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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After infusion of 500 ml of 6% hydroxyethyl starch into fifty-four patients an increase of serum amylase was observed which in fifty-one cases exceeded the upper limit of normal (190 U/l). In most cases serum amylase reached twice the basal value. Renal function influenced the duration of the increase in serum amylase, but not the maximum increase (201+/-15 U/l; mean+/-SEM). In patients with advanced renal failure (glomerular filtration rate (GFR) = 2-10 ml/min) serum amylase was still markedly elevated after 72 h (298+/-24 U/l; mean+/-SEM). In patients with normal renal function (GFR greater than 90 ml/min) serum amylase decreased to 183+/-40 U/l (mean+/-SEM) within 72 h without reaching basal values. After infusion of HES no changes were observed in serum lipase or in amylase or lipase activities in duodenal secretion. Amylase excretion in the urine decreased. The assumption of a macroamylasaemia caused by formation of an HES-amylase complex was confirmed by gel filtration. The elimination from plasma of this high molecular enzyme-substrate complex is slow and causes hyperamylasaemia. In no case was the macroamylasaemia associated with signs or symptoms. An awareness of this causal relationship seems to be important, to avoid the erroneous diagnosis of a pancreatic disease.
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PMID:Macroamylasaemia after treatment with hydroxyethyl starch. 7 Mar 54

Juvenile coho salmon (Oncorhynchus kisutch) were placed on five dietary regimes: fed 1 week, fasted 1 week, fed 3 weeks, fasted 3 weeks, and fasted 1 week/refed 2 weeks. Plasma levels of glucose, fatty acids, insulin, glucagon, and glucagon-like peptide (GLP) and the activities of key metabolic enzymes were determined. Plasma glucose levels in the fed control groups were 98.4 +/- 3.4 (SEM) and 104.8 +/- 4.7 mg/dl at 1 and 3 weeks, respectively. Plasma glucose in the fasted 1 week group was significantly elevated to 128.8 +/- 9.2 mg/dl. Animals fasted 3 weeks or fasted 1 week/refed 2 weeks displayed plasma glucose levels similar to those of fed animals. Fasted groups possessed significantly less liver glycogen than fed or fasted/refed groups. Plasma fatty acids were elevated only after 3 weeks of fasting (from 0.39 +/- 0.04 microEq/ml to 0.61 +/- 0.06 microEq/ml). This response was reflected in elevated liver lipase activity (from 6.02 +/- 0.44 nmol fatty acid released/hr/mg protein to 14.22 +/- 0.90 units). No significant alterations in liver lipogenesis, assessed by glucose-6-phosphate dehydrogenase activity and by 3H2O incorporation into fatty acids, were observed. Gluconeogenic flux, determined indirectly through kinetic parameters of pyruvate kinase, was enhanced in animals fasted 3 weeks and in animals recovering from a 1-week fast. Plasma insulin levels were highest in fed groups (7.7 +/- 2.3 and 5.9 +/- 1.4 ng/ml at 1 week and 3 weeks, respectively) and were significantly depressed in fasted groups. Plasma levels of glucagon and GLP were also depressed in fasted groups. These results indicate that plasma glucose levels are maintained in salmon during fasting and that fasting-induced hyperlipidemia is mediated by lipolytic enzyme activity. Insulin, glucagon, and GLP may interact with these enzyme systems to coordinate nutritional metabolism of fish.
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PMID:Effects of nutritional state on in vivo lipid and carbohydrate metabolism of coho salmon, Oncorhynchus kisutch. 205 44

The prevalence of marginal zinc nutriture in several populations of people in this country and the lack of reports on the effect of marginal zinc nutriture in experimental animals prompted us to look at pancreatic acinar cell function and morphology in rats fed a zinc-deficient diet ad libitum: 4 and 50 ppm zinc-supplemented diets in amounts isocaloric to a zinc-deficient diet and Rodent-Blox fed ad libitum for a period of 49 +/- 1 (SEM) days. Because of a diminished rate of energy expenditure in zinc-deficient rats, animals receiving 50 ppm zinc-supplemented diets were offered less food, resulting in decreased body weight and pancreas weight, DNA, RNA, total protein, lipase, amylase, and secretion of protein. Specific changes due to zinc deficiency included (a) further decrease in body weight and (b) increase in content, specific activity, and secretion of lipase. Both the size and volume fraction of zymogen granules were reduced in zinc deficiency. The lumina of acinar and small ducts were collapsed with paucity of secretion products. Zinc deficiency may therefore lead to a defect in discharge mechanism. A further reduction in volume fraction of zymogen granules in the 4 ppm zinc-supplemented group was associated with increased secretion of serine proteases (trypsinogen and chymotrypsinogen), which constitute approximately 46% of total secretory protein in the pancreas under normal dietary conditions. This indicated an accelerated discharge due to an unknown mechanism. Changes in the secretion of digestive enzymes in the present study simulated ethanol-induced secretory alterations that were previously observed. Because abnormal zinc nutriture and chronic alcoholism are commonly associated, it is speculated that zinc deficiency may play a role in the ethanol-induced secretory alterations.
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PMID:Pancreatic acinar cell function and morphology in rats fed zinc-deficient and marginal zinc-deficient diets. 241

The present study was done to determine interaction of ethanol and marginal zinc nutriture on morphology and function of rat pancreas. Sprague-Dawley rats were maintained on Wayne Rodent-Blox ad libitum; marginal zinc-deficient diet plus ethanol ad libitum and pair fed with animals fed marginal zinc-deficient liquid diet and zinc-supplemented liquid diet with ethanol for 33 (+/- 1 SEM) days. Body, pancreas, liver, heart, and kidney weights were determined, and studies of pancreatic DNA, RNA, total proteins and newly labeled proteins, amylase, lipase, trypsinogen, and chymotrypsinogen were done on pancreatic lobules in vitro. Ethanol feeding independent of the zinc content of the diet caused a decrease in zinc content of the liver, body weight, liver and pancreas weight, pancreatic DNA, total protein, and amylase concentration and an increase in lipase and trypsinogen concentrations and in secretion of amylase and lipase. Interaction of the marginal zinc diet and ethanol feeding resulted in a decreased synthesis of RNA and secretion of newly synthesized protein and an increase in secretion of serine proteases. Morphological studies revealed a reduction in the number of zymogen granules in animals fed low levels of zinc, also with an accumulation of lipid droplets when the diet contained ethanol. These studies confirmed our previous observations of specific injury to the pancreas due to marginal zinc nutriture or to ethanol, independent of each other. Marginal zinc nutriture in concert with ethanol resulted in impaired RNA synthesis and secretion of nascent proteins and increased secretion of serine proteases. These data indicate that altered zinc metabolism induced by ethanol per se may contribute to ethanol-induced disturbance of pancreatic function.
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PMID:Interaction between marginal zinc deficiency and chronic alcoholism: pancreatic structure and function in rats in vitro. 243 69

The lack of a potent and specific cholecystokinin (CCK) receptor antagonist has greatly hampered studies of the role of CCK in controlling pancreatic growth, enzyme release, pancreatitis, and pancreatic carcinoma. Asperlicin, a newly described, CCK antagonist, has been shown to be a potent, competitive inhibitor of CCK-induced gallbladder and ileal muscle contraction. In this study, the effects of asperlicin on CCK- and carbachol-stimulated pancreatic enzyme release from dispersed guinea pig acini were investigated. Cholecystokinin caused a dose-dependent release of amylase and lipase. Half-maximal release of amylase (17.9% +/- 2.1%, mean +/- SEM, percent of total content) and lipase (27.3% +/- 2.1%) was seen with CCK 10(-11) mmol/L) both p less than 0.01). Asperlicin (10(-11) to 10(-4) mmol/L) caused a substantial inhibition (10(-11) mmol/L) of CCK-induced amylase release with a 50% maximal effective inhibitory dose of 10(-9) mmol/L (p less than 0.01) and maximum inhibition at 10(-6) mmol/L. Asperlicin was approximately 1000-fold more potent than proglumide (a previously described CCK receptor antagonist) which had a 50% effective inhibitory dose of 10(-6) mmol/L) and a maximal effect at 10(-4) mmol/L. Asperlicin (10(-10) to 10(-4) mmol/L) failed to alter carbachol-induced amylase release. Asperlicin is a new, potent CCK antagonist for pancreatic CCK receptors and should prove useful as an investigational tool. Such receptor antagonists may have therapeutic potential.
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PMID:Asperlicin: a unique nonpeptide cholecystokinin antagonist. 244 81

The effect of a dietary fiber supplementation program (20 g/d) on exocrine pancreatic gland secretion was evaluated in six healthy male subjects who underwent quantitative assessment of pancreatic enzyme secretion both before and after 4 wk of dietary fiber supplementation. A duodenal perfusion technique was used to quantify the concentrations and output of pancreatic enzymes after ingestion of a standard test meal. Samples were aspirated from the ligament of Trietz and analyzed for pH, total protein, amylase, trypsin, and lipase activity. No significant changes were observed in duodenal flow rate pH, total protein, amylase, or trypsin concentrations and outputs after fiber supplementation. A marked increase in mean (+/- SEM) lipase concentration (U/mL) and output (kU/min) in both the resting and postprandial states was seen, reaching statistical significance (p less than 0.05) at 120 min postprandial. These data suggest that in man, a 4-wk dietary fiber supplementation program can modulate pancreatic lipase secretion.
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PMID:Dietary fiber supplementation: effect on exocrine pancreatic secretion in man. 247 53

To study the role of the two postheparin plasma lipolytic enzymes, lipoprotein lipase (LPL) and hepatic lipase (HL) in high density lipoprotein (HDL) metabolism at a population level, we determined serum lipoproteins, apoproteins A-I, A-II, B, and E, and postheparin plasma LPL and HL activities in 65 subjects with a mean HDL-cholesterol of 34 mg/dl and in 62 subjects with a mean HDL-cholesterol of 87 mg/dl. These two groups represented the highest and lowest 1.4 percentile of a random sample consisting 4,970 subjects. The variation in HDL level was due to a 4.1-fold difference in the HDL2 cholesterol (P less than 0.001) whereas the HDL3 cholesterol level was increased only by 32% (P less than 0.001) in the group with high HDL-cholesterol. Serum apoA-levels were 128 +/- 2.2 mg/dl and 210 +/- 2.8 mg/dl (mean +/- SEM) in hypo- and hyper-HDL cholesterolemia, respectively. Serum apoA-II concentration was elevated by 28% (P less than 0.001) in hyperalphalipoproteinemia. The apoA-I/A-II ratio was elevated only in women with high HDL-cholesterol but not in men, suggesting that elevation of apoA-I is involved in hyperalphalipoproteinemia in females, whereas both apoA proteins are elevated in men with high HDL cholesterol. Serum concentration of apoE and its phenotype distribution were similar in the two groups. The HL activity was reduced in the high HDL-cholesterol group (21.2 +/- 1.5 vs. 38.5 +/- 1.8 mumol/h/ml, P less than 0.001), whereas the LPL activity was elevated in the group with high HDL-cholesterol compared to subjects with low HDL-cholesterol (27.8 +/- 1.3 vs. 19.9 +/- 0.8 mumol/h/ml, P less than 0.001). The HL and LPL activities correlated in opposing ways with the HDL2 cholesterol (r = 0.57, P less than 0.001 and r = 0.51, P less than 0.001, respectively), and this appeared to be independent of the relative ponderosity by multiple correlation analysis. The results demonstrate major influence of both HL and LPL on serum HDL cholesterol concentration at a population level.
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PMID:Postheparin plasma lipoprotein and hepatic lipase are determinants of hypo- and hyperalphalipoproteinemia. 250 59

We studied the effects of intravenous infusion of synthetic oxyntomodulin (proglucagon 33-69), a potential hormone from the ileal mucosa, on fasting and postprandial gastric acid secretion, gastric emptying, gastroduodenal motility, and pancreatic secretion of trypsin and lipase measured simultaneously in six normal volunteers using multilumen tubes for infusion of markers, manometry, and aspiration of gastric and duodenal contents. The infusion resulted in plasma concentrations of 203 +/- 21 pmol/liter (mean +/- SEM) of oxyntomodulin, regarded as high but not unphysiological concentrations of the peptide. Oxyntomodulin almost abolished basal acid secretion and inhibited postprandial acid secretion by 35 +/- 10%. Gastric emptying decreased significantly; the time for 50% to leave the stomach increased from 17.3 +/- 2.2 min to 34.7 +/- 8.0 min. The postprandial gastroduodenal motility was massively inhibited by oxyntomodulin. Postprandial trypsin and lipase output was significantly inhibited by 56 +/- 12% and 42 +/- 11%, respectively, during oxyntomodulin infusion. However, pancreatic enzyme output was linearly related to gastric emptying and oxyntomodulin did not influence this relationship, suggesting that oxyntomodulins effect was due to its effect on gastric emptying. Oxyntomodulin seems to play an important role in the small intestinal inhibitory control of gastropancreatic functions.
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PMID:Oxyntomodulin from distal gut. Role in regulation of gastric and pancreatic functions. 267 Apr 87

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. 308 29

Serum HDL cholesterol, apolipoproteins AI and AII and post heparin lipolytic activities (PHLA) have been measured in a group of fourteen hypothyroid women without ovarian oestrogen secretion before and during a 2-month thyroxine treatment. The more rapid and consistent observed event was a decrease in apo AI levels (164 +/- 5 vs. 149 +/- 5 mg dl-1, mean +/- SEM, P less than 0.05) correlated (r = 0.79, P less than 0.05) to a slight increment of PHLA. A slight decrease in apo AII concentration was seen only after 5 days (25 +/- 2 vs. 22 +/- 2 mg dl-1, P less than 0.05) and in HDL cholesterol only after 60 days (1.3 +/- 0.6 vs. 1.1 +/- 0.5 mmol 1-1, P less than 0.05). Apo AI, HDL2 and HDL3 cholesterol were measured in another group of seven hypothyroid postmenopausal women before and after a 2-month thyroxine treatment. We observed a decrease in HDL2 cholesterol (1.69 +/- 0.20 vs. 1.17 +/- 0.09 mmol 1-1, P less than 0.02) with no changes in HDL3 cholesterol (0.88 +/- 0.09 vs. 0.99 +/- 0.06 mmol 1-1, NS). The decrease in HDL2 cholesterol correlated (r = 0.72, P = 0.05) with that for apo AI. The differential influence of thyroxine (T4) administration on the major HDL components might reflect changes in HDL composition due to the multiple effects of thyroid hormones on lipid metabolism. It can be hypothesized that the decrease in apo AI and HDL2 cholesterol concentrations are due, at least in part, to the increase in hepatic lipase activity.
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PMID:Time-course of alterations of high density lipoproteins (HDL) during thyroxine administration to hypothyroid women. 311 68


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