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Biomedical subjects

C M Mansbach

Publications and source records attributed to C M Mansbach.

At least 55 records · Page 3Linked to original sources
PubMed1984

Regulation of de novo phosphatidylcholine biosynthesis during renal growth.

Potential regulatory steps of de novo renal cortical synthesis of phosphatidylcholine (PC) were investigated during renal growth in rats. Twenty-four hours following unilateral nephrectomy, cortical PC content was increased in the remaining kidney when compared with sham-operated controls, 3.47 +/- 0.07 and 2.79 +/- 0.14 mumol/mg DNA, respectively (P less than 0.02). No alterations occurred in the cortical PC precursor pools of choline, phosphocholine, cytidine diphosphocholine, or diacylglycerol. At 15 min after the injection of 32P, the incorporation of isotope into the PC pool was increased in the contralateral kidney when compared with sham-operated controls. The calculated maximal velocities of choline kinase and cholinephosphotransferase were increased subsequent to unilateral nephrectomy, supporting a regulatory role for these enzymes in PC biosynthesis during renal growth.

Animals↗
PubMed1984

Hepatic uptake of chylomicrons and triglyceride emulsions in rats fed diets of differing fat content.

The hepatic removal of plasma chylomicrons was determined for rats fed the following diets: a) containing no triglyceride, b) regular chow diet with 4.5% of its mass as lipid and, c) a corn oil-supplemented chow with triglyceride accounting for 20% of the mass. The fractional hepatic uptake of either radiolabeled chylomicrons or a triglyceride emulsion was reciprocally related to the amount of lipid in the diet. The animals receiving only carbohydrate and protein calories had the most active hepatic uptake of particulate triglyceride and were observed to have a significant decrease in the plasma concentration of the C apolipoproteins. The addition of either C-I, C-II, or C-III apoproteins to the triglyceride emulsion prior to intravenous injection produced a significantly lower hepatic triglyceride recovery of emulsions containing apoC-III. When the plasma of animals fed a fat-free diet was supplemented with human C-III-1 apolipoprotein, the distribution into the liver of either enterally administered fatty acid or parenteral triglyceride was diminished. The triglyceride content in the liver of the rats fed fat-free or corn oil-supplemented diets was significantly greater than that of the control rats and composition was somewhat similar to that of lymph triglyceride. The studies indicate an important influence of dietary lipid on both the partition of plasma triglyceride into the liver and the steady state hepatic triglyceride content.

Animals↗
PubMed1983

Determination of intracellular choline levels by an enzymatic assay.

A sensitive enzymatic assay for the measurement of intracellular choline is described. The separation of choline from choline-containing phospholipids is accomplished by a minor modification of the Folch technique. The method is based on the specific oxidation of choline by choline oxidase. Phenol and 4-aminoantipyrine in the presence of hydrogen peroxide generated by the oxidation of choline and peroxidase form a red quinone dye which can be detected spectrophotometrically. The assay was useful between 12.5 and 100 nanomoles of choline. The recovery of standard choline in liver homogenates averaged 102 +/- 1.6%. Structurally similar compounds produced minimal interference.

Alcohol Oxidoreductases↗
PubMed1983

Effect of ethanol on intestinal lipid absorption in the rat.

The effect of ethanol infusion on intestinal lipid absorption was studied in rats with a duodenal cannula. Rats were infused with ethanol overnight and ethanol was included in a trioleoylglycerol emulsion infusion given for 3 hr the next day. These rats were compared to control animals infused with glucose (isocalorically). The ethanol-infused rats had a greatly impaired lipid absorptive capacity. The monoacylglycerol and free fatty acid contents in the intestinal lumen in the ethanol-infused rats were 4- and 7-fold greater, respectively, than controls. The inhibition of absorption was not due to an effect of ethanol on lipolytic activity. The lipase content of the ethanol-infused rats was greater than controls and the separate infusion of monoacylglycerol and fatty acids demonstrated impaired absorption of these end products of lipolysis as compared to controls. To observe if these changes were due to an effect of ethanol on the enterocyte brush border membrane, the membrane lipids were analyzed. The phosphatidylcholine, lysophosphatidylcholine, and phosphatidylethanolanine content was reduced but not the neutral lipids, sphingomyelin, or phosphatidylserine. The uptake of fatty acid into intestinal rings was also shown to be impaired by ethanol infusion. Lastly, the specific activity of the neutral lipids remaining in the intestinal lumen after [3H]glycerol-labeled trioleoylglycerol-infusion was similar to controls even though the mass was much greater. It is concluded that ethanol impairs neutral lipid absorption due to an effect on the enterocyte brush border membrane and by increasing the efflux of low specific activity lipid from the enterocyte back out into the intestinal lumen. A potential pathway for this efflux is the recently described increased porosity of the apical junctional complex in response to ethanol infusion.

Animals↗
PubMed1982

Novel intestinal phospholipase A2: purification and some molecular characteristics.

We purified to homogeneity a new phospholipase A2 from pig ileum which hydrolyzes phosphatidylglycerol at least 200 times more rapidly than phosphatidylcholine. The method involved the following steps: (1) complete delipidation of ileal homogenates by solvent extraction; (2) fractionation and partition between n-butanol and (NH4)2SO4 solution; (3) hydrophobic affinity chromatography on octyl-Sepharose; (4) adsorption chromatography on hydroxylapatite; (5) ion-exchange chromatography on carboxymethyl-Sepharose. Amino acid composition, molecular weight (15 000-16 000), N-terminal amino acid sequence to residue 48, and enzymatic activity on phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, and phosphatidylglycerol were determined.

Amino Acid Sequence↗
PubMed1982

Intestinal phospholipase, a novel enzyme.

We evaluated phospholipase activity in the intestine of rats and other species. Phospholipase activity was assayed by a surface barostat technique or an egg yolk titration system. Mucosal activity was found only by the surface barostat technique with phosphatidylglycerol as substrate; it was not found with phosphatidylcholine as substrate in assays by either technique. In gut luminal fluid activity was found when both phosphatidylcholine and phosphatidylglycerol were used as substrate in assays by the surface barostat technique, and phosphatidylcholine as substrate yielded activity in egg yolk titration. In rats in which pancreatic juice had been diverted, mucosal and gut luminal phospholipase activity was greater than in controls, thus demonstrating that enzyme activity was not due to pancreatic phospholipase. Bacterial origin of phospholipase activity was excluded in that phospholipase activity was found in germ-free rats; gastric and salivary gland origins were excluded in that continued phospholipase activity was found in rats with gastric fistula. The physiological importance of the enzyme was established by the finding that rats with pancreatic fistula absorbed 111 mumol of phosphatidylcholine and that controls absorbed 119 mumol of a 135-mumol load. Activity was found to be three times greater in the distal than in the proximal intestine; in cryptal cells it was 10 times greater than in villus tip cells. 65% of the activity in the gut lumen was tightly bound to particulate matter. We propose that intestinal phospholipase may be important in gut bacterial control, in the digestion of vegetable matter (phosphatidylglycerol is a major phospholipid in both plants and bacteria), and in the digestion of phospholipids in the gut lumen.

Animals↗
PubMed1982

A re-examination of the fate of glyceride-glycerol in neutral lipid absorption and transport.

Conventional ideas concerning the unidirectional movement of triacylglycerol from intestinal lumen to lymph with sn-2-monoacylglycerol being the major glyceride-glycerol precursor were challenged by our finding that steady state specific activities of radiolabeled triacylglycerol (glyceryl moiety) in the intestinal mucosa and lumen were greatly reduced as compared to the specific activity of intraduodenally infused triacylglycerol. Investigation of the point at which the radiolabel was diluted was performed in mesenteric lymph duct-cannulated rats with a duodenal cannula through which trioleoyl[3H]glycerol was constantly infused. Both within the bowel lumen and in the intestinal mucosa, monoacylglycerol, diacylglycerol, and triacylglycerol specific activities were 31% or less of the specific activity of the infusate; chylomicron triacylglycerol specific activity was 75%. Efflux of neutral lipid from the mucosa into the bowel lumen was directly demonstrated by finding that when 3H glucose was injected intraperitoneally during triolein infusion, luminal triacylglycerol had a higher specific activity than was present in the mucosa. We conclude that there are two pools of mucosal triacylglycerol. One is rapidly transported and derives most of its glyceride-glycerol from luminal monoacylglycerol. The second is slowly transported; it derives its glyceride-glycerol mainly from endogenous sources and may efflux back into the bowel lumen.

Animals↗
PubMed1980

The contribution of serum phosphatidylcholine and lysophosphatidylcholine to lymph phosphatidylcholine.

1. The contribution of serum phosphatidylcholine and 1-acyl lysophosphatidylcholine to chylomicron and mesenteric lymph lipoproteins of heavier buoyant density was studied in rats with catheters placed in the jugular vein, duodenum, common bile duct and mesenteric lymph duct. The effect of including 10 mM phosphatidylcholine in the triolein emulsion infused into the duodenum was also studied. 2. The intravenous infusion of phosphatidylcholine did not affect delivery of phosphatidylcholine into the lymph when phosphatidylcholine was included in the duodenal infusion. However, on intravenous lysophosphatidylcholine infusion, phosphatidylcholine transport into the lymph was increased both in chylomicrons and the other lipoproteins found in the lymph when phosphatidylcholine was included in the duodenal infusion. 3. The incorporation of serum phosphatidylcholine into chylomicron phosphatidylcholine was minimal and decreased further by intraduodenal phosphatidylcholine infusion. Incorporation into the heavier lymph lipoproteins was less than 20%. 4. The incorporation of serum lysophosphatidylcholine into chylomicrons was 17% at 4--6 h of infusion which was decreased by intraduodenal phosphatidylcholine as was the incorporation into the heavier lipoproteins of lymph. 5. It is concluded that serum phosphatidylcholine is a poor precursor of chylomicron phosphatidylcholine and that while lysophosphatidylcholine is a somewhat better precursor, its contribution to chylomicron phosphatidylcholine is limited by its serum concentration.

Animals↗
PubMed1980

Fat digestion in patients with bile acid malabsorption but minimal steatorrhea.

Patients with an interrupted enterohepatic circulation of bile acids and minimal or no steatorrhea were studied to determine if their fat absorption was aided by compensatory mechanisms which delivered increased amounts of lipid to the aqueous phase of post-prandial duodenal fluid. The data suggested that the molar stoichiometry of association of fatty acid and bile acid in an aggregated (micelle) form was reduced in the patients (0.8) as compared to normals (1.4). Each patient had either normal sized or undetectable micelles; one patient had a large fatty acid-rich aggregated species. The bile acid composition of the whole duodenal fluid was found to have an increased proportion of dihydroxy bile acids which were conjugated with glycine. There was a selective precipitation of dihydroxybile acids from the aqueous phase, such that the patients had a normal proportion of these bile acids in the aqueous phase. We were unable to identify a consistent compensatory mechanism whereby these patients could increase the concentration of lipid in the aqueous phase which would have led to a better understanding of their minimal steatorrhea. We believe that the reduced stoichiometry of aggregated fatty acid to aggregated bile acid is in part due to the altered bile acid pool composition of these patients.

Bile Acids and Salts↗
PubMed1978

beta-Sitosterol as a nonabsorbable marker of dietary lipid absorption in man.

beta-[14C]Sitosterol was evaluated for its usefulness as a nonabsorbable marker of lipid absorption in intubation studies. A liquid meal, including [3H]triolein as a marker of absorbable lipid, was used. The beta-sitosterol was shown to remain well mixed with triolein in the gastric antrum, validating its suitability for this type of study. In small bowel fluid, the beta-sitosterol was shown to partition into the aqueous phase in proportion to triolein and its hydrolysis products. With this system, lipid absorption was shown to take place chiefly in the jejunum in normal individuals.

Carbon Radioisotopes↗
PubMed1978

Enterocyte turnover and content in fat-fed hamsters.

Cryptal lecithin-synthesizing enzyme specific activities have been previously demonstrated to be increased by feeding a fat-supplemented diet to hamsters. To determine if a physiological basis exists for such changes [3H]thymidine incorporation, cellular migration rate, and mucosal concentration of DNA, protein, and lecithin were measured. Radioautographic studies showed that the labeling index and cell migration rate throughout the intestine in the fat-fed hamsters and in the proximal three-quarters of the intestine of the control group were the same. Both parameters were reduced in the distal quarter of the control intestine. The protein/DNA ratio was significantly increased in the proximal three-quarters and modestly in the distal quarter of the intestine of the fat-fed group as compared to controls, suggesting cellular hypertrophy. The lecithin content of the proximal three-quarters of intestine was the same in both groups but reduced in the distal quarter of the gut of the fat-fed group. These studies suggest that lipid feeding in the hamster can have profound effects on intestinal cellular content and turnover.

Animals↗
PubMed1978

Lymph-node bacilliform bodies resembling those of Whipple's disease in a patient without intestinal involvement.

A 38-year-old man developed symptoms of arthalgias and arthritis, lymphadenopathy, and weight loss. An axillary lymph-node biopsy was done in the diagnostic study; a periodic acid Schiff stain, done for evidence of fungal infection, showed periodic acid Schiff reagent-positive macrophages. Electron microscopy showed the typical morphologic features of the bacilliform bodies associated with Whipple's disease to be present in the macrophages of the lymph node. The patient had no intestinal symptoms. The absorption of a variety of substrates was found to be normal. Nine intestinal biopsies showed no organisms similar to those found in his lymph node. On tetracycline therapy, he symptomatically improved. The findings raise the question of the route of infection in Whipple's disease and point up the usefulness of periodic acid Schiff staining of lymph-node biopsies.

Adult↗
PubMed1977

Gastric ulcer: effect of healing on gastric acid secretion and fasting serum gastrin levels.

In 15 patients with uncomplicated gastric ulcers, basal and peak gastric acid outputs and fasting serum gastrin levels were studied before and after healing. The mean basal acid output [4.0 +/- 1.3 (SEM) mEq H+/hr], the mean peak acid output (29.5 +/- 5.1 mEq H+/hr), and the mean fasting serum gastrin level (80.3 +/- 16.7 pg/ml) in these patients did not change significantly with healing. Failure of gastric secretory function to change with healing suggests that mucosal resistance factors are more important than gastric acid secretion in the pathogenesis of a gastric ulcer.

Gastric Juice↗
PubMed1977

The origin of chylomicron phosphatidylcholine in the rat.

This study investigates the pathways of origin of chylomicron phosphatidylcholine (PC) using a lymph- and bile-fistulated rat infused with a stabilized triolein emulsion. [(14)C-glycerol]PC was used to evaluate chylomicron PC generated by lyso PC acyltransferase. The percentage of chylomicron PC derived from the PC infused was directly proportional to the PC concentration in the infusate. When the infusate PC concentration was 10 mM, essentially all the chylomicron PC was derived therefrom at 4-6 h of infusion. Incorporation of the radiolabel was not found to be as great in the lymph subnatant PC as in chylomicron PC, suggesting that chylomicron and lymph subnatant PC might be supplied from different PC precursor pools.(32)P(i) was infused into similarly prepared rats to judge chylomicron PC synthesized from de novo sources. In these experiments it was found that the percentage of chylomicron PC derived from de novo synthesis was inversely related to the PC concentration of the infusate. This suggests that exogenously infused PC inhibits de novo PC synthesis. When [(32)P]rat bile PC was infused with [(14)C-glycerol]potato PC, the bile PC was preferred as a chylomicron precursor despite the greater similarity of the saturated fatty acids of potato PC to those of chylomicron PC. When the saturated fatty acids of bile and chylomicron PC were compared, chylomicron PC was significantly richer in stearate, suggesting extensive enterocyte modification of the saturated fatty acids of bile PC.

Animals↗