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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hypothalamic regulatory hormones used for clinical studies are TRH, Gn-RH and somatostatin. In addition, as dopamine appears to be a physiological PIF, the dopamine agonists such as bromocriptine, could be considered as functional analogues of PIF. Gn-RH can be used to study the hypothalamic-pituitary gonadal relationship and to test the secretory reserve capacity of the gonadotrophs in disease states. Unfortunately Gn-RH testing discrimulates between pituitary and hypothalamic diseases only poorly. However gonadotrophin deficient men or women may be successfully treated with long-term Gn-RH with induction of puberty, potency, spermatogenesis and ovulation. Somatostatin has multiple actions in inhibiting endocrine and exocrine secretion but its actions are still being explored in diabetes. Bromocriptine, a long acting dopamine agonist (a functional analogue of PIF), suppresses prolactin and is highly effective in treating many hypogonadal states since hyperprolactinaemia is common. It also lowers growth hormone in acromegaly. TRH has provided a major, accurate, sensitive and safe test of thyroid function.
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PMID:Hypothalamic regulatory hormones: physiological and clinical implications. 2 68

Glycemia, growth hormone level and urinary catecholamine excretion were studied in 182 patients suffering from insulin-dependent diabetes mellitus during insulin therapy alone, and in 33 during treatment with insulin plus alpha- and beta-adrenoblockers. Under the effect of alpha-adrenoblockers glycemia proved to fall in the insulin-dependent patients, without increasing the insulin dose. The STH level diminished in these patients under the effect of alpha-adrenoblockers, even when glycemia persisted at the same level. But beta-adrenoblockers aggravated decompensation and the STH level remained unchanged. alpha and beta-adrenoblockers decreased the urinary adrenaline excretion and elevated noradrenaline, dophamine and DOPA excretion, irrespective of blood glycemia. The authors recommend the use of alpha-adrenoblockers to prevent the necessity of a considerable elevation of insulin doses during compensation in patients with the insulin-resistant form of diabetes mellitus. beta-adrenoblockers are not recommended in diabetes mellitus.
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PMID:[Effect of alpha and beta receptor blockaders on the degree of glycemia, growth hormone content of blood and catecholamine excretion in insulin-dependent diabetes mellitus]. 3 98

Diminished renal glomerular mesangial phagocytic function has been found in rats with streptozotocin induced diabetes. Similar impairment was produced by high dose cortisone and growth hormone, whereas oestrogen had a stimulant effect. The findings could be relevant to the understanding of human diabetic nephropathy.
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PMID:Mesangial cell dysfunction detected by accumulation of aggregated protein in rats with streptozotocin induced diabetes. 6 Jan 45

Changes in glucagon, growth hormone (GH), cortisol, renin and aldosterone accompanying the metabolic disturbances and dehydration of severe diabetic ketoacidosis were studied over a 24 h period in eight patients treated with a constant intravenous insulin infusion. Mean steady state plasma-free insulin levels achieved were 28.6--49 mu/1 in patients receiving 2 u/h but a satisfactory rate of fall of glucose was not always obtained until the infusion dose was increased to 4 u/h or more. The total insulin dose administered was positively correlated with the level of plasma glucagon and cortisol on admission. During insulin infusion, both glucagon and cortisol fell but the rate of fall was not related to dose or plasma level of free insulin achieved. In six of eight patients studied increments in plasma GH above admission levels were observed during insulin treatment. Admission values of both plasma renin activity and plasma aldosterone were raised. The renin levels were highest in newly diagnosed diabetics, and two patients with long-established diabetes showed only small increments despite profound dehydration. Plasma renin activity, but not plasma aldosterone correlated with the fluid and sodium retention over the initial 24 h treatment period, but not with potassium requirements. The urinary excretion rates of the small molecular weight proteins GH and insulin, were considerably elevated over the treatment and convalescent periods.
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PMID:Hormonal responses during treatment of acute diabetic ketoacidosis with constant insulin infusions. 10 71

Severe resistance to subcutaneous insulin but sensitivity to intravenous insulin persisted for 15 months in a 17-year-old diabetic girl. Heat-labile insulin-degrading activity was present in the patient's ketotic sera and in the 100,000 g fraction (soluble fraction) of adipose tissue. Serum-degrading activity was not inhibited by N-ethylmaleimide. The soluble fraction also degraded glucagon and B chain but not growth hormone or myoglobin. It was inhibited by incubation with the patient's nonketotic sera, normal sera, or Trasylol. Glutathione-insulin-transhydrogenase (GIT) activity was 66% of normal. The biopsy of adipose tissue at remission showed a normal level of insulin- and glucagon-degrading activity. The activity was eluted from Sephadex G200 as a single peak and had properties consistent with those of the insulin-specific protease (ISP). The increased degrading activity present during insulin resistance had properties not shared with ISP, suggesting the presence of an uncharacterized protease.
Diabetes 1979 Jul
PMID:Insulin resistance caused by massive degradation of subcutaneous insulin. 10 40

This study reviews the pathogenic hormonal abnormalities (insulin deficiency and stress hormone excess) in diabetic ketoacidosis. The data both supporting and negating a primary role for insulin deficiency in the pathogenesis of diabetic ketoacidosis are examined. Evidence implicating excess stress hormone secretion as a necessary event in the development of severe metabolic decompensation is discussed. The data suggest that diabetic ketoacidosis may be prevented by correcting either the relative deficiency of insulin or the excess secreation of one or a combination of the stress hormones. Studies supporting a primary role for insulin deficiency in the pathogenesis of diabetic ketoacidosis include the beneficial therapeutic response to insulin administration in ketoacidosis, development of ketoacidosis; and (3) stress hormone excess is necessary for fulminant ketoacidosis to be manifested.s following insulin withdrawal from diabetic man and animals, and hypoglycemic and hypoketonemic effects of insulin. Studies negating a primary role for insulin deficiency in ketoacidosis include the "normal" plasma insulin concentration in the majority of ketoacidotic cases, delayed onset of ketoacidosis after insulin withdrawal from diabetic man, and lack of hypolipolytic and hypoketonemic effect of insulin without prior stress hormone adipocyte and hepatocyte stimulation. Evidence that stress hormones (glucagon, catecholamines, cortisol, and growth hormone) contribute to the metabolic decompensation of ketoacidosis includes: (1) in all cases of ketoacidosis, at least one stress hormone is always elevated; (2) pharmacologic blockade of each of the stress hormones reduces the rate and/or frequency of metabolic decompensation in diabetic man; (3) removal of the pituitary and/or the adrenal gland in diabetic animals completely prevents the development of ketoacidosis after insulin withdrawal; and (4) administration of each of the four stress hormones under appropriate conditions induces metabolic decompensation in diabetic man with "normal" circulating levels of plasma insulin concentration. From these studies, the following conclusions are supported: (1) absolute insulin deficiency is an unusual cause of ketoacidosis; (2) the presence of relative insulin deficiency is necessary for the development of ketoacidosis; and (3) stress hormone excess is necessary for fulminant ketoacidosis to be manifested.
Diabetes Care
PMID:Pathogenesis of diabetic ketoacidosis: a reappraisal. 11 31

Ultrastrucutral examination of 184 pituitary adenomas demonstrated the presence of extracellular accumulations of electron dense material in 3 out of 64 cases with acromegaly. Fibrillary structures were seen in larger deposits of such material. This material was only observed in biopsies fixed directly with osmium tetroxide; initial fixation with glutaraldehyde did not retain the material and left empty spaces. Positive immuno-histochemical reaction with specific antibodies demonstrated that the extracellular material contained growth hormone (GH). The presence of this extracellular material could not be related to the age or sex of the patient nor to the duration of symptoms, size of the tumor, presence of diabetes mellitus, or concomitant secretion of prolactin. The pericapillary fibrous sheath was heavily thickened in the patient with the longest duration of symptoms, intermediate in thickness in the second and normal in the third.
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PMID:Extracellular growth hormone deposits in pituitary adenoma. 14 77

Acute insulin deficiency in rats results in a decrease in the in vitro protein synthetic activity of isolated hepatic membrane-bound ribosomes and an increase in activity of free ribosomes. These changes are prevented by concomitant insulin treatment and are reversed by the administration of insulin. The current study evaluated the role of the pituitary in the genesis of these changes. The severity of diabetes produced by streptozotocin was less in hypophysectomized (Hx) rats, and in Hx rats receiving hormone replacement, as compared with similarly streptozotocin-treated intact rats. Although acute insulin deficiency in intact rats produced the previously described increase in protein synthetic activity of free hepatic ribosomes and decrease in activity of hepatic bound ribosomes, these changes did not occur in Hx rats, even when Hx rats received replacement doses of thyroxine, ACTH, and growth hormone. Thus, the changes in hepatic protein synthetic activity that occur in rats with acute experimental diabetes mellitus are secondary to the metabolic sequalae of insulin lack and the response of the pituitary gland to insulin deficiency.
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PMID:Effect of hypophysectomy on protein synthetic-activity of free and bound hepatic ribosomes from insulin-deficient rats. 16 9

A chromophobic pituitary adenoma induced on BD IX-rats has been grafted on animals of the same strain. The transplanted tumour takes in 90-100%; it grows at a slow rate (in 7 months after grafting a weight of 7-20 g is attained). Tumour-bearing animals display gigantism and hypertrophy of adrenals; moreover, in 33% of cases, diabetes is observed. With non-diabetic animals, splenomegaly and marked leukocytosis are observed; immature white and red cells are present in the peripheral blood. Spontaneous regression of the tumour never occurs. After surgical removal, tumour regrowth and the formation of metastases are observed. Diabetes is characterised by pronounced hyperglycaemia, glucosuria, polyphagia and polydipsia. Histochemically, insulin cannot be detected in pancreas. Splenomegaly is never observed in diabetic animals. Transplanted adenoma frequently tends to stop growing. No recurrence is observable after extirpation. Spontaneous regression of the tumour sometimes occurs. Gigantism, hypertrophy of adrenals and diabetes are considered as consequences of growth hormone- and ACTH-secretion of the transplanted adenoma. At present the tumour is running in the 8th passage. It did not change its characteristics over a period of 5 years.
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PMID:Transplantable, STH-producing and diabetogenic pituitary adenoma of the BD IX-strain of rats. 17 13

Twelve acromegalic patients with clinical and biochemical evidence of active disease were studied whilst on bromocryptine (Sandoz) at a maximum dosage of 10--60 mg. The patients were followed for a period of 9--23 months. Clinically, ten patients showed a reduction or disappearance of sweating and seven patients had a reduction in soft tissue mass. Of the five patients who had diabetes prior to treatment, three reverted to normal glucose tolerance during treatment. Biochemically, there was no difference between mean plasma levels of growth hormone (hGH) before and on maximum therapy with bromocryptine. There was a significant difference between fasting plasma hGH before treatment with bromocryptine and following treatment for 9--23 months in five individual patients. Side effects were not disabling in this series except for a reversible paranoid psychosis in one patient. The overall results are disappointing; although some clinical features improved, plasma hGH levels returned to normal in only three patients. Bromocryptine has a limited place in the management of acromegaly for those patients in whom conventional therapy has been ineffective or is contraindicated.
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PMID:Treatment of acromegaly with bromocryptine. 28 86


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