

Insulin-like growth factors (IGFs) I and II, which are present in normal human beings, were measured in serum samples from 11 pygmies from the Central African Republic, 31 controls, and 12 patients with growth hormone deficiency. The mean serum concentration of IGF-I (+/- S.E.M.) was 68.6 +/- 8 ng per milliliter in pygmies, as compared with 193 +/- 10 ng per milliliter in controls (P less than 0.001) and 24 +/- 4 ng per milliliter in patients with growth hormone deficiency (P less than 0.05). Mean serum concentrations of IGF-II in controls, pygmies, and growth hormone-deficient patients were 647 +/- 22, 503 +/- 37, and 252 +/- 29 ng per milliliter, respectively. The serum IGF-I concentration was within the normal range in only one pygmy, whereas IGF-II values were within the normal range in 10 of 11. Pygmies appear to have a major defect in the production of IGF-I.

Adolescent↗
PubMed1981

[Incidence and clinical manifestation of ACTH-producing pituitary adenoma after bilateral adrenalectomy for Cushing's syndrome (Nelson syndrome)].

29 out of 39 patients bilaterally adrenalectomized for pituitary-dependent Cushing's syndrome between 1958 and 1979 have been followed up at regular intervals. ACTH-producing pituitary adenomas were detected and removed in 9 of them up to 1981. In 4 additional patients an enlarged sella turcica was already found at the time they had Cushing's syndrome, and therefore they were first treated by pituitary surgery or radiotherapy. In the adrenalectomized patients hyperpigmentation was the major clinical symptoms of the adenoma. Only in three instances did extrasellar growth of the adenoma cause ophthalmoplegia or narrowing of the visual fields. The existence of intrasellar ACTH-producing microadenomas in 5 additional patients seems highly probable in view of hyperpigmentation, excessively elevated plasma ACTH concentrations and radiological evidence of sella deformations. These observations indicate that in patients adrenalectomized for pituitary-dependent Cushing's syndrome ACTH-producing adenomas are more common than previously assumed. Moreover, according to recent reports, ACTH-producing microadenomas are frequently found in pituitary-dependent Cushing's syndrome and are assumed by many clinical endocrinologists to be the primary cause of this disease. Therefore, bilateral adrenalectomy is no longer the undisputed therapy of first choice and it is necessary in each individual case to consider carefully whether an attempt to remove selectively an ACTH-producing pituitary adenoma by microsurgery might not be preferable.

ACTH Syndrome, Ectopic↗
PubMed1981

[Control of the juvenile diabetic with the insulin dosage device: indications and uses].

The Clinitest was used to assess the effect of inpatient treatment in 24 labile insulin-dependent diabetics with a portable open loop insulin infusion device. The Clinitest results one month prior to hospitalization were compared with those during 3 months following inpatient treatment. During the first month after the hospital stay 21 patients (88%) were better controlled. Only 15 (63%) maintained better control for the whole period of 3 months. After the hospital stay the patients experienced an average of 4 more slight hypoglycemic episodes than before hospitalization. In patients who were better controlled for the whole period of 3 months the insulin dose had been adjusted considerably. Besides inadequate daily adjustment of the insulin dose, half the patients were not sufficiently motivated and did not cooperate with their diabetologists. One third of the patients did not follow a diet and one fifth practiced inadequate insulin injection techniques. These were the major causes of poor control prior to hospitalization. The results show that short term treatment with an open loop insulin infusion device is worth while for all diabetics in whom less than one third of all Clinitests are sugarfree, and also for all those in whom there are doubts about the actual insulin requirement.

Adolescent↗