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

Ninety-five nonobese, nonketotic subjects were divided into five groups (one normal and four with varying degrees of glucose intolerance) according to their plasma glucose responses during an oral glucose tolerance test. These five groups were then compared on the basis of their insulin response during the oral glucose tolerance test and on the ability of exogenously infused insulin to limit hyperglycemia during a continuous infusion of glucose and insulin, while endogenous insulin was inhibited by the infusion of epinephrine and propranolol. The mean plasma insulin response of patients with either borderline abnormalities of glucose tolerance or chemical diabetes was equal to or greater than that of normal subjects at all points during the glucose tolerance test. Thus, the glucose tolerance of these two patient groups cannot be attributed to lack of insulin. On the other hand, the mean insulin response of patients with moderate fasting hyperglycemia (plasma glucose of 110 to 150 mg/100 ml) was somewhat attenuated, and patients with severe fasting hyperglycemia (plasma glucose greater than 150 mg/100 ml) had unequivocal insulin deficiency. In contrast, all four patient groups with abnormal carbohydrate metabolism were more resistant than normal subjects to the action of insulin. These results indicate that there is a very complex relationship between insulin deficiency and insulin resistance in patients currently classified as having nonketotic diabetes. Patients with either borderline abnormal glucose tolerance or chemical diabetes are more resistant to insulin than normal subjects, and are not insulin deficient. In these patients it seems reasonable to assume that their glucose intolerance is a direct function of their insulin resistance. Patients with severe fasting hyperglycemia are suffering from both insulin deficiency and insulin resistance, and the relationship between these two variables in the genesis of hyperglycemia in these subjects remains obscure. It seems apparent from these studies that nonketotic diabetes mellitus can no longer be considered to be a simple function of insulin lack, and that in order to understand this syndrome we will need to increase our knowledge of the relationship between insulin deficiency and insulin resistance in these patients.
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PMID:Nonketotic diabetes mellitus: insulin deficiency or insulin resistance? 81 10

Muscle tissue obtained by needle biopsy from 20 diabetic subjects and from 20 age-matched control subjects was divided into two portions, one of which was fixed and processed by our routine procedure (primary glutaraldehyde fixation followed by osmium fixation and embedment in araldite) and the other was fixed initially in osmium tetroxide and embedded in maraglas, the procedure employed by Siperstein et al. Basement-membrane width of capillaries was measured by the 20-point method of Siperstein et al. and by the two-minimum-point technic developed in our own laboratory. Contrary to the experience of Siperstein et al., the prevalence of basement-membrane thickening in diabetic subjects based on mean width values and/or standard deviations in excess of 95 per cent tolerance intervals was highest (65 per cent) in minimum measurements of glutaraldehyde-fixed tissues and lowest (30 per cent) in osmium-fixed tissues (X2 = 4.9123, p less than 0.05). Internal discrepancies in the data of Siperstein et al. indicate that (1) their basement-membrane-width values derived from multiple measurements from control subjects are anomalous (low) and (2) the very high prevalence of basement-membrane thickening they reported in diabetic and in prediabetic subjects and considered as strong support for their conclusion that basement-membrane disease is independent of and precedes glucose intolerance is suspect.
Diabetes 1976 Jul
PMID:Influence of fixation and morphometric technics on capillary basement-membrane thickening prevalence data in diabetes. 81 19

The question of whether iron overload causes glucose intolerance was studied in a group of 26 multiply transfused homozygous beta thalassemics. Of the 26, 13 (50%) had some abnormality in their oral glucose tolerance test, 5 fitting criteria for definite diabetes. Glucose intolerance correlated significantly with number of transfusions received and with age of the subjects, while a positive family history for diabetes was more common in the subjects with glucose intolerance. These data and a chart review of four deceased thalassemics with overt diabetes are consistent with the following conclusions: (1) glucose intolerance is common in multiply transfused thalassemics; (2) the incidence of abnormal glucose tolerance correlates with the number of transfusions received and the age of the subject; (3) a family history of diabetes may predisose multiply transfused thalassemics to glucose intolerance.
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PMID:Abnormal glucose tolerance in beta-thalassemia major. 83 42

Thirty-one patients with subclinical diabetes, who showed diabetic or impaired glucose tolerance after treatment for diabetes, were investigated in order to clarify the abnormalities of insulin response in diabetes mellitus. These patients showed a delayed response of plasma insulin during oral glucose loading. In the tolbutamide-glucose test, in which glucose loading followed the intravenous tolbutamide injection at a 60-min interval, the insulin level at 90 min was significantly lowered in a group of 20 patients with subclinical diabetes. In the tolbutamide-glucagon test, in which 1 mg of glucagon was injected 60 min after tolbutamide injection, the maximal level of plasma insulin was significantly decreased in a group of 10 subclinical diabetes except for one patient. These results indicate that insulinogenesis and/or release of insulin were decreased even in subclinical diabetes, suggesting that such a defect in islet function might be one of the abnormalities in primary diabetes.
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PMID:Insulin response to glucose or glucagon in subclinical diabetes previously injected with tolbutamide. 83 36

The effect of ethanol on stimulus-induced insulin secretion was studied, and possible mechanisms were examined in fasting unanesthetized and unrestrained rats with indwelling jugular and aortic catheters. Glucose (150 mg.) or tolbutamide (10 mg.) was given rapidly, i.v., one hour after agavage of ethanol or saline (control). Acutely, ethanol treatment caused marked inhibition of glucose-induced insulin secretion and impaired glucose disappearance rate. Tolbutamide-induced insulin secretion was also significantly inhibited, and decline in glucose was significantly less in ethanol-treated rats. In response to ethanol, serum calcium concentration significantly declined for two hours. In another study, an ethanol metabolite, acetate (0.4 micronmole/min.) or vehicle (control) was infused for 60 minutes prior to 150 mg. glucose pulse. Acetate priming significantly potentiated glucose-induced insulin secretion and also improved glucose tolerance. It is proposed that (1) ethanol in vivo acutely induces hypocalcemia, which inhibits glucose- and tolbutamide-induced insulin secretion--which, in turn, causes glucose intolerance and prevents tolbutamide-induced hypoglycemia. (2)Acetate might be the actual petentiating influence on glucose-induced insulin secretion observed several hours after ethanol treatment.
Diabetes 1977 Apr
PMID:Effect of ethanol on stimulus-induced insulin secretion and glucose tolerance. A study of mechanisms. 84 8

The importance of genetically determined antigens of the HLA system in etiology and pathogenesis of juvenile onset diabetes (JOD) was studied in 93 JOD-patients and 68 blood relations. A close association was found between JOD and B-locus antigens B8 and Bw15, and C-locus antigen Cw3. Patients positive for one of these antigens have a 2-3 times -- and those positive for both B8 and Bw15 -- a 8.6 times greater chance of developing JOD, Evidence for a genetic heterogeneity between childhood type and later onset JOD could be obtained. B8 seems to play a particularly important role in childhood-type diabetes, whereas in the later onset JOD the antigens Cw3 and/or Bw15 might possibly represent an additional predisposing factor. Family studies have revealed a close correlation between glucose intolerance and those genes associated with JOD in blood relations below age 35. HLA-B7 which could be detected in that group of blood relations, and which was found statistically decreased in JODs might even exert some protective role. Incidence of haplotye identity in glucose intolerant siblings was almost three times higher than expected. These data provide evidence for the existence of a genetic basis which determines the susceptibility to develop JOD.
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PMID:The importance of HLA genes to susceptibility in the development of juvenile diabetes mellitus. A study of 93 patients and 68 first degree blood relations. 87 Mar 54

In 21 patients with liver cirrhosis, 35 normal subjects, 8 patients with chemical and 11 with manifest diabetes 0.5 g glucose/kg together with 14C-glucose were injected intravenously. 71% of the cirrhotics showed an impaired glucose tolerance. IRI response was exaggerated. The insulinogenic index was elevated in patients with liver cirrhosis and normal glucose tolerance and normal or subnormal in those with carbohydrate intolerance, as well as in diabetics. Decrease of the specific activity of glucose, expressing supply of non-labelled glucose to the body pool, was much more rapid in patients with carbohydrate intolerance, either hepatogenic or not, when compared at equal glucose concentrations. Moreover all groups with deteriorated glucose tolerance exhaled less 14CO2. Consequently, diabetes in chronic liver disease displays the same abnormalities as diabetes in obesity with respect to liver glucose supply and glucose oxidation. In both conditions diminished glucose assimilation is usually the result of reduced removal and increased supply. Therefore it is concluded that impaired hepatic uptake of glucose cannot be implicated as a single cause of hepatogenic diabetes.
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PMID:[Insulin resistance and blood glucose replacement rates in liver cirrhosis. Studies with 14C-glucose (author's transl)]. 90 3

Oral tolerance of glucose was determined in 40 aged subjects with fasting blood sugar values of less than 100 mg/100 ml 56% had normal tolerance, 22% normal for age, and 22% values of diabetic type. In young subjects, only 2% display sugar metabolism disturbances. After 21 days' administration of potassium salts, 34.78% of the normal and 62.5% of the diabetic subjects showed reduced mean blood sugar values for the test, with significant falls at 120' and 180'. Reference is made to other conditions in which potassium depletion is coupled with glucose intolerance, e.g. old age. The pathogenetic significance of potassium depletion with respect to senile diabetes is discussed.
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PMID:[Potassium depletion. Glucose intolerance. Senile diabetes. Study on eventual pathogenetic relationships 1]. 91 43

Plasma levels of total immunoreactive insulin and immunoreactive proinsulin were studied in 10 normal children and 15 children with chemical diabetes ranging in age from 5 to 13 years. Eleven of the children with chemical diabetes demonstrated significantly elevated TIRI during fasting and following glucose administration. There was a delay in the increment of plasma TIRI in four children with chemical diabetes, but otherwise their TIRI levels were normal. In these four children IRP was not significantly different from normal; however, in the remaining children with chemical diabetes, those with elevated TIRI, the IRP was elevated following glucose administration. Although the IRP was significantly elevated in the hyperinsulinemic group, the TIRI was also increased to such an extent that the glucose intolerance demonstrated in these patients could not be attributed to the elevated IRP.
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PMID:Insulin and proinsulin in normal and chemical diabetic children. 93 2

A study of forty patients with active lichen planus and a negative family history for diabetes showed that 42% had unequivocally abnormal oral glucose tolerance. The pattern of insulin response to glucose is similar to that seen in typical mild maturity-onset diabetes. There was no association between the presence of glucose intolerance and the duration or type of lesions. None of the patients with glucose intolerance had demonstrable islet-cell antibodies.
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PMID:Carbohydrate metabolism in lichen planus. 95 47


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