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

Glycosylated hemoglobin (HbA1) is considered to be representative of prior blood-glucose levels and is being used in pregnant and nonpregnant diabetic patients as a possible index of both long and short-term glucose-control. Factors other than blood-glucose concentration have been reported to affect its value. Variant hemoglobin is one of them. HbA1 and blood-glucose levels were measured in pregnant patients at high risk for diabetes for screening for abnormal carbohydrate metabolism. HbA1 was measured by cation exchange column chromatography and glucose was measured by hexokinase reaction. The mean HbA1 in patients with normal blood sugars was 6.17 +/- 0.6 percent. A value of HbA1 of less than 5 percent as measured by cation exchange column chromatography was highly predictive (P less than 0.001) of hemoglobinopathies (S or C). The mean HbA1 of randomly selected matched patients with "normal" Hb was 5.94 +/- 0.72 percent. In patients with thalassemia, HbA1 values as measured by cation exchange column chromatography were elevated despite normal carbohydrate tolerance. While interpreting the results of HbA1 in the management of pregnant diabetics, the above fact should be kept in mind.
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PMID:Glycosylated hemoglobin (HbA1) and hemoglobinopathies in pregnancy. 650 39

The level of fructose 2,6-bisphosphate is markedly decreased in the rat V.renal gland in diabetes, falling to 23% of the control value. There is parallel decrease in the flux of 14C-labelled glucose through the glycolytic route and tricarboxylic acid cycle. Only minimal changes in hexokinase (EC 2.7.1.1.), a 22% decrease in Type I hexokinase of the soluble fraction, were observed, highlighting the probable significant involvement of fructose 2,6-bisphosphate in the regulation of glycolysis in the adrenal. In contrast, there was evidence for a marked rise in the flux of glucose through the pentose phosphate pathway, which may be linked to enhanced corticoid synthesis in the diabetic state.
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PMID:Regulation of glucose metabolism in rat adrenal gland in alloxan-diabetes: the possible role of fructose 2,6-bisphosphate. 654 41

The effects of a high fat diet (30% (w/w) corn oil) on chronic streptozotocin-diabetic rats were investigated at the whole body level and at the enzyme level. The diet caused significant decreases in the extent of polydipsia (66% decrease), polyphagia (49%), polyuria (67%) and glycosuria (70%). The activities of selected hepatic enzymes from the glycolytic, gluconeogenic, ureogenic and lipogenic clusters were determined. The fat diet caused significant decreases (range: 47 to 54%) in the activity of the ureogenic enzymes carbamyl phosphate synthetase, ornithine transcarbamylase and arginase; had no effect on the glycolytic enzymes glucokinase, hexokinase and pyruvate kinase; partially decreased the diabetes-induced elevated activities of the gluconeogenic enzymes phosphoenolpyruvate carboxykinase (63% decrease), serine dehydratase (90%), alanine aminotransferase (31%) and aspartate aminotransferase (65%), and partially reversed the activity of one lipogenic enzyme, ATP citrate lyase.
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PMID:The effects of a high fat diet on chronic streptozotocin-diabetic rats. 692 68

The accuracy and reliability of new blood glucose measurement strips, BM Test-Glycemie 20-800, were assessed in 99 consecutive patients attending the diabetic clinic and seven subjects at home. The BM Test-Glycemie 20-800 strip technique was compared with the automated hexokinase method and the Reflotest-Glucose test strip technique employing the Boehringer Reflomat. The mean of the blood glucose values was 12.6 +/- 0.6 mmol/L for the hexokinase method and 12.9 +/- 0.6 mmol/L for the 20-800 strip technique, with a mean difference between the hexokinase and the 20-800 strip methods of 1.9 +/- 0.2 mmol/L. In the range 4 mmol/L to 12 mmol/L, the 20-800 strips were found to be extremely accurate, but for blood glucose levels less than 3.5 mmol/L and greater than 12 mmol/L, they were less reliable. Importantly, the strips were often misleading in indicating hypoglycaemia. It is concluded that the BM Test-Glycemie 20-800 strips have a practical and valuable role when used by suitably instructed staff members, or by patients in the management of diabetes, and represent a major advance over urine testing on previously available direct reading enzyme strip methods.
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PMID:Appraisal of a new rapid enzyme strip. 721 5

Venous serum glucose concentrations determined by a laboratory hexokinase technique were compared over a wide range of glucose concentrations with concentrations of capillary blood glucose determined by three reflectance meter techniques currently available in the United States (Eyetone and Dextrometer, Ames Company; StatTek, Bio-Dynamics BMC) and by visual interpretation of reagent strips (Chemstrip bG, Bio-Dynamics BMC). The Chemstrip bG reagent strip was read by patients, nurses, and a physician. In all cases, there was an excellent correlation between laboratory serum glucose concentrations and reflectance meter blood glucose determinations (r = 0.90-0.94, P less than 0.0001) or visual interpretation of Chemstrip bG (r = 0.85-0.92, P less than 0.0001). Chemstrip bG appears to be the least expensive method of glucose measurement. This method offers additional advantages in not requiring a reflectance meter, which needs frequent recalibration and other ancillary equipment for blood glucose determination.
Diabetes Care
PMID:A comparison of accuracy and estimated cost of methods for home blood glucose monitoring. 734 86

The ultrastructure of dog cardiomyocytes was studied one month after reproducing alloxan diabetes, with respect to myocardial extraction from the blood of glucose, nonesterified fatty acids, beta-lipoproteins and ketone bodies as well as to respiration in conjunction with oxidative phosphorylation of mitochondria, hexokinase and phosphorylase activity. Destructive changes in mitochondria, increased glycogen content in cardiomyocytes were revealed in the absence of glucose consumption by the myocardium which absorbed only lipoid metabolites. Lipoid inclusions were rarely seen in cardiomyocytes. The myocardium showed the increased content of lysosomes and hydrolytic phosphorylase. It is suggested that lipoid metabolites transform to glycogen, with lysosomes participating in the process.
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PMID:[Ultrastructural manifestations of early metabolic disorders in the myocardium of dogs with alloxan diabetes]. 739 46

Glucokinase is the beta-cell glucose sensor, i.e., the site in glucose metabolism that determines the glucose set-point (sensitivity) for insulin secretion. Hexokinase is also present, but it normally contributes little to glucose metabolism because of end-product inhibition by glucose 6-phosphate. There is a lowered glucose set-point for insulin secretion in 90% pancreatectomized (Px) diabetic rats. We investigated the mechanism by measuring hexokinase and glucokinase activity in islet extracts. Glucokinase activity was minimally raised in Px islets (Vmax 125% of sham-operated control rats). In contrast, hexokinase Vmax was 250% of the control value, suggesting that the increased hexokinase activity caused the beta-cell glucose hypersensitivity. Additional evidence was obtained with a 40-h fast that was performed because of a previous observation that the inhibitory effect of fasting on insulin secretion was impaired in Px rats. Glucokinase activity fell normally in the Px rats (32 +/- 4% reduction in sham vs. 37 +/- 4% in Px rats) as opposed to hexokinase activity, which was unaffected in either group. In summary, a feature of hyperglycemia is upregulated islet hexokinase activity. The result is that hexokinase assumes partial control over the glucose set-point for insulin secretion. As such, regulatory effects on insulin secretion, such as fasting, that are mediated through glucokinase activity may be altered.
Diabetes 1995 Nov
PMID:Upregulated hexokinase activity in isolated islets from diabetic 90% pancreatectomized rats. 758 32

The hexokinases, by converting glucose to glucose-6-phosphate, help maintain the downhill gradient that results in movement of glucose into cells through the facilitative glucose transporters. GLUT4 and hexokinase (HK) II are the major transporter and hexokinase isoforms in skeletal muscle, heart, and adipose tissue, wherein insulin promotes glucose utilization. To understand whether hormones influence the contribution of phosphorylation to cellular glucose utilization, we investigated the effects that catecholamines, cyclic AMP (cAMP), and insulin have on HKII gene expression in cells representative of muscle (L6 cells) and brown (BFC-1B cells) and white (3T3-F442A cells) adipose tissues. Isoproterenol or the cAMP analog 8-chlorophenylthio-cAMP selectively increase HKII gene transcription in L6 cells, as does insulin (Printz RL, Koch S, Potter LP, O'Doherty RM, Tiesinga JJ, Moritz S, Granner DK: Hexokinase II mRNA and gene structure, regulation by insulin, and evolution. J Biol Chem 268:5209-5219, 1993), and cause a concentration- and time-dependent increase of HKII mRNA in both muscle and fat cell lines without changing HKI mRNA. Isoproterenol and insulin also increase the rate of synthesis of HKII protein and increase glucose phosphorylation and glucose utilization in L6 cells.
Diabetes 1995 Dec
PMID:Regulation of hexokinase II gene transcription and glucose phosphorylation by catecholamines, cyclic AMP, and insulin. 758 50

The aim of the present study is to compare normal and tumoral pancreatic islet cells in terms of both the activity of selected cytosolic and mitochondrial enzymes participating to nutrient catabolism and the intrinsic properties of FAD-glycerophosphate dehydrogenase. The activity of the glycolytic enzymes hexokinase and lactate dehydrogenase was higher in tumoral (RINm5F) than normal islet cells. The opposite was seen for glutamate decarboxylase, glutamate-oxaloacetate transaminase, glutamate-pyruvate transaminase, glutamate dehydrogenase, 2-ketoglutarate dehydrogenase and FAD-glycerophosphate dehydrogenase (m-GDH). These findings are consistent with the high rates of glycolysis and protein synthesis seen in tumoral islet cells compared with normal islet cells, which favour mitochondrial oxidative events associated with the catabolism of D-glucose and amino acids. The intrinsic catalytic properties of m-GDH were comparable, albeit not identical, in normal and tumoral islet cells. Since a deficiency of m-GDH in pancreatic islets may represent a contributing factor in the pathogenesis of non-insulin-dependent diabetes, it is proposed that RINm5F cells may readily yield sufficient islet m-GDH for purification and further gene cloning.
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PMID:Activity of cytosolic and mitochondrial enzymes participating in nutrient catabolism of normal and tumoral islet cells. 776 86

Recent studies have demonstrated that reduced insulin-stimulated muscle glycogen synthesis is the major cause of insulin resistance in patients with non-insulin-dependent diabetes mellitus (NIDDM). This reduced rate has been assigned to a defect in either glucose transport or hexokinase activity. However it is unknown whether this is a primary or acquired defect in the pathogenesis of NIDDM. To examine this question, we measured the rate of muscle glycogen synthesis and the muscle glucose 6-phosphate (G6P) concentration using 13C and 31P NMR spectroscopy as well as oxidative and nonoxidative glucose metabolism in six lean, normoglycemic offspring of parents with NIDDM and seven age/weight-matched control subjects under hyperglycemic (approximately 11 mM)-hyperinsulinemic (approximately 480 pM) clamp conditions. The offspring of parents with NIDDM had a 50% reduction in total glucose metabolism, primarily due to a decrease in the nonoxidative component. The rate of muscle glycogen synthesis was reduced by 70% (P < 0.005) and muscle G6P concentration was reduced by 40% (P < 0.003), which suggests impaired muscle glucose transport/hexokinase activity. These changes were similar to those previously observed in subjects with fully developed NIDDM. When the control subjects were studied at similar insulin levels (approximately 440 pM) but euglycemic plasma glucose concentration (approximately 5 mM), both the rate of glycogen synthesis and the G6P concentration were reduced to values similar to the offspring of parents with NIDDM. We conclude that insulin-resistant offspring of parents with NIDDM have reduced nonoxidative glucose metabolism and muscle glycogen synthesis secondary to a defect in muscle glucose transport/hexokinase activity prior to the onset of overt hyperglycemia. The presence of this defect in these subjects suggests that it may be the primary factor in the pathogenesis of NIDDM.
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PMID:Decreased muscle glucose transport/phosphorylation is an early defect in the pathogenesis of non-insulin-dependent diabetes mellitus. 786 78


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