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

A newborn infant, small for her gestational age with macroglossia and transient insulinopenic diabetes mellitus is described. Two similar cases have been found in the literature. Flat glucose tolerance test results were found in the mother, the mechanism of which was not disclosed; there was no evidence of hyperinsulinism or malabsorption syndrome and the response of plasma growth hormone, and cortisol, and of urinary epinephrine to insulin-induced hypoglycemia was adequate. It is suggested that the triad of intrauterine growth retardation, macroglossia, and transient neonatal diabetes mellitus constitutes a distinct clinical entity. The link to the maternal abnormalities of carbohydrated homeostasis remains speculative.
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PMID:Macroglossia, transient neonatal diabetes mellitus and intrauterine growth failure: a new distinct entity? 111 Aug 57

The recent literature relating to the pathogenesis of diabetic retinopathy, with or without nephropathy, is critically reviewed. Particular attention is given to the (GH) growth hormone hypothesis. The various procedures of hypophysectomy are discussed including the possible ways of suppressing GH production or overproduction by drugs, especially with (MAP) medroxyprogesterone acetate. Personal results obtained with long-term administration of MAP in depot form on alternate days in 10 patients with advanced retinopathy are described. An inconstant and barely significant suppression of the GH response to insulin-induced hypoglycemia was noted in 6 cases showing that a complete pituitary inactivation had not been achieved. Therefore, the modifications observed in the fundus picture seem to have no relationship with such a condition. The features involved were Microaneurysms and Hemorrhages and Exudates. New vessels and retinitis proliterans were unaffected. Subjective improvement in visual acuity appeared to be more frequent with various possible explanations. MAP was without appreciable effect on the clinical and metabolic course of the diabetes or on renal function in cases of concomitant nephropathy. In light of these preliminary results, further investigation seems to be justified. (author's modified) (summary in ENG).
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PMID:[Trial treatment of diabetic retinopathy by inhibition of pituitary somatotropin secretion with MAP]. 112 48

To detect abnormalities in the secretion of insulin and growth hormone in monozygotic twin siblings of patients with juvenile-onset diabetes, their responses during oral, cortisone-primed oral, and intravenous, glucose tolerance tests and intravenous tolbutamide tests were compared to those of matched controls. The twins had higher mean serum insulin levels during all tests, but differences reached statistical significance (P less than 0.02) only in the cortisone-primed test. Growth hormone levels were higher in the twins (P less than 0.04) in the intravenous tolbutamide tolerance test. The frequency of abnormal oral glucose tolerance tests among controls, diabetic monozygotic twins and the offspring of two diabetic parents was also compared. Twins and controls had nearly the same frequency of normal tests; however, the diabetic offspring had a significantly higher (P less than 0.001) prevalence of abnormal tests. These data suggest that magnitudes of environmental and genetic factors operating in monozygotic "pre-diabetic" children of diabetic parents.
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PMID:Serum insulin and growth hormone response patterns in monozygotic twin siblings of patients with juvenile-onset diabetes. 112 40

Thirty-seven cases of neonatal hypoglycaemia were studied at follow-up at the age of 2 6/12-r 9/12 years. Two of them had had hypoglycaemia were stuafter the newborn period, and another patient died in a hypoglycaemic state following surgery at 10 weeks of age. Twenty-three children had oral glucose tolerance tests and intravenous insulin tolerance tests performed. Diabetic glucose tolerance was noted in 3 children. None of them showed symptoms of diabetes mellitus, neither was there any family history of diabetes. One of these patients had experienced hypoglycaemia after the newborn period and responded with hyperinsulinism during the glucose tolerance test. The other hypoglycaemic patient showed an exaggerated insulin release in response to tolbutamide. Deficient serum cortisol response to insulin-induced hypoglycaemia was demonstrated in 7 patients and 6 of these had concomitant minimal growth hormone response. One of these patients also had a diabetic glucose tolerance. None were of short stature. It is probable that a disturbance in the hypothalamic-pituitary-adrenal axis may contribute to an impaired carbohydrate metabolism in some patients with neonatal hypoglycaemia.
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PMID:Endocrinological aspects at follow-up studies in neonatal hypoglycaemia. 113 Jan 86

In vivo studies were undertaken in rats to provide evidence of the neural nature, tentative localization and mode of excitation of the insulin-sensitive central nervous system (CSN) glucoregulator center. In rats under light barbiturate anesthesia minute amounts of insulin injected into the carotid artery resulted in an immediate decrease of the systemic blood sugar. This hypoglycemic action of regional insulinzation of the CSN was lost when the animals were subjected to prolonged, deep barbiturate narcosis. Competitive inhibition of glucose utilization in the CSN region by intracarotid administration of 2-deoxy-D-glucose did not block the systemic hypoglycemic effect of subsequent intracarotid insulin injection. Chronic endogenous hyperinsulinemia produced by daily growth hormone treatment resulted in an insensitivity of the CNS glucoregulator center to exogenous insulin. The ratio of the quantity of the injected insulin and the pre-existent plasma insulin concentration showed direct correlation with the systemic hypoglycemic response that followed intracarotid injection. Present data support the hypothesis that the insulin-sensitive glucoregulator center located in the area supplied by the carotid artery is neural in nature, because of its inhibition by barbiturate anesthesia. The data are compatable with the working hypothesis that the center is located in the hypothalamus, since light cortical barbiturate anesthesia did not, but deep anesthesia did have an inhibitory effect on it. Marked interference by chronic hyperinsulinemia suggests that the receptor center estimates the metabolic status of the animal through means related to physicochemical binding of insulin to specific receptors. However, since our attempt to inhibit glucose utilization in the CNS was without effect on the activity of the center, it appears that the singal for the glucoregulatory impulse is not insulin facilitation of glucose utilization in the receptor area, but another parameter of insulin action.
Diabetes 1975 Apr
PMID:Studies on the nature and mode of action of the insulin-sensitive glucoregulator receptor in the central nervous system. 113

Oral administration of 1.0 or 2.5 mg bromocriptine (CB 154: 2-brom-alpha-ergocryptine) in nine of twelve patients with active acromegaly resulted in a reduction of growth hormone level by 80-90% over 8-10 hours. During treatment for 2-9 months with daily doses of 4.0 to 10.0 mg bromocriptine, there was a sustained reduction of growth hormone levels in these patients. At the same time soft-tissue swellings and tendency towards sweating decreased. In two patients with diabetes mellitus the blood sugar profile improved and in one of them the insulin dose could be markedly reduced. The rise in growth hormone levels after TRH administration also occurred during bromocriptine treatment. In those patients in whom growth hormone levels failed to react to either acute or chronic administration of bromocriptine no rise followed TRH administration. It is possible that in these patients there is a hypophyseal adenoma without hypothalamic control. On gradually increasing dosage bromocriptine was tolerated without side effects.
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PMID:[Therapy of acromegaly using bromocriptine]. 114 34

Experience in the management of 100 cases of acromegaly is described. Three quarters of these had been referred directly to the endocrine clinic at the Middlesex Hospital. The remainder were referred from the Royal Post-graduate Hospital because they were thought unsuitable for yttrium implantation. The patients were studied by clinical assessment of severity, by measurement of basal growth hormone levels on three separate mornings, and by a review of possible complications. Particular attention was paid to diabetes, hypertension, cardiomegaly, respiratory, vascular and skeletal changes as well as visual field defect. Aggressive treatment was recommended in 77 patients. It was not recommended in the remainder on account of age, intercurrent illness or the apparent mildness of the condition. Fifty-nine patients were treated by trans-sphenoidal hypophysectomy. In 46 of the 59 patients the mean basal growth hormone level has been reduced to 5 ng/ml or less. In 39 this followed operation, in five operation and subsequent X-ray therapy and in two operation and the continuing effect of previously implanted yttrium. Of these 46 patients in whom the growth hormone level has been reduced to normal, 26 do not show any deficiency of anterior pituitary trophic hormones, 13 have gonadotrophin defect (in eight of these it was present before the operation) and seven require full replacement therapy. One patient died at home six weeks after the operation from a pulmonary embolus. There was one case of CSF rhinorrhoea which stopped spontaneously and three of acute frontal sinusitis. Trans-sphenoidal hypophysectomy is shown to be an effective means of treating acromegaly. If the basal level of growth hormone is not reduced to normal by six weeks after operation, it is recommended that a course of X-ray therapy should be given. This does not apply if irradiation has been used before operation.
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PMID:The treatment of acromegaly with special reference to trans-sphenoidal hypophysectomy. 115 91

Glucose tolerance tests were carried out on 35 recently discovered Indian and Black maturity-onset diabetic patients. Differences were found between the two ethnic groups although they were of comparable age, body weight, and probable duration of diabetes at the time of investigation. Glucose tolerance was worse among Blacks and was associated with low plasma insulin levels. Blacks also had lower plasma triglyceride and cholesterol values than Indian diabetics. Plasma growth hormone respone was similar in both groups. The possible role of these factors in determining the relative frequency of ischaemic heart disease in the two racial groups is discussed.
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PMID:Carbohydrate tolerance, plasma insulin, growth hormone and lipid levels in Indian and Black diabetics. 115 33

The effect of hyperglycemia on the growth hormone response to oral L-dopa (500 mg.) was assessed in eight normal and eight insulin-dependent diabetic subjects. A peak growth hormone response of 21.0 +/- 4.0 ng./ml. (mean +/- S.E.M.), significantly above baseline (p less than 0.01), was achieved in the normal group following oral L-dopa. Glucose concentrations did not change and were approximately 80 mg./100 ml. throughout. Administration of 100 gm. oral glucose with the L-dopa, or thirty minutes thereafter, totally suppressed the growth hormone response in all eight and six of the subjects, respectively. A peak growth hormone response of 20.0 "/- 1.7 ng./ml. (mean +/- S.E.M.), significantly above baseline (p less than 0.001), was obtained in eight nonobese, insulin-dependent diabetics, in spite of prevailing hyperglycemia (mean plasma glucose 243-258 mg./100 ml.) throughout the test. Endogenous hyperglycemia was achieved in these patients by lessening the usual strict adherence to plasma glucose control for the purpose of the study. These results suggest an abnormality in the hypothalamus or pituitary of diabetic subjects allowing growth hormone responsiveness in spite of hyperglycemia.
Diabetes 1975 Jul
PMID:Effect of glucose on the growth hormone response to L-dopa in normal and diabetic subjects. 115 29

The effect of muscular exertion of moderate intensity on blood sugar (BS), plasma levels of growth hormone (GH), glucagon, and cortisol (F) has been studied in endocrinologically normal children with short stature and compared with children with clinical diabetes mellitus and obese children with normal and diminished carbohydrate tolerance. In diabetic children, physical exertion induces a rise in plasma GH levels comparable to that in controls; in obese children with normal or with diminished glucose tolerance, the rise is considerably smaller. Physical exertion caused no change in F levels in the groups tested, although basal level in the obese children was significantly higher than in the controls. Basal glucagon levels were similar in all groups and showed no change on physical exertion. The behavior of GH and glucagon in diabetic children was comparable to that in the controls even where blood sugar level was high.
Diabetes 1975 Aug
PMID:Effect of physical exercise on secretion of growth hormone, glucagon, and cortisol in obese and diabetic children. 115 40


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