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

Electrophysiological, biochemical, and morphometric observations were made on the peripheral nerves of rats after galactose feeding. Motor nerve conduction velocity was found to be reduced. This was associated with an accumulation of galactitol in the peripheral nerves and a diminution in their myoinositol content. An increased water content and fascicular area, taken in conjunction with a probable increase in the area of the endoneurial spaces, indicated overhydration of the peripheral nerves. Morphometric observations on the myelinated fibre population in the tibial nerve showed no loss of fibres and although both the maximal and the average diameter of the myelinated fibres was slightly less than in age-matched controls, this was insufficient to explain the reduction in conduction velocity. Segmental demyelination was not detected and the relationship between myelin thickness and axon circumference was not altered. Electron microscope observations revealed no ultrastructural changes in the myelinated fibres and, in particular, no abnormalities at the nodes of Ranvier or indication of abnormal hydration of the Schwann cells. The relevance of these findings to the peripheral nerve changes in human and experimental diabetes is discussed.
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PMID:Peripheral nerve abnormalities related to galactose administration in rats. 18 26

Exposing micro-dissected pancreatic islets of non-inbred ob/ob mice to 2-5 mM-alloxan for 10 min decreased the ability of the islets to accumulate Rb+. Rb+ accumulation in pieces of exocrine pancreas was unaffected by alloxan. When islets were treated with alloxan in the presence of 2-20 mM-D-glucose, the Rb+-accumulating ability was protected in a dose-dependent manner. The protective action of D-glucose was reproduced with 3-O-methyl-D-glucose but not with L-glucose or D-mannoheptulose; mannoheptulose prevented D-glucose from exerting its protective action. The inhibition of Rb+ accumulation was due to a decreased inward pumping, since alloxan did not affect Rb+ efflux from pre-loaded islets. The inhibitory effect of alloxan had a latency of about 1 min, as revealed by experiments with dispersed islet cells in suspension. Alloxan-treated islets showed only a marginal decrease in ATP and no change in glucose 6-phosphate concentration. Although alloxan slightly decreased the hydrolysis of ATP in a subcellular fraction enriched in plasma membranes, this effect could not be attributed to a ouabain-sensitive adenosine triphosphatase. The plasma membranes exhibited a K+-activated hydrolysis of p-nitrophenyl phosphate; this enzyme activity too was insensitive to alloxan. Glucose may protect the univalent-cation pump by preventing permeation of alloxan via a path coupled to the hexose-transport system. Inhibition of the pump may be fundamental to the induction of alloxan-diabetes.
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PMID:Alloxan cytotoxicity in vitro. Inhibition of rubidium ion pumping in pancreatic beta-cells. 19 15

The subcellular localization of the incorporation of 2-(3H)-myoinositol into lipids has been studied in isolated pancreatic islets of the rat. The recovery of lipid-bound myoinositol increased with time in the nuclear, mitochondrial, microsomal, and secretory granule fractions. The utilization of a filtration technique for the more complete separation of mitochondrial and secretory granule elements permitted us to show that the recovery of lipid-bound 2-(3H)-myoinositol increased most rapidly in the secretory granule fraction. A 30-minute exposure of prelabeled islets to a stimulatory concentration of D-glucose (3.0 mg./ml.) resulted in a statistically significant decrease in the amount of lipid-bound 2-(3H)-myoinositol that was recovered from the secretory granule fraction (p less than 0.001). In contrast, exposure of islets to the elevated glucose concentration had no statistically significant effect on the recovery of lipid-bound radioactivity from other subcellular fractions. Since the majority of lipid-bound radioactivity associated with the secretory granule fraction could be recovered with the presumptive secretory granule membranes, these data suggest that the hydrolysis of phosphatidylinositol that accompanies glucose-induced insulin secretion from the rat pancreatic islet may be localized to the beta granule and, in particular, to its limiting membrane.
Diabetes 1977 Dec
PMID:Subcellular localization of the alterations in phosphatidylinositol metabolism following glucose-induced insulin release from rat pancreatic islets. 33 3

The rate of alloxan-induced insulin release was measured from rat islets maintained in a simple perifusion system. Insulin release during the five-minute exposure to alloxan reached its maximum rate after two to three minutes of the exposure and then rapidly declined. This insulin release was dependent upon extracellular calcium and was associated with an increased 45Ca uptake by isolated islets. Once exposed to alloxan, however, the islets did not release insulin when stimulated again with D-glucose or alloxan. These effects of alloxan on insulin release (stimulation and subsequent inhibition) and the increased 45Ca uptake were prevented by the presence of 3-0-methyl-D-glucose during the alloxan exposure. These findings indicate a close correlation between alloxan-induced insulin release and the subsequent inhibition of further insulin release. D-glucose, when present during the entire five-minute exposure to alloxan, protected competitively against alloxan inhibition of insulin release. In addition, D-glucose, when present immediately after brief (one to three minutes) alloxan exposures, reversed some of the subsequent inhibition of insulin release. These findings suggest that alloxan and D-glucose were competing for a common site on the beta-cell. The possibility of this site being a receptor responsible for the initiation of insulin release is discussed.
Diabetes 1978 Dec
PMID:Alloxan stimulation and inhibition of insulin release from isolated rat islets of Langerhans. 36 92

The effect of a new complex oligosaccharide exhibiting potent inhibitory action on alpha-glucoside hydrolases on intestinal absorption of sucrose in man was tested by constant in vivo perfusion of the jejunum. At concentrations of 4.65 or 15.5 X 10(-6)M the alpha-glucosidehydrolase inhibitor (alpha-GHI) markedly inhibited absorption of glucose from sucrose and absorption of sodium and water. Oral administration of the alpha-GHI resulted as well in depression of solute, sodium, and water absorption. This new compound can serve as an interesting tool to induce carbohydrate malabsorption by inhibition of final digestion and may possibly be of beneficial therapeutic effect in dietary control of diabetes or obesity.
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PMID:Effect of alpha-glucosidehydrolase inhibition and intestinal absorption of sucrose, water, and sodium in man. 38 40

The effect of variations in kind and amount of dietary carbohydrate on plasma glucose and insulin responses was studied in normal subjects and in patients with chemical diabetes. Plasma glucose and insulin responses fell when the proportion of total calories given as carbohydrate were decreased by 15% (coincidental with a comparable increase in dietary fat). Associated with the lower plasma glucose and insulin concentrations was a fall in fasting and postprandial triglyceride levels. Plasma glucose and insulin responses were also lower when equivalent carbohydrate challenges were given as part of a mixed meal, as compared to a drink. Furthermore, carbohydrate given as starch also led to an attenuated glucose and insulin response when compared to an equivalent amount of glucose administered as either dextrose or sucrose. Finally, significant differences were also seen after the ingestion of different kinds of starch, with potato being the most like dextrose, and rice the least. These results indicate that differences in amount and kind of ingested carbohydrate can modify ensuing plasma glucose and insulin responses, and raise the possibility that such dietary manipulation may have some therapeutic utility in patients with abnormal carbohydrate and lipid metabolism.
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PMID:Effects of differences in amount and kind of dietary carbohydrate on plasma glucose and insulin responses in man. 38 23

Maternal hypoglycaemia (plasma glucose below 5th centile) had a highly significant association with fetal growth retardation, and perinatal mortality was significantly increased in the presence of both hypoglycaemia and hyperglycaemia (plasma glucose above 95th centile) when pregnancy outcome was analyzed in 5000 consecutive patients who had a glucose tolerance test performed during the third trimester of pregnancy. This study confirms the significance of abnormal glucose tolerance as a causative factor of feto-placental dysfunction. The flat glucose tolerance test pattern had no significance beyond the presence of associated hypoglycaemia, but reactive hypoglycaemia, and persistent abnormalities of plasma glucose levels during the test, were associated with higher incidences of complicated outcome. Hypertonic dextrose therapy administered to the patient with persistently subnormal urinary oestriol excretion was less likely to cause a favourable response in oestriol excretion if glucose tolerance was abnormal, perhaps because the adverse influences of abnormal glucose tolerance were not reversible by the third trimester of pregnancy. Hypoglycaemia and hyperglycaemia, additional to diabetes mellitus, are significant factors in the aetiology and diagnosis of abnormal pregnancy, and point to the need to investigate therapeutic measures.
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PMID:The significance of abnormal glucose tolerance (hyperglycaemia and hypoglycaemia) in pregnancy. 42 63

1. Effects of dietary composition, energy restriction, and diabetes on hexose absorption were examined by feeding male rats isoenergetic, semi-synthetic diets of differing carbohydrate and protein content. Diets were carbohydrate, (g/kg): 890 sucrose; carbohydrate-protien, 500 sucrose, 390 casein; or protein, 890 casein. An additional group was fed on commercial rat chow ad lib. 2. Hexose (3-O-methyl-D-glucose) absorption was measured by luminal perfusion of the entire small intestine in situ. Absorption by the total small intestine, i.e. absorption per rat, and absorption per g dry weight of mucosa (specific absorption) were calculated. 3. When semi-synthetic diets were fed at 210 kJ/d to normal animals absorption depended on composition of diets: carbohydrate enhanced or protein suppressed hexose absorption. Dietary carbohydrate as glucose, dextrimaltose or starch gave the same hexose absorption response as sucrose. 4. When diets of normal rats were restricted to 118 kJ/d, specific absorption was independent of dietary composition and was increased for all dietary groups to the level of the group fed on the carbohydrate diet at 210 kJ/d. 5. When diabetic rats were given 210 kJ/d, hexose specific absorption was the same for all diabetic groups independent of dietary composition and was equal to that of controls given carbohydrate, but greater than that of protein-fed controls. 6. Thus, when two of the three stimuli (i.e. carbohydrate diet plus energy restriction or diabetes) were combined, the effect was not additive, and the response of hexose specific absorption to diabetes and energy restriction was the same: absorption was independent of dietary composition and was stimulated relative to controls fed on diets containing protein. 7. The pattern of response of total small intestinal hexose absorption to the stimuli of dietary composition, energy restriction and diabetes was similar to that of specific absorption. 8. Compared with groups given semi-synthetic diets, rats eating commercial rat chow ad lib. (approximately 286 kJ/d) showed increased mucosal mass and decreased specific absorption, but total absorption was similar to that of the carbohydrate and carbohydrate-protein-fed groups. 9. In a separate study in control rats, specific and total intestinal absorption of L-leucine did not respond to dietary composition, i.e. level of protein fed.
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PMID:Effects of diet, energy restriction and diabetes on hexose transport in the rat. 46 35

Miles Laboratories has developed a Glucose Controlled Insulin Infusion System (GCIIS) designated by the Trademark (BIOSTATOR) as a tool to investigate the physiologic control parameters of carbohydrate metabolism and regulatory deficiencies in diabetes. It consists, in principle, of a rapid on-line glucose analyzer, a computer/controller for the calculation and control of insulin or dextrose infusion, and a multichannel infusion system. A silent printer records, on a minute-by-minute basis, the glucose value measured, the insulin and/or dextrose infusion rates, and the cumulative total of the insulin infused. The on-line glucose analyzer employs an electrochemical sensor with immobilized glucose oxidase and measures the hydrogen peroxide produced. Its linearity extends beyond 700 mg/dl glucose; it permits a rapid two-point calibration of the sensor and the overall calibration of the on-line analyzer without disconnecting the catheter from the patient. The system's response time, including blood sample transport from the patient, is less than 90 seconds with a blood loss of approximately 50 ml per 24 h. The insulin and dextrose infusions are governed by control algorithms; various mathematical models have been developed and employed toward improved feedback control dynamics. The rapid glucose analyzer eliminates the need for the calculation of a "predicted" glucose value and permits, instead, the use of a derivative function for dynamic control. A multichannel infusion system combines the principles of a peristaltic pump with the advantages of a precision pump performance and individual computer control for each of the pump channels.
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PMID:Feedback control dynamics for glucose controlled insulin infusion system. 48 65

We have studied the effects of dextrose, rice, potato, corn, and bread on postprandial plasma glucose and insulin responses in 16 subjects. All carbohydrate loads were calculated to contain 50 gm. of glucose. The data demonstrate (1) that dextrose and potato elicited similar plasma glucose responses whereas rice, corn, and bread elicited lower responses; (2) similarly, dextrose and potato elicited similar and greater plasma insulin responses than rice and corn, with the response to bread being intermediate; (3) when the study group was divided in half, on the basis of each subject's one-hour plasma glucose response to dextrose, the differences in the plasma glucose and insulin responses were greater in the subjects with the highest glucose response to dextrose than in the low responders. In conclusion, there is a range of plasma-glucose and insulin responses to different complex carbohydrates, with rice and corn producing the lowest response curves. Furthermore, these differences are accentuated in patients with reduced glucose tolerance.
Diabetes 1977 Dec
PMID:Postprandial plasma-glucose and -insulin responses to different complex carbohydrates. 59 Jun 39


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