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

Nineteen patients suffering from chemical diabetes either with (group A, ten cases) or without (group B, nine cases) reactive hypoglycaemia were included in the study and compared with seven control (group C). The following variables were measured over a 5 hour period during a standard oral glucose tolerance test (OGTT): (i) blood glucose by continuous monitoring; (ii) plasma insulin and glucagon levels by radioimmunoassay. Furthermore, in five diabetics of group A, the data from the standard OGTT were compared with those from a pectin-supplemented OGTT (9 g per square meter of body surface). Although the insulin response was similar glucagon levels were significantly higher (45.1 +/- 11.8 pmol/l) (p less than 0.01) in group B than in group A (9.6 +/- 1.3) and C (8.1 +/- 1.4 at 30 minutes). The high glucagon levels noted in group B may explain the absence of reactive hypoglycaemia. The pectin supplementation improved the OGTT pattern by blunting the blood glucose peak (p less than 0.05), and avoiding the reactive hypoglycaemia (p less than 0.01). The addition of pectin did not produce any significant effect on the insulin response while a significant increase in glucagon concentrations (p less than 0.05) was observed beyond the 150th minute. Therefore, the data suggest that pectin may improve the OGTT pattern by increasing the glucagon response in the late period of the test. The development of postprandial reactive hypoglycaemia seldom coincides with a plasma glucagon peak, while the absence of reactive hypoglycaemia tends to be associated with high levels of glucagon, as is the case in overt diabetes mellitus.
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PMID:[Late hypoglycaemia in chemical diabetes. Abnormalities of pancreatic glucagon secretion and effect of pectine (author's transl)]. 54 86

Two patients are described with asymptomatic low blood glucose and excessive in vitro consumption of glucose by leukocytes before separation of the serum for assay. This may be a more common problem than is appreciated and need not be associated with leukemia or extreme leukocytosis. The circumstances that allow this avoidable type of artifactual hypoglycemia may also produce factitious euglycemia during evaluation of suspected diabetes mellitus.
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PMID:Leukocytosis and artifactual hypoglycemia. 57 9

In spite of the continuing debate, it is possible to summarize the present state of our knowledge and to draw the following conclusions: 1. Microangiopathy of diabetes can be produced by pure insulin-deficiency in human subjects and experimental animals. 2. Evidence supports the concept that the pathology is due mainly to the deranged metabolism following insulin deprivation. 3. Repair of the insulin deficiency in animals has been shown to prevent the vascular damage associated with insulin deficiency. 4. Present methods of therapy have not been successful in preventing vascular complications in the noninsulin-dependent middle-aged diabetic patient; and, based on the findings of the University Group Diabetes Program, there is reason to believe that new methods of therapy must be realized to improve this outlook. 5. The efficacy of "compulsive control" for prevention of microangiopathy in insulin-dependent diabetic patients has not been adequately studied. Based on the results of animal experiments, the prudent physician should make every attempt to restore a normal physiological cellular environment in these patients with the expectation that this will offer the patient the best opportunity to minimize degenerative complications. Prospective observations are needed on the effects of hypoglycemic episodes which may be inevitable under these circumstances, but there is no evidence at present to suggest that mild hypoglycemia is of itself detrimental. 6. All individuals interested in the prevention of the complications of diabetes using available therapeutic methods should work to encourage a prospective clinical trial carefully designed from both an ethical and scientific point of view to obtain answers to the questions raised here.
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PMID:The role of diabetic control in diabetic retinopathy. 58 92

A study was made of 149 patients with various endocrine diseases, and 30 healthy persons. Despite the sharply increased initial level of growth hormone, somatotropic function of the adenohypophysis was considerably depressed. In patients with hypophysial, cerebral, and somatogenic nanism somatotropic function of the hypophysis proved to be lowered. In diabetes mellitus of moderate severity without any vascular affections with the normal initial blood somatotropin level reaction to insulin hypoglycemia was sharply diminished. Persons suffering from prediabetes displayed a tendency to the change of the somatotropic function of the hypophysis. With increasing adiposity there is a reduction of the initial level of blood growth hormone and of the somatotropic activity of the hypophysis in Itsenko-Cushing's disease and thyrotoxicosis was apparently connected with disturbances of the hypothalamo-hypophysial interrelations.
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PMID:[Somatotropic function of the hypophysis in endocrine diseases]. 60 Sep 25

Glucose disappearance and insulin response were determined in mother--infant pairs of normal, gestational diabetic and diabetic pregnancies following an intravenous glucose load. Mothers were studied in the third trimester of pregnancy and at least 6 wk postpartum. Significant differences were present in glucose disappearance and insulin response in both gestational diabetic and diabetic mothers during pregnancy compared with the control group. Infants were studied within 4 h of birth while fasting, and glucose and insulin levels followed through the first 3 days of life. Neonatal hypoglycemia did not occur and glucose disappearance (KT) was not different among the three groups. There was no correlation between maternal glucose tolerance or insulin production and that of their infants. The only distinguishing factor among the infants was higher insulin production in infants of diabetic mothers during the 60-min intravenous glucose tolerance test which persisted up to 4 h following the infusion. It is concluded that factors other than the degree of maternal glucose tolerance are responsible for the development of neonatal hypoglycemia in infants of diabetic mothers, most notably control of maternal diabetes, the amount of glucose infused immediately before delivery and neonatal glucose production.
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PMID:Glucose disappearance in infants of diabetic mothers. I. Relationship to maternal glucose tolerance and insulin production. 61 12

To examine the effects of leg exercise on insulin absorption from various injection sites, 125I-labelled rapid actin insulin (9 units) was injected subcutaneously into the leg, arm or abdomen of patients with insulin-dependent diabetes before one hour of intermittent leg (bicycle) exercise and on a resting, control day. Insulin disappearance from the leg increased by 135 per cent during the first 10 minutes of leg exercise (P less than 0.05) and remained 50 per cent above resting levels after 60 minutes (P less than 0.02). Leg exercise had no effect on insulin disappearance from the arm, but insulin disappearance from the abdomen was reduced during the post-exercise recovery period (P less than 0.02). As compared to leg injection, arm or abdominal injection reduced the hypoglycemic effect of exercise by 57 per cent (P less than 0.02) and 89 per cent (P less than 0.005), respectively. Leg exercise accelerates insulin absorption from the leg. Arm or abdominal injection avoids this acceleration during leg exercise and reduces exercise-induced hypoglycemia.
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PMID:Effects of leg exercise on insulin absorption in diabetic patients. 61 37

In the course of familial idiopathic haemochromatosis with diabetes, after stimulation with arginine, the alpha cell responds perfectly to stimulation, in contrast to the case of chronic pancreatic diseases. After an oral glucose load, there is no reduction in plasma glucagon concentrations, and a paradoxal increase is sometimes seen. These results are quite similar to those reported in common diabetes. Secretion of growth hormone after an infusion of arginine and insulin hypoglycaemia seem to be significantly reduced in comparison with normal subjects and those suffering from common diabetes, paired and explored using the same protocol. This may perhaps explain the low degree of severity and slow course of associated vascular disease.
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PMID:[Familial idiopathic haemochromatosis with diabetes. Study of glucagon and growth hormone secretions (author's transl)]. 63 72

In two cases of chronic schizophrenia complicated by diabetes mellitus, the concomitant use of the neuroleptica and oral antidiabetics was attended by the appearance of symptoms simulative of syndrome malin, i.e. hyperpyrexia, tachycardia, blood pressure instability, disturbances of consciousness, muscle rigidity, tremor, dysphagia, salivation and urinary incontinence. In one of these cases, the patient, a 47-year-old man, died 10 days later. In the other case, a 62-year-old woman, almost all the symptoms subsided after 14 days, and oral dyskinesia persisted for only one additional month. In both cases, hypoglycemia due to oral antidiabetics was not seen. In Case 2, a combined regimen of oral antidiabetics and neuroleptica was later resumed. Again, a similar set of symptoms as seen initially were noted, along with an elevation of the serum CPK level. Parenterally administered biperiden proved to be highly effective in the control of the symptoms. The pathogenetic mechanism of these symptoms might possibly be explained as potentiation of the action of the neuroleptica by oral antidiabetics.
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PMID:"Syndrome malin"-like symptoms probably due to interaction between neuroleptica and oral antidiabetic agents. 65 48

Fourteen adults in whom diabetes mellitus and coeliac disease coexist, are described. In no patient was coeliac disease diagnosed (biopsy proven) before the age of 28 years. Diabetes was recognized before coeliac disease in all except one. Diabetic control was very unstable and hypoglycaemia particularly troublesome before treatment with a gluten free diet. Following gluten restriction, insulin requirement increased in six patients, and diabetic control became more stable. Diarrhoea due to coeliac disease in a patient with coexisting diabetes, may be mistakenly diagnosed as 'diabetic diarrhoea'. However, certain clinical and laboratory features should arouse suspicion that the diarrhoea is not of diabetic origin. These included a history of gastrointestinal symptoms preceding the diagnosis of diabetes, the occurrence of repeated hypoglycaemia, absence of neuropathy, anaemia, low serum folate, low serum albumin and a malabsorption pattern on small bowel radiography. A definitive diagnosis of coeliac disease can be made only jejunal biopsy. The opportunity to diagnose coeliac disease in adult diabetics will usually fall to the diabetologist and wider use of jejunal biopsy in diabetics with chronic or recurrent diarrhoea is suggested.
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PMID:Diabetes mellitus and coeliac disease: a clinical study. 67 52

Induction of alloxan diabetes in 5 lactating goats resulted in reduced milk yields in 3 of the animals, while the yield was unchanged in two. After treatment of the diabetic goats with insulin for 4--5 days--the last 24 h intravenously--lactose secretion returned to the control values before alloxan administration provided that normoglycemia developed. In 2 experiments infusion of a large dose of insulin caused hypoglycemia and a 20--30 per cent reduction in lactose secretion rates. In the course of 1 h after withdrawal of the insulin infusion, patent signs of insulin deficiency developed as evidenced by steadily increasing plasma glucose concentrations. Nevertheless, lactose secretion continued at the same rate as during insulin infusion for the 4 h studied after discontinuation of the insulin infusion. In the goats where lactose secretion was reduced due to insulin-induced hypoglycemia, lactose secretion returned to control values when following discontinuation of insulin infusion the plasma glucose concentrations increased into normal and diabetic ranges. It is concluded that during insulin deficiency of short term duration, mammary lactose secretion was maintained at a normal rate. Since lactose is the major product of mammary glucose utilization, it is suggested that glucose uptake in the mammary gland was not reduced by short term insulin deficiency.
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PMID:Maintenance of lactose secretion during acute insulin deficiency in lactating goats. 67 68


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