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

To evaluate hemoglobin AIc (Hb AIc) as an indicator of prolonged glucose control in pregnant diabetics, four groups of subjects were studied--16 pregnant diabetic, 13 pregnant nondiabetic, 12 nonpregnant diabetic, and 18 healthy control subjects. Hb AIc was significantly lower in the pregnant diabetic than in the nonpregnant diabetic subjects, 7.8% +/- 1.6 vs, 9.9% +/- 1.9 (mean +/- SD). No difference was present in the nondiabetic groups (4.0% +/- 0.7 vs. 4.3% +/- 0.8, respectively). Hb AIc correlated significantly with the average glucose concentrations of the preceding 60 days in both diabetic groups, suggesting that the lower concentration of Hb AIC in pregnant as compared with nonpregnant diabetic patients was because of better control of blood glucose. This was also borne out by the average of fasting glucose levels being 6.1 +/- 1.7 mmol/L in the pregnant diabetic and 10.7 +/- 2.2 mmol/l in the nonpregnant diabetic subjects.
Diabetes 1979 Jul
PMID:Hemoglobin AIc as an index of long-term blood glucose regulation in diabetic pregnancy. 44 24

Seven patients with diabetes mellitus were hospitalized and their blood sugar concentrations regulated as a result of fasting blood sugar, sugar around meals, urinary sugar, and hemoglobin AIC assays. Erythrocyte half-life as measured by 51 Cr increased in all patients from a mean of 27 days to 31 days, while hemoglobin AIC levels decreased from a mean of 10.1% to 5.6%. Leukocyte adherence increased in all patients from a mean of 28% to 51%. Most striking were the changes observed in platelet function in response to epinephrine. The length of the secondary lag phase of platelet aggregation, after a stimulus with final concentration of 70 muM of epinephrine, increased from a mean of 19 seconds to 65 seconds. Studies in additional patients confirmed an inverse correlation between hemoglobin AIC concentration and the secondary lag phase (r = 0.87, P less than 0.001). These studies found that certain secondary sequelas of diabetes can be corrected by strict carbohydrate control and confirmed that hemoglobin AIC assays provide a useful means of showing the degree of control of glucose metabolism in diabetic patients.
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PMID:Reversible hematologic sequelae of diabetes mellitus. 84 4

5-Amino-4-imidazolecarboxamide riboside (AICAriboside; Z-riboside), the nucleotide corresponding to AICAribotide (AICAR or ZMP), an intermediate of the 'de novo' pathway of purine nucleotide biosynthesis, has been shown to inhibit gluconeogenesis in isolated rat hepatocytes [Vincent, Marangos, Gruber & Van den Berghe (1991) Diabetes 40, 1259-1266]. We now report that glycosis is also inhibited and even more sensitive to AICAriboside in these cells. In hepatocyte suspensions from fasted rats, production of lactate from 15 mM-glucose was half-maximally inhibited by 25-50 microM-AICAriboside. AICAriboside influenced two regulatory steps of glycolysis: (1) it decreased the release of 3H2O from [2-3H]glucose and the concentrations of both glucose 6-phosphate and fructose 6-phosphate, indicating that it diminished the phosphorylation of glucose by glucokinase; (2) it decreased the concentration of fructose 2,6-bisphosphate (Fru-2,6-P2), the main physiological stimulator of liver 6-phosphofructo-1-kinase. Further studies showed that AICAriboside induced an inactivation of 6-phosphofructo-2-kinase, the enzyme that produces Fru-2,6-P2, without affecting the concentration of cyclic AMP. Similarly to the inhibiton of gluconeogenesis by AICAriboside, the inhibition of glycolysis became apparent after an approx. 10 min latency and persisted when the cells were washed after addition of AICAriboside, strongly suggesting that the effects were also exerted by the Z-nucleotides, which accumulate after addition of AICAriboside to hepatocytes. An increased uptake of lactate was evident when 50-200 microM-AICAriboside was added 15 min after addition of glucose. This can be explained by the higher sensitivity of glycolysis, as compared with gluconeogenesis, to inhibition by AICAriboside, and reveals the simultaneous operation of both processes.
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PMID:Inhibition of glycolysis by 5-amino-4-imidazolecarboxamide riboside in isolated rat hepatocytes. 153 Oct 10

5-Amino-4-imidazolecarboxamide (AICA) riboside, the nucleoside corresponding to AICA ribotide (AICAR or ZMP), an intermediate of the de novo pathway of purine biosynthesis, was found to exert a dose-dependent inhibition on gluconeogenesis in isolated rat hepatocytes. Production of glucose from lactate-pyruvate mixtures was half-maximally inhibited by approximately 100 microM and completely suppressed by 500 microM AICA riboside. AICA riboside also inhibited the production of glucose from all other gluconeogenic precursors investigated, i.e., fructose, dihydroxyacetone, and L-proline. Measurements of intermediates of the glycolytic-gluconeogenic pathway showed that AICA riboside provoked elevations of triose phosphates and fructose-1,6-bisphosphate and decreases in fructose-6-phosphate and glucose-6-phosphate. The effects of AICA riboside persisted when the cells were washed 10 min after its addition but were suppressed by 5-iodotubercidin, an inhibitor of adenosine kinase. AICA riboside provoked a dose-dependent buildup of normally undetectable Z nucleotides. After 20 min of incubation with 500 microM AICA riboside, ZMP, ZTP, and ZDP reached 3, 0.3, and 0.1 mumol/g cells, respectively. Concentrations of ATP were not significantly modified by addition of up to 500 microM AICA riboside when the cells were incubated with lactate-pyruvate but decreased with fructose or dihydroxyacetone. The activity of rat liver fructose-1,6-bisphosphatase was inhibited by ZMP with an apparent Ki of 370 microM. It is concluded that AICA riboside exerts a suppressive effect on gluconeogenesis because it provokes an accumulation of ZMP, which inhibits fructose-1,6-bisphosphatase.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1991 Oct
PMID:Inhibition by AICA riboside of gluconeogenesis in isolated rat hepatocytes. 165 65

An asymptotic lifetime growth model of height is introduced by modifying a fundamental growth model considering a relative measure of maturity. This model is compared with the Preece-Baines model and the Jolicoeur et al. model for 365 Japanese females collected in Hiroshima. The pooled residuals and the amount of the AIC can evaluate the goodness of fit to the longitudinal growth records. The proposed growth model is the best among three models from a viewpoint of the goodness of fit. Some special points of growth curve are characterized mathematically and the estimates of these points are compared with ones of other growth models. The larger the value of growth velocity at take-off is, the higher the final height is. An empirical Bayesian approach is applied to an asymptotic lifetime growth prediction of an insulin-dependent diabetes mellitus patient.
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PMID:On a growth model of human height. 209 15

This study reviews the new diagnostic criteria for diabetes mellitus proposed by NIH. We measured insulin levels during 75 g oral glucose tolerance test (75 g OGTT) and hemoglobin AIC levels in patients diagnosed as having impaired glucose tolerance (IGT) or non-insulin dependent diabetes (NIDDM) according to the NIH criteria. In a 75 g oral glucose tolerance test, there was no significant difference in insulin-glucose ratio between nonobese IGT and nonobese NIDDM who had fasting blood glucose levels of less than 120 mg/dl (NIDDM-A group). However, in nonobese NIDDM with fasting blood glucose higher than 120 mg/dl (NIDDM-B group), the insulin-glucose ratio was significantly lower than in the IGT or NIDDM-A group. The NIDDM-B group had a higher hemoglobin AIC levels than the IGT and NIDDM-A groups, with no significant difference between the levels of the two latter groups. These observations suggest that the impairment in the function of pancreatic B cells and the state of chronic hyperglycemia are the same in IGT & NIDDM-A groups. Therefore, the NIH standards do not appear refined enough to truly differentiate between IGT and nonobese NIDDM with fasting blood glucose of less than 120 mg/dl.
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PMID:An assessment of the new NIH diagnostic criteria for diabetes mellitus according to insulin response in a 75 g oral glucose tolerance test and levels of hemoglobin AIC. 675 57

Recently, a minor component of normal adult hemoglobin has been discovered. This hemoglobin is referred to as glycohemoglobin or Hgb AI, and it is made up of subgroups A-E (Hgb AIA-AIE). As the name implies, these hemoglobins are simply Hgb A with a hexose residue attached to each of the beta chains. The most important of the subgroups is Hgb AIC wich has a glucose molecule attached to the beta chains. The degree of glycosylation of Hgb A is directly dependent upon the concentration of blood glucose. Hgb AIC and total glycohemoglobin levels have been found to be two to three times greater in diabetics than in nondiabetics. It has also been determined that Hgb AIC and glycohemoglobin levels are reduced to near normal values when the blood glucose is well controlled. Since glycosylated hemoglobin levels represent a time-averaged blood glucose level, it is considered to be a better indicator of control than individual blood glucose levels. The glycohemoglobins are eluted quite easily before the major Hgb A component on ion exchange columns. Although Hgb AIC can be isolated by column exchange, most methods separate total glycohemoglobins, not just Hgb AIC. Thus, glycohemoblobin levels by ion exchange column separation may become the test of choice in monitoring treatment of diabetes mellitus.
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PMID:Glycosylated Hemoglobin: a literature review. 741 94

AICA riboside (0.1 to 1.0mM) caused a concentration-related increase of insulin output caused by D-glucose (5.6 to 20.0mM) in either rat isolated pancreatic islets or perfused pancreases. In the latter model, the rate of insulin release was further enhanced upon removal of AICA riboside from the perfusate. No insulinotropic action of AICA riboside was observed in the absence of D-glucose or at a low concentration (2.8mM) of the hexose. Preincubation of isolated islets for 30 min in the presence of AICA riboside (0.5 to 1.0mM) also enhanced insulin release recorded over 60 min incubation, in the absence of AICA riboside, but presence of either D-glucose (8.3mM), 2-ketoisocaproate (10.0mM), or the association of D-glucose (5.6 mM) and 2-ketoisocaproate (5.0 mM). The preincubation of the islets with AICA riboside failed, however, to augment the later secretory response to the association of L-leucine (10 mM) and either L-glutamine (10 mM) or L-asparagine (10 mM). In perfused pancreases exposed to 6 mM D-glucose, the presence of L-asparagine (10 mM) did not augment the insulinotropic action of AICA riboside. It is concluded that AICA riboside displays positive insulinotropic potential. However, the determinants of such an insulinotropic action remain to be elucidated.
Diabetes Res 1994
PMID:Insulinotropic action of AICA riboside. I. Insulin release by isolated islets and the perfused pancreas. 764 78

Preincubation of rat pancreatic islets with AICA riboside (0.1 to 1.0mM) caused a concentration-related stimulation of both 45Ca net uptake and insulin release evoked by 8.3 mM D-glucose, but failed to affect the conversion of D-[5-3H]glucose to 3HOH, the generation of 14CO2 and 14C-labelled amino acids or acidic metabolites from D-[U-14C]glucose, and the islet content in ATP, ADP or AMP. The secretory response to AICA riboside was not suppressed in islets preincubated with methotrexate. AICA riboside caused a progressive decrease in 86Rb outflow from prelabelled islets perifused at 2.8 or 6.0mM D-glucose. This effect faded out at a higher concentration of D-glucose (16.7 mM), in which case AICA riboside nevertheless provoked a delayed, progressive and not rapidly reversible enhancement of insulin output. At concentrations up to 0.4 mM, ZTP only exerted a modest effect on the activity of KATP-channels in inside-out patches of dispersed mouse islet cells. These findings raise the question whether the insulinotropic action of AICA riboside may be attributable to the sequential generation of ZMP, ZDP and ZTP from the nucleoside.
Diabetes Res 1994
PMID:Insulinotropic action of AICA riboside. II. Secretory, metabolic and cationic aspects. 764 79

It has previously been reported that exercise causes an increase in glucose uptake in skeletal muscle and also an increase in 5' AMP-activated protein kinase (AMPK) activity. 5-Aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICA-riboside), an analog of adenosine, is taken up into cells and phosphorylated to form AICA-riboside monophosphate (ZMP), which can also activate AMPK. This study was designed to determine whether the increase in glucose uptake observed with AMPK activation by AICA-riboside is due to GLUT4 translocation from an intracellular location to the plasma membranes, similar to that seen in response to contraction. Rat hindlimbs were perfused with Krebs-Henseleit bicarbonate containing 4% bovine serum albumin, washed bovine erythrocytes, 8 mmol/l glucose, and +/-2 mmol/AICA-riboside or +/-60 nmol/l insulin. Perfusion medium containing AICA-riboside was found to significantly increase AMPK activity, glucose uptake, and GLUT4 translocation in skeletal muscle above basal levels. Insulin-perfused muscles showed significant increases in glucose uptake and GLUT4 translocation, but AMPK activation was not significantly changed from basal levels. These results provide evidence that the increased glucose uptake observed with AMPK activation by AICA-riboside in perfused rat hindlimb muscles is due to an increase in the translocation of GLUT4 to surface membranes.
Diabetes 1999 Aug
PMID:5' AMP-activated protein kinase activation causes GLUT4 translocation in skeletal muscle. 1042 89


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