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

Biceps, triceps, subscapular, and suprailiac skinfolds were measured in 40 newborn infants of diabetic mothers. Maternal fasting blood-glucose and mean blood-glucose in the third trimester correlated significantly with neonatal skinfold thickness. Skinfold measurement, when compared with a reference range for gestational age, may be a convenient way of assessing one effect of maternal diabetes on the fetus. Gluteal adipose-cell diameter was measured in 31 infants of diabetic mothers. The fattest babies had the largest adipose cells and there was a significant positive correlation between maternal fasting blood-glucose and neonatal adipose cell diameter. These findings are consistent with the hypothesis that in diabetic pregnancy fetal hyperglycaemia and hyperinsulinism stimulate increased triglyceride synthesis in adipose cells and enlargement of adipose cells and lead to an increase in fetal subcutaneous fat.
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PMID:Subcutaneous fat in newborn infants of diabetic mothers: An indication of quality of diabetic control. 6 56

The present experiments have tested the hypothesis that ventromedial hypothalamic (VMH) lesions enhance insulin secretion by neural mechanisms. Rats were made diabetic by injecting streptozotocin to destroy their own pancreatic beta-cells. Subsequently, transplants of fetal pancreatic tissue were placed under the renal capsule. VMH lesions were placed in rats whose diabetes was cured with transplants as well as sham-transplanted animals. The animals were followed for 4 wk. The lesioned rats with pancreatic transplants gained no more weight than the sham-operated controls. There was no significant rise in insulin in the transplanted rats after VMH lesioning, but the VMH lesioned rats with intact pancreatic tissue showed the expected rise in insulin. Food intake rose 71% in the VMH lesioned rats with intact beta-cells, but only 23% in the VMH lesioned rats with transplants. Hypertrophy of the pancreatic islets was also observed in the VMH lesioned rats with an intact pancreas, but was not found in the VMH lesioned rats with a transplanted pancreas. Thus, transplantation of pancreatic tissue beneath the renal capsule of diabetic rats prevented the characteristic hyperphagia, hyperinsulinemia, and obesity in VMH lesioned rats whose pancreas was free from intact innervation. The results support the hypothesis that neural mediation of the rise in insulin is the primary factor in the development of hypothalamic obesity.
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PMID:Transplantation of pancreatic beta-cells prevents development of hypothalamic obesity in rats. 10 13

Longitudinal studies of the rhesus monkey reveal a syndrome of diabetes mellitus in those that become middle-aged and obese. The sequence of events in the development of the disease progresses from normoinsulinemia with normoglycemia through stages of hyperinsulinemia followed by below normal insulin levels with hyperglycemia and glycosuria. We believe the rhesus to be an excellent nonhuman primate model for maturity-onset diabetes in humans.
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PMID:The course of development of glucose intolerance in the monkey (Macaca mulatta). 10 70

Prolactin levels were measured in 84 patients aged 20 years with hypogonadism, both under baseline conditions and after stimulation with TRH. In those with impuberty from delayed puberty or gonadotropin insufficiency, baseline blood prolactin levels were normal but the response after stimulation was reduced in a significant manner. In patients with Klinefelter's syndrome, both baseline and reserve blood prolactin levels were increased. No correlation was observed between these abnormal levels and the usual clinical and biological disturbances found in this disorder (gynaecomastia, diabetes, hyperinsulinism, changes in 5-alpha-reduction). The significance of this hyperprolactinaemia remains obscure.
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PMID:[Blood prolactin levels in male hypogonadism (author's transl)]. 12 17

The decrease of insulin binding to plasma membranes of liver, adipose, and muscle tissues observed in obese-hyperglycemic (ob/ob) mice was reversed towards normal by prolonged fasting or streptozotocin treatment. The extent of this reversal was related to that of the decrease in hyperinsulinemia of the obese mice. In contrast, binding of glucagon to liver plasma membranes was little influenced by fasting or streptozotocin treatment of obese animals. The relationship between insulin binding and metabolic effects of the hormone did not appear to be identical in all tissues. In muscle, insulin binding and insulin effect on glucose uptake and metabolism changed in parallel--i.e., when binding increased, tissue sensitivity to the hormone increased. In the liver, the increase in insulin binding that followed fasting or streptozotocin treatment was not accompanied by any detectable metabolic effect of insulin on hepatic metabolism. A similar situation appeared to prevail in adipose tissue. The varying relationships observed between the state of insulin binding to membranes and the target tissue responsiveness to the hormone probably reflect the multiplicity of the factors operative in these processes and help us to understand why the over-all obese-hyperglycemic syndrome of ob/ob mice cannot be improved simply by decreasing endogenous hyperinsulinemia.
Diabetes 1977 Jun
PMID:Effect of fasting and streptozotocin in the obese-hyperglycemic (ob/ob) mouse. Apparent lack of a direct relationship between insulin binding and insulin effects. 14 Aug 28

Diabetes mellitus was induced in female Wistar rats by injections of either alloxan or streptozotocin, and their embryos were found to have significantly higher incidences (7.5%) of brain and heart abnormalities (non-closure of neural folds, and deformities of heart chambers) at mid-gestation than controls (2.2%). There were also increased numbers of resorptions (25% in diabetic animals: 7.2% in controls). Both drugs produced similar abnormalities. External and X-ray examination of 488 foetuses from streptozotocin-treated animals at 20 days showed eight cases of exomphalos, two cases of micrognathia with tongue protrusion, and 34 cases of incomplete sacral ossification. This last deformity occurred also in foetuses of mildly diabetic animals, and has been seen occasionally in infants of human diabetic mothers. Other evidence suggests that skeletal deformities may be due to hyperinsulinism in the foetuses of diabetic mothers. Even a mild or pre-diabetic condition may set the foetus at risk.
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PMID:Embryonic malformations in rats, resulting from maternal diabetes: preliminary observations. 14 55

In view of the potent influences of the central nervous system on glucose metabolism and on its hormonal regulators, and our recent finding of insulin and insulin receptors throughout the central nervous systsem, we have examined extreme conditions of hyperinsulinemia (obese mice) and hypoinsulinemia (streptozotocin-treated rats) with respect to changes in brain insulin and receptor content. Sprague-Dawley rats given streptozotocin (100 mg/kg body wt) developed severe diabetes and by 48 h showed no change in brain insulin. Rats given 65 mg/kg streptozotocin also had severe diabetes, but survived longer. Both at 7 d and at 30 d after streptozotocin treatment there was no significant change in brain insulin or in brain content of insulin receptors, despite the fact that peripheral hepatic receptors were elevated and pancreatic insulin was markedly depleted. The obese mice were studied at 8-10 wk when peripheral plasma insulin concentrations were 50-fold elevated and receptors on peripheral target cells were reduced to congruent with40-50% of normal; brain insulin concentrations and receptor content were indistinguishable from those of thin littermates. Thus, brain insulin, which is typically 10 times higher than plasma insulin concentrations, and brain receptor content, which is equivalent to receptor content on peripheral tissues, appears to be regulated entirely independently of hormone and receptor in the periphery. These findings are consistent with the hypothesis that insulin in the central nervous system is synthesized by the neural elements, and plays a role in the central nervous system which is unrelated to peripheral glucose metabolism.
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PMID:Concentrations of insulin and insulin receptors in the brain are independent of peripheral insulin levels. Studies of obese and streptozotocin-treated rodents. 15 37

An insulinoma was diagnosed in a fifty-seven-year-old woman suffering from frequent hypoglycemic attacks. Propranolol--a beta-adrenergic blocker--in a dose of 80 mg. per day effectively prevented recurrent hypoglycemic attacks. It also corrected the basal hyperinsulinemia as well as the increased insulin secretion which results from stimulation with glucose or arginine.
Diabetes 1975 Jun
PMID:Prevention of hypoglycemic attacks by propranolol in a patient suffering from insulinoma. 16 95

Glycogen accumulates in human fetal liver beginning at the eighth week of gestation. A parallel increase in total glycogen synthase activity is found, although the I-form activity remains low and constant throughout the first two thirds of gestation. Total phosphorylase activity increases slightly during this period, with the proportion in the active form amounting to about one half of the total throughout. After an initial rapid decline, the glycogen concentration in explants of human fetal liver remained constant for twenty to forty hours at about 20 per cent of the in vivo level. Incubation with glucagon, cyclic AMP (adenosine 3',5'-monophosphate) or its dibutyryl derivative markedly reduced tissue glycogen concentrations while insulin brought about a small increase. The effect of maximal doses of dibutyryl cyclic AMP and glucagon were the same, and the combination of agents produced no further effect. The response to dibutyryl cyclic AMP was apparent by one hour and maximal by three to six hours, whereas the response to insulin required about six hours to be detected, and it continued for at least eighteen hours. Insulin antagonized the glycogenolytic effect of low doses of glucagon or theophylline but was without significant effect in the presence of high glucagon concentrations. Glucagon stimulated cyclic AMP output from explants, and this effect was further augmented by theophylline. Insultin had no consistent effect on cyclic AMP output in either the presence or the absence of glucagon or theophylline. Incubation with dibutyryl cyclic AMP resulted in a decrease of glycogen synthase I-form activity, while insulin tended to increase this enzyme activity. In neither circumstance was the proportion of active phosphorylase altered. These results suggest that the regulation of glycogen levels in human fetal liver by cyclic AMP, glucagon, and insulin may entail alterations in the activity of glycogen synthase activity without necessitating alterations in phosphorylase activity. Cyclic AMP or glucagon was capable of depleting tissue glycogen stores in tissue from fetuses of six weeks' gestation. Insulin increased tissue glycogen concentrations in tissue from fetuses of seven or more weeks.
Diabetes 1975 Dec
PMID:Hormonal regulation of glycogen metabolism in human fetal liver. I. Normal development and effects of dibutyryl cyclic AMP, glucagon, and insulin in liver explants. 17 97

What is the interest of insulin determinations in diabetics? The interest is considerable, scientifically, particularly in obese patients with hyperinsulinism. In practice, in intermediate cases of diabetes, it may help in deciding whether or not to administer insulin. The authors studied insulin secretion in various varieties of diabetes and its role in the onset of vascular complications. Low insulin secretion seems to favour the development and frequency of the latter.
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PMID:[Our experience with the radioimmunoassay of insulin: Its practical value. Apropos of 140 cases]. 17 76


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