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

Pancreatic lipase was revealed by immunocytochemistry and analyzed biochemically in pancreatic tissue from control, diabetic, and insulin-treated diabetic rats. In the three groups of animals, lipase antigenic sites were detected with high resolution in the acinar cells in the compartments involved in protein secretion: rough endoplasmic reticulum, Golgi apparatus, and secretory zymogen granules. The quantitative evaluation of the intensities of labeling has demonstrated that, in contrast to other pancreatic proteins, lipase is concentrated only at the transition between the Golgi apparatus and the condensing vacuoles. This indicates that, although sharing the same secretory pathway as amylase and chymotrypsinogen, lipase may in fact be processed differently. On the other hand, when compared with controls, lipase immunolabelings in tissues with diabetic condition were higher in all the cellular compartments. Treatment of diabetic animals with insulin was found to restore these levels to those obtained in control condition. The biochemical determination of lipase activities in pancreatic tissues confirmed the immunocytochemical data. These results, together with those obtained previously for amylase and chymotrypsinogen, indicate that in diabetic condition secretion from the acinar cells is significantly altered, which may influence intestinal digestion and absorption processes. These modifications, and the enhancement of lipase in particular, could play a role in the pathogenesis of the hyperlipidemic condition present in diabetes.
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PMID:Immunocytochemical and biochemical evaluation of pancreatic lipase in acinar cells of control and streptozotocin-induced diabetic rats. 329 Aug 94

Among 88 unselected patients with chronic pancreatitis 35% (95% confidence limits 25 to 46) had insulin-dependent diabetes, 31% (21% to 41%) had non-insulin-dependent diabetes or impaired glucose tolerance (by intravenous glucose tolerance test), and 34% (24% to 45%) had normal glucose tolerance. B cell function measured by C-peptide concentration after 1 mg glucagon IV correlated with the pancreatic enzyme secretion (meal stimulated duodenal lipase content). B cell function was preserved to a greater extent (P less than .01), and glycosylated hemoglobin and fasting level of glucose were lower (P less than .01 to .05) in the 31 patients with pancreatogenic diabetes than than in 35 otherwise comparable patients with type I (insulin-dependent) diabetes, yet daily insulin dose was similar in the two groups. Glucagon stimulated C-peptide was inversely correlated to glycosylated hemoglobin in insulin-dependent patients with pancreatogenic diabetes and in type I diabetes. Since body mass indices were identical in the two groups, better glucoregulation was not due to reduced food intake or malabsorption in pancreatogenic diabetes. Rather residual B cell function and/or different secretion of other pancreatic hormones in pancreatogenic diabetes may account for different metabolic control in type I IDDM compared with insulin-dependent pancreatogenic diabetes.
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PMID:Metabolic control and B cell function in patients with insulin-dependent diabetes mellitus secondary to chronic pancreatitis. 330 47

Four-five months after the induction of diabetes, salivary tissues of male Wistar rats were preserved by glutaraldehyde fixation or rapid freezing in dry-ice cooled hexane. Fixed tissues were either processed and embedded for light and electron microscopy, or frozen and, together with unfixed tissues, sectioned and stained with Oil Red 0 or by the calcium-lipase method. All diabetic glands had considerably more intracellular lipid than control ones. Lipid accumulation within parenchymal cells varied with the type of gland, and was more pronounced in animals with the highest serum-glucose levels. Serous cells of parotid and sublingual glands accumulated the greatest amount of lipid; lesser amounts were present in seromucous acinar cells of submandibular glands; little or none in mucous acinar cells of sublingual glands. There was no lipid in striated, granular or excretory ducts. Histochemical staining suggested that the intracellular lipid was mainly triglyceride which may accumulate by increased uptake for use as an energy source, or by decreased use in the synthesis of secretory granule and plasma-membrane material.
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PMID:Lipid accumulation in the major salivary glands of streptozotocin-diabetic rats. 346 70

Exocrine and endocrine pancreatic functions were studied in 30 patients with homozygotic beta-thalassaemia. All were treated with continuous subcutaneous deferoxamine infusions for a mean period of 30 months. Three patients (aged 18-22 years) had insulin-dependent diabetes, two before and one shortly after the onset of deferoxamine administration. There was no improvement during the treatment. An abnormal glucose tolerance test was demonstrated in 14 patients (47%) before and in seven (23%) during deferoxamine infusion. Enzyme activity of alpha-amylase and lipase as an expression of exocrine pancreatic function was normal in all during the observation period. Improvement in endocrine pancreatic function was apparently age-dependent: the younger the patient at the onset of treatment the more likely is normalization of the oral glucose tolerance test.
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PMID:[Continuous subcutaneous deferoxamine infusions in thalassemia major. Improvement in glucose tolerance]. 348 6

High vitamin E supplementation in the diets of streptozocin-induced diabetic rats eliminates accumulation of lipid peroxides in the plasma and the liver, returns the plasma triglycerides toward normal levels, and increases the activity of lipoprotein lipase. Vitamin E has no effect on the levels of insulin or glucose. These findings suggest that vitamin E increases the total hepatic triglyceride lipase activity by increasing the lipoprotein lipase activity possibly by protecting the membrane-bound lipase against peroxidative damage.
Diabetes 1986 Mar
PMID:Triglyceride-lowering effect of dietary vitamin E in streptozocin-induced diabetic rats. Increased lipoprotein lipase activity in livers of diabetic rats fed high dietary vitamin E. 351 38

To study postheparin plasma lipase activities in nonfed newborn infants immediately after birth and to investigate the possible influence of fetal hyperinsulinemia on lipoprotein lipase activity, we measured lipoprotein and hepatic lipase activities in 55 macrosomic newborn infants: group I consisted of 21 infants born to mothers with insulin-dependent diabetes. The infants were hyperinsulinemic at birth and had hypoglycemia and poor lipolysis at the age of 2 h. Group II consisted of 18 infants born to mothers with gestational diabetes. Group III consisted of 16 large-for-date infants born to nondiabetic mothers. The mean postheparin plasma lipoprotein lipase activities at 2 h of age were similar (mean 36 mumol free fatty acids/ml/h; SEM 15) in groups I-III. Lipoprotein lipase activity correlated negatively with cord-serum triglycerides (range 0.13-1.2 mmol/liter) but did not correlate with serum insulin (range 5.4-524 microU/ml) or C-peptide (range 0.6-21.0 micrograms/liter). Hepatic lipase activity was somewhat higher in group I (mean 68 mumol free fatty acids/ml/h; SEM 23) than in groups II and III (mean 55 mumol free fatty acids/ml/h; SEM 14). Hemoglobin Alc was the only important factor explaining the difference in hepatic lipase activities between groups. Lipoproteins and apolipoproteins A-I, A-II, and B were similar in all three groups. We conclude that in large-for-date infants lipoprotein lipase is active at birth without exogenous fat induction, and that these infants are capable of hydrolyzing fat, their main source of energy, immediately after birth. In addition, we conclude that postheparin plasma lipoprotein lipase activity is not affected by fetal hyperinsulinemia.
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PMID:Postheparin plasma lipoprotein and hepatic lipase activities in hyperinsulinemic infants of diabetic mothers and in large-for-date infants at birth. 352 12

The placental transfer of non-esterified fatty acids, predominantly in the direction of mother to fetus, is regulated on a gross scale by the transplacental non-esterified fatty acid gradient. This is maintained by fetal liver lipid uptake and by enhanced lipolysis of circulating triacylglycerol in the pregnant mother. It is also dependent upon maternal placental blood flow, which is reduced in diabetes, upon the fetal umbilical blood flow, upon maternal and fetal albumin concentrations and upon intratrophoblastic fatty acid binding protein, which appears to be altered in diabetes. Circulating maternal triacylglycerols also directly contribute non-esterified fatty acids to the fetus by intraplacental hydrolysis and the hypertriglyceridaemia associated with maternal diabetes, in concert with changes in lipase levels will enhance maternal to fetal lipid flux.
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PMID:Placental transfer of non-esterified fatty acids in normal and diabetic pregnancy. 355 63

Diabetes was induced by the administration of streptozotocin (55 mg/kg or 70 mg/kg) to rats. After 21-25 days, myocardial cells (myocytes) were isolated from control and diabetic rat hearts. Rates of endogenous lipolysis, measured as the output of glycerol, were elevated in the chronically diabetic myocytes. Lipoprotein lipase activity was reduced in homogenates of diabetic myocytes. Neutral triacylglycerol lipase activity was increased in myocytes from rats made diabetic with the lower dose of streptozotocin, but not in myocytes from diabetic rats given the higher dose. Diabetes had no effect on acid lysosomal lipase activity.
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PMID:Triacylglycerol lipase activities in isolated myocardial cells from chronically diabetic rat hearts. 366 9

The effect of progressive, diabetes-associated adiposity on reproductive tract structure and function was examined in 4- to 16-week-old C57BL/KsJ, control (+/?) and diabetic (db/db) mice. Uterine and ovarian tissues were analyzed by transmission electron microscopy for ultrastructural changes associated with increased intracellular lipid accumulation. In addition, the same tissues were analyzed for changes in activity of tissue lipoprotein lipase, an enzyme that hydrolyzes lipoprotein-associated triacylglycerols and supports the cellular uptake and storage of free fatty acids. Between 8 and 16 weeks of age, intracellular lipid deposits increased dramatically in the ovarian granulosa, thecal and stromal cell populations, as well as in the uterine epithelium, of diabetic mice compared to controls. By 16 weeks of age, the lipid deposits essentially occupied the entire cytoplasmic area of both the ovarian and uterine cell types in diabetics. The basal lamina underlying the uterine epithelium was expanded in the diabetics relative to controls, and the hyperglycemic condition induced an observable increase in endometrial intercellular space that was occupied by a hyaline type of ground substance of unknown composition and origin. In association with these structural changes, both ovarian and uterine lipase activities were greatly increased in the db/db mice compared with controls. These data suggest that the structural adiposity and functional decline in reproductive tract condition of the db/db mutants are related to the enhanced cellular lipid deposition observed in this species. These changes in structural and metabolic parameters are related to the reproductive incompetence characteristic of this murine model.
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PMID:Ultrastructural and metabolic changes associated with reproductive tract atrophy and adiposity in diabetic female mice. 378 18

A neutral triacylglycerol lipase activity that is separate and distinct from lipoprotein lipase (LPL) could be measured in homogenates of myocardial cells if protamine sulphate and high concentrations of albumin were included in the assay. This neutral lipase was predominantly particulate, with the highest relative specific activity in microsomal subcellular fractions. The induction of diabetes by the administration of streptozotocin to rats resulted in a decrease in LPL activity in myocyte homogenates and in particulate subcellular fractions, but the percentage of cellular LPL activity that was released during incubation of myocytes with heparin was normal. In contrast, neutral lipase activity was increased in diabetic myocyte homogenates and microsomal fractions. Acid triacylglycerol lipase activity was not changed in diabetic myocytes. The decrease in LPL in myocytes owing to diabetes may result in the decreased functional LPL activity at the capillary endothelium of the diabetic heart.
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PMID:Effect of diabetes on acid and neutral triacylglycerol lipase and on lipoprotein lipase activities in isolated myocardial cells from rat heart. 380 Sep 35


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