PubMed Health⌕ Search

Biomedical subjects

F Stephan

Publications and source records attributed to F Stephan.

At least 37 records · Page 2Linked to original sources
PubMed1982

[Hormonal adaptation to chronic self-starvation in patients with anorexia nervosa (author's transl)].

An intravenous glucose tolerance test (glucose 0.33 g/kg bodyweight) was performed in 35 women with chronic anorexia nervosa (AN) and in 19 age-matched women of normal weight. Plasma free fatty acids (FFA), immunoreactive insulin (IRI) and growth hormone (GH) levels were measured before and after the test. Although the mean value of glucose disappearance rate K was significantly reduced in the patient group as compared with the control group, K was in fact normal (greater than or equal to 1.10 +/- 10(-2)) in 20 anorectic women (AN 1) and lowered in 15 (AN 2). The basal and post-stimulation IRI levels were decreased in all anorectic women, but particularly in the AN 2 group with impaired glucose tolerance. The glucose load elicited a striking rise in GH in patients of the AN 2 group, a slight increase in those of the AN 1 group and no change in women of the control group. FFA values before the test were high mainly in the AN 2 patients but the difference with reference values did not reach statistical significance owing to the large s.e.m. After the glucose load there was a similar decrease in FFA levels in all three groups, but levels in the AN 2 group remained significantly higher than in the control group. Hyposecretion of IRI and hypersecretion of GH may account for the impaired glucose tolerance observed in all patients of the AN 2 group. Both hormonal changes facilitate neoglucogenesis and lipolysis, thereby providing the energy substrates required for survival of the self-starved subjects. The anorectic women also had low plasma T3 enabling adjustment of the oxidative metabolism to the reduced food supply.

Adolescent↗
PubMed1982

Effect of diabetic control on the level of circulating thyroid hormones.

Basal plasma levels of thyroxine (T4), triiodothyronine (T3) and reverse T3 were determined by radioimmunoassay in 44 control subjects, 44 Type 1 (insulin-dependent) and 39 Type 2 (non insulin-dependent) diabetic patients aged from 15 to 75 years. All were clinically euthyroid. The quality of diabetic control was assessed by the percentage of glycosylated haemoglobin. In both the diabetic groups there was a significant decrease in T3 and a rise in reverse T3 whereas T4 was normal. We found no significant differences between plasma thyroid hormone levels in Type 1 and Type 2 diabetic patients. In the poorly controlled diabetics (glycosylated haemoglobin greater than or equal to 12%), T3 was 90 +/- 5 ng/dl, which differed significantly from the level found in the better controlled patients (106 +/- 5 ng/dl, p less than 0.01). In the diabetic patients without associated illness, a negative linear correlation was found between T3 and glycosylated haemoglobin and a positive correlation between reverse T3/T3 and glycosylated haemoglobin. No correlation between T3 or reverse T3 and fasting blood glucose could be established. In conclusion, many diabetics showed a low T3 syndrome suggesting that there may be an impairment in the extrathyroidal conversion of T4 to T3. This may well be enhanced by a poor diabetic control (glycosylated haemoglobin greater than or equal to 12%).

Adolescent↗
PubMed1982

Enhancement of renal compensatory hypertrophy by hyperadrenocorticism and its modulation by nutritional factors.

Renal compensatory hypertrophy (RCH) is enhanced by ACTH in the uninephrectomized rat. In the present experiments, the kidney weight and its content in protein, RNA and DNA were determined in 48 adult, female rats; 24 had free access to a NaCl solution (9 g/l) and the others to a glucose solution (50 g/l). In each group 12 rats were sacrificed 2 or 7 d. after uninephrectomy (UN). In each subgroup 6 rats were treated with ACTH (18 micrograms/100 g B.W./d) from operation until autopsy. RCH has been evaluated by the arithmetical difference between the data determined in the right control kidney excised at UN and those determined in the left solitary kidney. In all the rats, hyperadrenocorticism increased significantly the weight of the solitary kidney and its content in protein and RNA. There was a significant decrease of the DNA content of the solitary kidney in the rats sacrificed 7 d. post-UN, treated with ACTH and drinking the saline solution. DNA was not affected by ACTH in the 7 other groups suggesting that ACTH favours cellular hypertrophy mainly in the rats drinking the saline solution. The renotrophic action of hyperadrenocorticism may be related to an altered handling of Na+ and K+: there was a positive correlation between the weight gain of the solitary kidney and the urinary excretion of Na+ (r = 0.507, p less than 0.001) and of K+ (r = 0.460, p less than 0.001). Hyperinsulinism was present in all the rats given ACTH; it may act as a growth factor. Hyperglycemia played an important role in former experiments but it was absent in the present studies.

Adrenocorticotropic Hormone↗
PubMed1982

Growth hormone response to thyrotropin-releasing hormone in insulin-dependent diabetics with or without severe microvascular lesions.

Plasma levels of growth hormone (GH) were determined in fifty-two non obese insulin-dependent diabetics (IDD) and in twenty eight control patients before and after the i.v. administration of 250 micrograms in thyrotropin-releasing hormone (TRH). The mean basal plasma GH level in the IDD was normal. Administration of TRH elicited a rise of GH above 6 ng/ml in 40% of the IDD whereas no elevation occurred in any control subject. The basal and post-stimulative GH levels were similar in diabetics with mild retinopathy and in diabetics without microvascular lesions. The basal and peak plasma GH levels as well as the GH increase after TRH were significantly higher in ten patients with nephropathy and severe retinopathy than in 42 IDD having no detectable renal damage. It is concluded that there is a disturbance of GH secretion in IDD. This abnormality seems to be independent of the short-term glycemic control and appears to be partially related to the presence of severe microvascular lesions. The present results do not prove a causal relationship between the abnormal GH secretion and the development of the diabetic microangiopathy as the pituitary dysfunction could also be a consequence of central microvascular lesions.

Adolescent↗
PubMed1981

[Correlation between renal compensatory hypertrophy and urinary sodium excretion in the ACTH treated rat].

In the rat, renal compensatory hypertrophy (RCH) is enhanced by the administration of ACTH (beta 1-24 corticotrophin) given at a dose of 18 micrograms/100 g. body weight/d. after uninephrectomy. In the rats drinking tap water, the enhancement of RCH by ACTH occurs without any significant change in urinary Na+ excretion. But, in the animals drinking a NaCl solution (9 g/l), ACTH determines a polyuria with hypernatriuria and a more striking increase of RCH positively correlated with the urinary Na+ excretion.

Adrenocorticotropic Hormone↗
PubMed1980

[Metabolic risks of salbutamol in diabetic patients. A study using somatostatin (author's transl)].

Salbutamol-induced diabetic ketoacidosis having recently been reported, the authors have studied the metabolic changes produced by the drug in 6 nondiabetic patients. All patients received a 3-hour infusion of salbutamol (S) 20 z g/minm. On the following day, three of these were given somatostatin (SRIF) 100 mg/hour mixed with S infused at the same rate, whilst the remaining 3 patients received SRIF alone. On the 3rd day, patients of the first sub-group received the same infection of S and SRIF as before plus exogenous glucagon 90 ng/kg/hour. Somatostatin is know to inhibit insulin and glucagon secretion. Exogenous glucagon was given in order to reproduce the metabolic conditions of insulin-deficient diabetes mellitus. Salbutamol alone induced a small rise in blood glucose and insulin, free fatty acids, glycerol and ketonic bodies, but no changes in endogenous glucagon. SRIF alone produced no significant metabolic variations. In the presence of SRIF, all salbutamol-induced metabolic changes were increased. Adding glucagon mainly resulted in high levels of ketonic bodies. All variations correlated with each other. Thus, whilst the hyperglycaemic, lipolytic and ketogenic effects of S in non-diabetic patients are partly masked by insulin hypersecretion, they are enhanced in the absence of insulin and, to an even greater extent, by an excess of glucagon. Diabetic patients treated with salbutamol should therefore be under close surveillance and have their insulin dosage increased.

Adult↗
PubMed1980

[Thyrotoxicosis with low T3 and high reverse T3 levels. 9 cases (author's transl)].

In common forms of hyperthyroidism serum levels of triiodothyronin (T3) are higher than those of thyroxin (T4) and isolated elevations of serum T3 have even been noted. We report 9 cases of proven hyperthyroidism with normal or low levels of T3 and elevated T4 and reverse T3 (rT3). Most out of the patients were more than seventy years old and had associated diseases. Our data show that the low T3 with elevated rT3 syndrome--which has been noted in many metabolic and pathologic conditions--can coexist in hyperthyroidism. They emphasize the lack of diagnostic discrimination of T3 assays in thyroid dysfunction especially in the older patient or one with associated disease.

Adult↗
PubMed1979

Influence of nutritional factors on the renotrophic action of ACTH in the uninephrectomized rat.

In the rat, renal compensatory hypertrophy (RCH) was apparent 48 h after uninephrectomy; it was significantly enhanced by long-acting beta1-24-corticotrophin (ACTH) when the animals had free access to food and a NaCl solution (9 g/l). In rats starved after uninephrectomy but drinking the NaCl solution freely, RCH was suppressed: the weights of the body, heart, liver, and solitary kidney were reduced. In similarly starved rats treated with ACTH, the weights of the heart and the solitary kidney were normal. RCH was also impaired in rats fed only a glucose solution (30 g/dl) after uninephrectomy, but it is restored by ACTH, which significantly increases the weight of the remaining kidney. This renotrophic action of ACTH may be related to hyperglycemia and, perhaps, elevated urinary K excretion, which occur in hyper-adrenocorticism and increase the work load of the nephron.

Adrenocorticotropic Hormone↗
PubMed1979

[Lithium and thyroid function. Significance of the TRH test in the diagnosis of lithium-induced thyroid dysfunction].

The treatment by lithium is known to involve certain endocrine complications. Those concerning the thyroid function, with risk of a frank hypothyroidy, are the most important. Aiming to appreciate the frequence and the intensivity of the endocrine effects of lithium, the thyroid parameters and the steady state of the hypothalamo-pituitary-thyroid axis were tested using the TRH test in 52 patients with maniaco-depressive psychosis with special attention to TSH, prolactin and growth hormone: 24 out of them were treated for 1 month to 6 years by lithium; the 28 others were considered as controls. The lithium treatment involves a decrease in the free thyroxine index (1.78 +/- 0.09 vs 2.16 +/- 0.09; p less than 0.01), an increase in the mean baseline TSH level (5.80 +/- 1.49 vs 2.70 +/- 0.24 microU/ml; p less than 0.05) and a noteworthy increase in the TSH responsiveness to TRH (22.7 +/- 2.14 vs 9.75 +/- 1.63 microU/ml; p less than 0.005). The TSH supranormal responses were neither correlated with the length of the treatment nor with the age of the patients. They appear as the consequence of a decrease in the thyroidal hormone secretion. The basal and stimulated prolactinemias remain comparable in the two groups of patients and no response of growth hormone occured after TRH. The TRH test must be considered as a useful complement for the surveillance of the patients treated with lithium because it permits to diagnose early the lithio-induced thyroid dysfunction.

Adolescent↗
PubMed1978

[Anorexia: a redoubtable complication of the surgical treatment for obesity after jejuno ileal by-pass (author's transl)].

Three cases of severe anorexia are reported. It results in a strong protein malabsorption with hepatic steatosis and in a syndrome of mental depression which needed the re-establishment of the intestinal-continuity. Although a mild post-operative anorexia is regular and contributes to the weight loss, massive anorexia must be considered as a new and redoubtable unpredictible complication of the surgical treatment for obesity, which may hinder the intestinal adaptation and increase the protein malabsorption.

Adult↗
PubMed1978

[Effects of fasting and of ACTH on renal compensatory hypertrophy in the 48 hour uninephrectomized rat].

Renal compensatory hypertrophy (R.C.H.) is determined 48 h. after uninephrectomy in fed and fasting rats having free access to a NaCl solution. ACTH (18 gamma/100 g BW/d/2d) enhances R.C.H. in the fed animals. R.C.H. is severely impaired by food deprivation and the remaining kidney looses weight; a normal kidney weight can be maintained if the fasted, uninephrectomized rat is treated with ACTH. These experiments suggest that the stimulation of the adrenal cortex by ACTH has a renotrophic effect. This action may be related to the elevation of blood glucose or/and to the fall of the concentration of plasma K+.

Adrenal Cortex↗