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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetes stimulates the functional activity of the intestinal brush border membrane with enhancement of both hydrolytic enzyme activity and membrane transport systems. To determine the mechanism of this effect, we studied the effects of streptozotocin diabetes on the metabolism of one membrane protein, sucrase-isomaltase, which increases its activity in diabetes. The protein was purified and an antiserum prepared. Sucrase-isomaltase from control and diabetic rats was immunologically identical as shown by Ouchterlony double-diffusion analysis of papain-solubilized mucosal proteins. The increase in sucrase enzyme activity in diabetic animals (31.0+/-1.4 U SEM 5 days after streptozotocin vs. 13.1+/-1.0 in controls) was the consequence of increased enzyme protein and not an alteration in catalytic efficiency as demonstrated by quantitative immunoprecipitin reactions. To account for increased sucrase-isomaltase protein in diabetes we studied papain-solubilized mucosal proteins labeled by injection of [(14)C]carbonate and [(14)C]leucine and analyzed incorporation into sucrase-isomaltase protein (anti-serum precipitable) and total protein (trichloroacetic acid precipitable). We found that diabetes did not affect the decay of labeled total protein, but prolonged the decay of labeled sucrase-isomaltase. t((1/2)) of sucrase-isomaltase was 4.4 h in control animals after [(14)C]carbonate injection and 8.8 and 10.2 h, respectively, 2 and 5 days after induction of streptozotocin diabetes. We obtained similar results in experiments with [(14)C]leucine with diabetes increasing t((1/2)) from 6 to 13.6 h. Diabetes did not appear to increase the rate of addition of sucrase-isomaltase to the brush border membrane, since it did not affect the 10- and 60-min incorporations of isotope into sucrase-isomaltase protein relative to incorporation into total protein and did not alter rate constants for synthesis calculated from the t((1/2)) and the change in enzyme mass over time.Thus, enhanced sucrase activity in the diabetic animal is the consequence of an increase in sucrase-isomaltase protein which develops because of a decrease in its rate of degradation.
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PMID:The intestinal brush border membrane in diabetes. Studies of sucrase-isomaltase metabolism in rats with streptozotocin diabetes. 14 62

Addition of HCO3- to the serosal side (S) of the isolated turtle bladder results in a HCO3- flow from S to the mucosal side (M) which markedly reduces the net rate of acid secretion. To characterize the driving forces for this downhill HCO3- flow, the effects of metabolic inhibitors and substrates were examined. In short-circuited bladders with the M pH lowered to the point of zero net H+ secretion, the rate of HCO3- entry into M in response to a 20-mM HCO3- gradient was measured by pH stat titration. Deoxygenation reduced the HCO3- flux from 1.24 plus or minus 0.1 mum/h/8 cm2 (SEM) to 0.50 plus or minus 0.1 muM/h with glucose (2 times 10-3 M) AND FROM 1.32 PLUS OR MINUS TO 0.47 PLUS OR MINUS 0.1 MUM/h without glucose. A similar reduction (61 per cent) was observed in the presence of 1 per cent C92. Dinitrophenol (10-4 M), cyanide (10-3 M), and deoxyglucose (10-2 M) inhibited the HCO3- flux by 39 per cent, 37 per cent, and 38 per cent, respectively. The combination of any of these inhibitors with N2 caused the same inhibition as N2 alone. In bladders depleted of substrate, pyruvate (5 times 10-3 M) increased the HCO3- flux from 0.36 plus or minus 0.05 to 0.58 plus or minus 0.01 muM/h (P smaller than 0.005); the increment was abolished by deoxygenation. The results indicate that the bulk of the downhill HCO3- flow in this system is dependent on metabolic energy derived primarily from oxidative sources, and that this energy-dependent flow approximates the electroneutral component of HCO3- secretion that is coupled to Cl- absorption.
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PMID:Energy dependence of urinary bicarbonate secretion in turtle bladder. 23 65

Microsomal fractions from homogenates of pig gastric fundic mucosa showed high levels of K+-stimulated adenosine triphosphatase (ATPase) and K+-stimulated phosphatase. Similar preparations from antral mucosa showed virtually no such activity. Because of mitochondrial contamination the fundic microsomes were further separated by sucrose density gradient centrifugation. A low density band of membranes (peak 1.12 to 1.13 g per ml) possessed all of the K+-stimulated enzyme activities. Morphological features and the abundant glycoproteins of the low density microsomes suggested they might be derived from the tubulovesicles of oxyntic cells. Mitochondrial and ribosomal markers were associated with membranes with much higher densities (greater than 1.22). The K+-stimulated ATPase has a pH optimum of 7.5 and required Mg++, but neither Na+ nor ouabain had any appreciable effect on the activity. Stimulation of basal ATPase by K+ ranged from 1.5 to 3.0-fold with an apparent Ka for activation between 0.2 to 0.4 mM K+. Addition of various K+ ionophoretic substances (e.g., gramicidin) produced further stimulation of K+-ATPase up to 6 times the basal rate. The mean activities for seven separate preparations of purified low density pig fundic microsomes were as follows (micromoles of ATP hydrolyzed per mg protein per hr +/- SEM); basal ATPase, 15.8 +/- 2.8; plus 10 mM K+, 29.3 +/- 4.5; plus 10 mM K+ and 10(-5) M gramicidin, 45.2 +/- 5.2. Neither the basal ATPase nor the K+-stimulated rates were altered by HCO3- or Cl-. The occurrence of these active and unique enzyme activities in the oxyntic region of gastric mucosa suggest some relation with secretory activity. Possible functional roles are discussed.
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PMID:Unique enzymes of purified microsomes from pig fundic mucosa. K+-stimulated adenosine triphosphatase and K+-stimulated pNPPase. 23 96

A multilumen balloon tube constructed to separate duodenal and jejunal perfusion segments was placed in the proximal small bowel of 6 healthy volunteers. The effect of nutrient mixture in the duodenum on net jejunal water and electrolyte flux was then determined. The duodenum was perfused with a balanced electrolyte solution before and after the nutrient perfusion. Net water flux in the perfused jejunum changed from absorption 27.0 +/- 6.0 microliter/min/cm, (mean +/- SEM) to secretion 7.7 +/- 7.3 microliter/min/cm (P less than 0.025) during nutrient perfusion. There was also net chloride secretion and decreased net absorption of Na, K, and HCO3 (P less than 0.05). The jejunal absorption of water and electrolytes before and after the duodenal nutrient perfusion was the same. Results indicate that intestinal secretion may occur under physiologic conditions at sites remote to the application of food in humans.
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PMID:Jejunal secretion in response to a duodenal mixed nutrient perfusion. 75 54

In patients with chronic renal failure (CRF) (CCr less than 20 ml/min), we have previously demonstrated greater rates of Na excretion (ex) when Na intake was nearly all NaHCO3 as compared to NaCl (both 200 mEq Na daily). Chloride (Cl) wasting on NaHCO3 (with severe Cl restriction) occurred, however, and may in part explain the results. To avoid Cl restriction in 6 patients with CRF (CCr 10-15 ml/min) on an estimated 10 mEq Na and Cl diet, electrolyte ex was compared on NaCl supplements of 200 mEq/day versus a daily mixture of NaHCO3 (100mEq) and NaCl (100 mEq). Periods on NaCl and the mixture lasted 4 days (order randomized) separated by re-equilibration to baseline weight (wt). Mean +/- SEM ex of Na, Cl, HCO3 mEq/day and CCr and deltawt (lbs) are compared below for the 4th day of NaCl vs NaHCO3 intake. (see article). Also there were no significant differences in K excretion, blood pressure, or plasma renin activities. Mean serum HCO3 increased from 21.2 to 25.8 mEq/l (day 1 vs 5, P less than 0.01) reflecting the net positive HCO3 balance on the mixture indicated above. Thus increments of Na intake above a fixed NaCl intake were excreted similarly whether given as NaCl or NaHCO3. Greater Na ex on NaHCO3 may depend on severe Cl restriction and/or higher serum HCO3 levels. If dietary NaCl intakes are near maximum tolerance, NaHCO3 supplementation should be accompanied by reductions in NaCl intake to maintain Na balance,
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PMID:NaHCO3 and NaCl tolerance in chronic renal failure II. 83 32

In patients with chronic renal failure, NaHCO3 therapy may correct or prevent acidemia. It has been proposed that the NaHCO3 required will not result in clinically significant Na retention comparable to that from similar increases in NaC1 intake. In each of ten patients with chronic renal failure, creatinine clearance (Ccr) range 2.5-16.8 ml/min, on an estimated 10-meq Na and C1 diet, electrolyte excretion was compared on NaHCO3 vs NaC1 supplements of 200 meq/day. Periods of NaHCO3 and NaC1 (in alternate order for successive patients) lasted 4 days, separated by reequilibration to base-line weight. Mean +/- SEM excretion (ex) of Na, C1, and HCO3 and deltaCcr and deltaweight (day 4-1) are compared below for the 4th day of NaC1 vs. NaHCO3 intake. Mean Ccr +/-SEM on day 4 of NaC1 and NaHCO3 were 10.8 +/-1.6 and 9.0 +/-1.4 ml/min, respectively (P less than 0.02). Mean systolic blood pressure (but not diastolic) increased significantly on NaC1 (P less than 0.05). No significant blood pressure changes were seen on NaHCO3. Net positive HCO3 balance occurred on NaHCO3 as indicated above and reflected a rise in mean serum HCO3 from 19 to 30 meq/liter (day 1 vs. 4) (P less than 0.01). Mechanisms for the greater excretion of Na on NaHCO3 may relate to C1 wasting as noted above on low C1 intake and limited HCO3 reabsorptive capacity. Thus, Na excretion by day 4 was greater on NaHCO3 than on NaHCO3 did Na excretion near intake (210 meq/day).
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PMID:NaHCO3 and NaC1 tolerance in chronic renal failure. 115 Aug 79

By means of the newly developed Replamineform process, the unique pore microstructures found in the skeletal calcium carbonate of certain reef corals can be replicated or reproduced with high precision in a wide variety of materials suitable for hard tissue implant and prosthetic applications. The advantages of fabricating porous biomaterials with this method include closely controlled size of both the pore diameters and the diameters of the pore interconnections, and virtually complete interconnection of the uniformly spaced pores. These properties are of great importance in implant devices, because tissue ingrowth, the stimulation of new bone formation, the suppression of undesirable scar tissue, the inhibition of adverse body responses, and firm biological fixation of the implanted material all depend upon the nature of the pore-microstructure configuration. Replamineform preparation of Al2O3, TiO2, hydroxyapatite, silver, Co-Cr-Mo alloys, and polymers is described in detail, and the characterization procedures used to determine the physical and structural properties of their materials are discussed. A few of the routinely measured characteristics include (1) quantitative computerized SEM image analysis for determining the volume, size and shape distributions of the macro and microporosity and the grain size measurement of the solid; (2) nondestructive x-radiography of specimens to reveal any internal defects; (3) mechanical strength measurements of randomly selected specimens. Experimental results up to now clearly demonstrate the superiority of microstructures imparted to metals, ceramics, and polymers with the Replamineform process.
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PMID:Replamineform porous biomaterials for hard tissue implant applications. 117 5

1. Renal and systemic responses to infusion of angiotensin II (1.25 and 2.5 ng min-1 kg-1 body weight) were examined in ten normal males 12 h after single doses of 750 mg of lithium carbonate, 250 mg of lithium carbonate (n = 6) or placebo. 2. Baseline mean arterial pressure [mean (SEM)] was higher after 750 mg of lithium [93.1 (1.7) versus 89.5 (1.9 mmHg, P = 0.014], and the subsequent rise in blood pressure during angiotensin II infusion was lower [8.2 (1.8) versus 12.2 (2.4) mmHg, P less than 0.02]. 3. Lithium at a dose of 750 mg increased overnight urinary sodium excretion before the study. The fall in fractional sodium excretion during angiotensin II infusion was reduced after pretreatment with 750 mg of lithium [750 mg of lithium, 2.73 (0.24) to 1.34 (0.08)%; placebo, 2.69 (0.26) to 1.01 (0.11)%; P = 0.02]. The increases in effective filtration fraction [750 mg of lithium, 5.4 (1.0)%; placebo, 8.6 (0.7)%; P less than 0.05] and total effective renal vascular resistance [750 mg of lithium, 3700 (390) dyn s cm-5; placebo 5100 (460) dyn s cm-5; P = 0.03] during angiotensin II infusion were also attenuated after 750 mg of lithium. Responses after 250 mg of lithium did not differ from those after placebo. 4. The fall in plasma renin activity and the increase in plasma aldosterone concentration during angiotensin II infusion were similar on each study day. 5. Renal responses to exogenous angiotensin II are altered after pretreatment with a 750 mg dose of lithium in normal man. This dose of lithium is not an inert marker of sodium handling.
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PMID:Lithium pretreatment affects renal and systemic responses to angiotensin II infusion in normal man. 131 64

1. The influences of lithium dosage, urine flow rate and acute administration of amiloride on the renal handling of lithium in normal conscious dogs were investigated. 2. Lithium was administered in the diet at daily doses of 100 mg or 2 mg of lithium carbonate for the 2 days preceding the investigation. Urine flow rate was altered by water loading with and without arginine vasopressin infusion (5 pg min-1 kg-1). Amiloride was administered as an intravenous bolus (130 micrograms/kg) followed by a continuous infusion (1.22 micrograms h-1 kg-1). 3. Glomerular filtration rate (exogenous creatinine clearance) did not change within series and was not different between series; it averaged 3.27 ml min-1 kg-1. Control levels of fractional lithium excretion (12.4 +/- 1.2%, mean +/- SEM) were not influenced by hydration, hydration plus arginine vasopressin administration or the lithium dosage. However, in hydrated dogs having a plasma lithium concentration of 130-140 mumol/l, amiloride administration was associated with a 5% increase in fractional lithium excretion (P less than or equal to 0.01). 4. It is concluded that distal tubular lithium reabsorption may take place in sodium-replete conscious dogs undergoing water diuresis. The low fractional lithium excretion even during amiloride infusion (14.1-16.8%) may well be due to a high fractional reabsorption of lithium in the proximal tubules; however, a significant reabsorption of lithium distal to the proximal straight tubules by amiloride-insensitive pathways cannot be excluded.
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PMID:Lithium clearance in dogs: effects of water loading, amiloride and lithium dosage. 132 May 43

We studied the effect of converting 100 established CAPD patients from aluminium- to calcium-based phosphate binders. After a follow-up of 1 year only 60% of patients remained on calcium carbonate. Hypercalcaemia was the major problem, with more than 40% of patients having a serum calcium in excess of 3.0 mmol/l. Several patients required hospitalization for symptomatic hypercalcaemia. Hypercalcaemia was more common in patients with normal serum parathyroid hormone concentrations (65 versus 25%, P less than 0.01). Serum phosphate control was better prior to commencing calcium carbonate when patients were treated with aluminium phosphate binders mean 1.71 +/- 0.15 mmol/l (SEM) than at the time of maximum serum calcium concentration, 1.81 +/- 0.25, P less than 0.05. This study does not confirm the findings of others, which have suggested that calcium carbonate is a safe and effective phosphate binder for patients with end-stage renal failure.
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PMID:Audit of the use of calcium carbonate as a phosphate binder in 100 patients treated with continuous ambulatory peritoneal dialysis. 838 46


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