[Evaluation of an automated assay of thyrotropin receptor antibody (TRAb) on Elecsys Analyser 2010]. / Evaluation du dosage automatisé des auto-anticorps anti-récepteur de la TSH sur l'analyseur Elecsys 2010.

2nd generation assays are currently available to determine the concentration of thyrotropin receptor antibody (TRAb) present in Graves' disease. The aim of this study was to evaluate the analytical performance of TRAb assay on Elecsys 2010 and Cobas(R)e of Roche Diagnostics, a new test using electrochemiluminescence immunoassay (ECLIA). The analytical performance observed with this assay is accurate (repetability and reproductibility, analytical and functional sensitivities). Comparing this method with Brahms' assay (TRAK human RIA), the correlation observed can be put in the equation: y = 1.013 x + 1.381; r = 0.92. With a positive value in ECLIA at 0.9 UI/L and at 1 UI/L in RIA (functional sensitivity fixed by manufacturers), concordance study shows a false negative and two false positive. With a positive value at 0.8 UI/L with ECLIA (functional sensitivity calculated from precision's profile for a CV inferior to 10%), there is no false negative and two false-positive results, this value seems to give a better sensitivity.

Parallel increase of plasma apoproteins C-II and C-III in Type 2 diabetic patients.

AIMS: To determine plasma levels of apoprotein (apo) C-II and apoprotein C-III in Type 2 diabetic patients and to examine the clinical and biological factors that are associated with elevated apoC concentrations. METHODS: We measured apoC-II and apoC-III in total plasma and in non-high-density lipoprotein fractions by an immunoturbidimetric assay in 88 Caucasian Type 2 diabetic patients and in 138 healthy control subjects. RESULTS: Plasma levels of both apoC-II and apoC-III were increased in Type 2 diabetic patients. The clinical conditions associated with an increase of plasma apoC-II and apoC-III were abdominal obesity, body mass index, poor glycaemic control and lack of insulin treatment. However, when multivariate analysis was used, plasma apoCs levels correlated with triglyceride levels only. The apoC-III/apoC-II ratio was similar in the Type 2 diabetic and control subjects. CONCLUSIONS: Our study shows the parallel increase of apoC-II and C-III in Type 2 diabetic patients. This parallel increase is related to hypertriglyceridaemia only.

Multivariate optimization of a derivatisation procedure for the simultaneous determination of nine anabolic steroids by gas chromatography coupled with mass spectrometry.

The medical commission of the International Olympic Committee forbids the use of anabolic androgenic steroids to improve sporting performances. Nine anabolic steroids (androsterone (A), nandrolone, estradiol, testosterone propionate, nandrolone-17 propionate, dydrogesterone, testosterone, epitestosterone, boldenone) and alpha-cholestane as internal standard were studied by gas chromatography coupled with mass spectrometry (GC/MS). The derivatisation reagent employed for the derivatisation of anabolic steroids was a mixture of N-methyl-N-trimethylsilyltrifluoroacetamide (MSTFA), ammonium iodide and 2-mercaptoethanol (1000:2:6, v/w/v). Trimethylsilyl (TMS) derivatives were obtained. Anabolic steroids can be derivatised into one or two forms, mainly for androsterone into A-monoTMS and A-diTMS. The aim of this study was to research the optimization conditions of the derivatisation process (maximum yield of silylation reaction) of each anabolic steroid into only one form. A two-level factorial Doelhert design was used to determine the influence of different parameters and their interactions on each compound, thanks to response surface methodology. The parameters to be optimized were the reaction time and the temperature. The interaction "temperature-reaction time" is significant and has a positive effect on the improvement of the effectiveness of the derivatisation. Considering the large amount of information, often not convergent, a global desirability function was applied for multi-responses optimization. Thus, the optimized temperature and the reaction time of silylation were 85 degrees C and 24 min, respectively. Several GC/MS analytical parameters were also studied: linearity (regression coefficient upper than 0.99 for each compound, sensibility (range of concentration 0.05-0.30 microg/ml). Confirmatory experiments were applied to check the predicted values and to validate the model. The confirmatory assay responses are relatively close to the responses predicted. We observed satisfactory resolutions by GC/MS and a run lower than 12 min.

Lack of toxicity of hydroethanolic extract from Mitragyna inermis (Willd.) O. Kuntze by gavage in the rat.

In traditional medicine in Mali, extracts derived from Mitragyna inermis (Willd.) O. Kuntze (Family: Rubiaceae) are commonly used to treat malaria. The antimalarial activity and the lack of genotoxicity in vitro and in vivo have been demonstrated in previous studies. Acute and chronic evaluation of the toxicity of the hydroethanolic extract of Mitragyna inermis leaves was performed in this study, according to the recommendations (cahier de l'Agence no. 3) of the French Drug Office. Two dosages (300 mg/kg and 3 g/kg) were given in one single administration by gavage to male and female rats. No animal died and no behavioral signs of acute toxicity were observed. Chronic toxicity studies over 28 days showed no changes in body weight and no macroscopic abnormality in the 14 organs examined after the animals were sacrificed. With the 3 g/kg/d drug dosage (100-fold higher than those proposed in man), only slight histological abnormalities were observed. Statistically significant differences, compared to control animals, in the weight of some organs and the values of some haematological or biochemical parameters were observed. However, these values always remained in the range given by the breeder for naive animals of the same strain. These investigations thus seemed to indicate the safety of repeated oral administration (up to 3 g/kg/d) of the hydroethanolic extract of Mitragyna inermis leaves, which can therefore be continuously used with safety by the African population in traditional treatment of malaria.

Effects of salmon oil and corn oil on plasma lipid level and hepato-biliary cholesterol metabolism in rats.

The aim of this work was to compare the effects of n-3 and n-6 fatty acids on plasma lipid level and hepato-biliary cholesterol metabolism by studying rats fed semi-synthetic diets enriched with either 10% salmon oil, 10% corn oil, or a blend of 6% corn oil and 4% salmon oil. After 4 weeks of feeding, a drop in plasma lipid level was noted in the salmon oil group in comparison to the control group, whereas no change was observed in the corn oil group. An increase in production of cholesterol ester by the liver was recorded in the salmon oil group with a marked enhancement in acyl-CoA:cholesterol acyltransferase (ACAT: EC 2.3.1.26) activity and hepatic cholesterol concentration. Corn oil did not affect either ACAT activity or hepatic cholesterol storage. All bile parameters (flow, bile salts, phospholipids, cholesterol) increased in the salmon oil group, but the molar ratio of cholesterol participation in the bile secretion decreased. These changes in bile composition, as well as in hepatic metabolism of cholesterol, may help to explain the hypolipidemia following the intake of fish oil.

Subcellular localization of rat gastric phospholipase A2.

In the present study, we have performed experiments to gain some insight into the subcellular localization and biochemical properties of gastric mucosal phospholipase A2. After classical subcellular fractionation of whole glandular stomach mucosa, we found that gastric phospholipase A2 was essentially enriched in the 105,000 x g pellet that contains microsomes and plasma membranes. Except for the cytosol, all the subcellular fractions exhibited similar phospholipase A2 activity (i.e., optimum of pH, calcium dependence, apparent Km and positional specificity). The high-speed pellet was further characterized by ultracentrifugation on a sucrose gradient. Data showed that the sedimentation profile of phospholipase A2 was quite similar to those of plasma membrane markers and more specifically to an apical membrane marker. These results, taken together, showed that a gastric phospholipase A2 is distributed among the various subcellular fractions (as a result of cross-contamination) together with the membrane fraction on which it is associated. It is proposed that this fraction is the apical plasma membrane which would be the main site of phospholipase A2 action for arachidonic acid release. Lysophospholipase showed the same sedimentation profile as phospholipase A2, whereas acyl CoA-lysophosphatidylcholine: acyltransferase mainly sedimented with heavy microsomes. The substrate specificity of the enzyme was assessed by endogenous hydrolysis of gastric mucosal phospholipids. We were able to show that the enzyme acts at nearly the same rate on two major gastric membrane phospholipids, namely phosphatidylcholine and phosphatidylethanolamine.

Effect of increasing amounts of dietary fish oil on brain and liver fatty composition.

Increasing dietary fish oil in rat had the following effect on brain lipids: Arachidonic acid regularly decreased; eicosapentanenoic acid, normally nearly undetectable, was present; 22:5(n - 3), dramatically increased but remained below 1% of total fatty acids; cervonic acid was increased by 30% at high fish oil concentration. Saturated and monounsaturated fatty acids were not affected regardless of chain-length. In contrast, in the liver, nearly all fatty acids (saturated, monounsaturated and polyunsaturated) were affected by high dietary content of fish oil, but liver function was normal: serum vitamin A and E, glutathione peroxidase, alkaline phosphatase, transaminases were not affected. Serum total cholesterol, unesterified cholesterol and phosphatidylcholine were slightly affected. In contrast, triacylglycerols were dramatically reduced in proportion to the fish oil content of the diet.

Acute hyperinsulinism modulates plasma apolipoprotein B-48 triglyceride-rich lipoproteins in healthy subjects during the postprandial period.

The role of postprandial insulin in the regulation of postprandial lipid metabolism is still poorly understood. The roles of hyperinsulinemia and insulin resistance in the alteration of postprandial lipid metabolism are not clear either. To improve knowledge in this area, we submitted healthy men to acute hyperinsulinemia in two different ways. In the first study, we compared in 10 men the effects of four isolipidic test meals that induce different degrees of hyperinsulinemia on postprandial lipid metabolism. Three different carbohydrate sources were compared according to their glycemic indexes (GIs; 35, 75, and 100 for white kidney bean, spaghetti, and white bread test meals, respectively); the fourth test meal did not contain any carbohydrates. Postprandial plasma insulin levels were proportional to the GIs (maximal plasma insulin concentrations: 113 +/- 16 to 266 +/- 36 pmol/l). We found a strong positive correlation during the 6-h postprandial period between apolipoprotein (apo) B-48 plasma concentration and insulin plasma concentration (r2 = 0.70; P = 0.0001). In a second study, 5 of the 10 subjects again ingested the carbohydrate-free meal, but during a 3-h hyperinsulinemic- (550 +/- 145 pmol/l plasma insulin) euglycemic (5.5 +/- 0.8 mmol/l plasma glucose) clamp. A biphasic response was observed with markedly reduced levels of plasma apoB-48 during insulin infusion, followed by a late accumulation of plasma apoB-48 and triglycerides. Overall, the data obtained showed that portal and peripheral hyperinsulinism delays and exacerbates postprandial accumulation of intestinally derived chylomicrons in plasma and thus is involved in the regulation of apoB-48-triglyceride-rich lipoprotein metabolism, in the absence of insulin-resistance syndrome.

Effect of lithium on norepinephrine metabolic pathways.

We investigated lithium-induced changes in norepinephrine (NE) catabolism. NE and its major metabolites 3-methoxy-4-hydroxyphenylglycol (MHPG) and 3,4-dihydroxyphenyl glycol (DHPG), ions such as lithium (Li(+)), magnesium (Mg(2+)), and potassium (K(+)) were measured in rat plasma and cerebral cortex using an HPLC method with electrochemical detection for amines. The results obtained with a group of rats treated by lithium chloride (2 mmol/kg/IP) were compared with a control group receiving sodium chloride (2 mmol/kg/IP). Animals were killed at different times over a period of six hours in the morning following salt administration to minimize possible chronobiological effects. There are two pathways leading to MHPG formation: way A, without DHPG, and way B, with DHPG. In plasma and cerebral cortex of lithium treated rats, way A catabolism seems to be preferential. Lithium increases Mg(2+) and K(+) plasma levels. These results suggest that lithium may increase inactivation of NE and decrease NE available for adrenergic receptors.

Lipoprotein profile and prevalence of cardiovascular risk factors in urban Moroccan women.

OBJECTIVE: The study aimed to characterize the lipid and apolipoprotein profile and the prevalence of cardiovascular risk factors in a population of urban adult women of Morocco. DESIGN: A total of 213 women 25-55 y old were sampled from an agricultural province of Morocco: El Jadida. The following parameters of lipid and apolipoprotein profile were measured: plasma triglycerides (TG), plasma cholesterol (TC), triglyceride-rich lipoprotein triglycerides (TRL-TG), TRL-cholesterol (TRL-C), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and apolipoproteins A1, B, B48, CIII and E. Waist circumference (WC), body mass index (BMI) and blood pressure (BP) were also determined. RESULTS: The women studied showed the following pattern: elevated TC, LDL-C levels and TC/HDL-C in 10, 19.4 and in 43.8%, respectively; low HDL-C levels in 45.3% (<0.9 mmol/l) or in 95% (when the cutoff <1.3 mmol/l is used), elevated TG levels in 11.8%. Elevated TRL-C (>0.6 mmol/l) and TRL-TG (>0.8 mmol/l) were observed in 13.4%. Obesity and hypertension were highly prevalent in 23.9 and 16.5%, respectively. Plasma triglyceride concentrations were closely correlated with plasma concentrations of TRL-TG (R = 0.86, P = 0.0001), apoB (R = 0.50, P = 0.0001) and apoCIII (R = 0.52, P = 0.0001) and moderately correlated with HDL-C levels (R = -0.3, P = 0.0001) and BMI (R = 0.4, P = 0.0001). The association between BMI and systolic blood pressure was statistically significant (R = 0.3, P = 0.0001). Obesity, BP, TRL-C, TRL-TG, TG, apoB and apoCIII increased with age. CONCLUSION: There is a high prevalence of some risk factors for cardiovascular disease including altered lipid and lipoprotein profiles in the Moroccan urban women studied, some of these risk factors are associated with age.

Influence of obesity and body fat distribution on postprandial lipemia and triglyceride-rich lipoproteins in adult women.

We know that upper body obesity is associated with metabolic complications, but we don't know how regional body fat distribution influences postprandial lipemia in obese adults. Thus, this study explored the respective effects of android or gynoid types of obesity and fasting triglyceridemia on postprandial lipid metabolism and especially triglyceride-rich lipoproteins. Twenty-four obese and 6 lean normotriglyceridemic women (control), age 24-57 yr, were enrolled. Among obese women with an android phenotype, 9 exhibited normal plasma triglyceride levels (mean: 1.38 mmol/L) (NTAO), and 7 displayed a frank hypertriglyceridemia (mean: 2.40 mmol/L) (HTAO). The 8 patients with a gynoid phenotype had normal triglyceride levels (mean: 1.00 mmol/L) (GO). All were given a mixed test meal providing 40 g triglycerides. Serum and incremental chylomicron triglycerides 0-7 h areas under the curve (AUCs) as well as triglyceride levels in apoB-48-containing triglyceride-rich lipoprotein (TRLs) or chylomicrons were significantly higher in HTAOs and NTAOs than in GOs and controls postprandially. The size of chylomicron particles was bigger in controls and GOs than in HTAOs and NTAOs postprandially. Android obese subjects showed abnormally elevated fasting apoB-48 and apoB-100 triglyceride-rich lipoprotein (TRL) levels. Most abnormalities that were found correlated to plasma levels of insulin and apoC-III. In conclusion, an abnormal postprandial lipid pattern is a trait of abdominal obesity even without fasting hypertriglyceridemia.

Effects of oat bran, rice bran, wheat fiber, and wheat germ on postprandial lipemia in healthy adults.

Six normolipidemic males ingested on separate days a low-fiber test meal [2.8 g dietary fiber (TDF)] containing 70 g fat and 756 mg cholesterol, enriched or not with 10 g TDF as oat bran, rice bran, or wheat fiber or 4.2 g TDF as wheat germ. Fasting and postmeal blood samples were obtained for 7 h and chylomicrons were isolated. Adding fibers to the test meal induced no change in serum glucose or insulin responses. The serum triglyceride response was lower (P less than or equal to 0.05) in the presence of oat bran, wheat fiber, or wheat germ and chylomicron triglycerides were reduced with wheat fiber. All fiber sources reduced chylomicron cholesterol. Cholesterolemia decreased postprandially for 6 h and was further lowered in the presence of oat bran. Serum apolipoprotein (apo) A-1 and apo B concentrations were not affected. Thus, dietary fibers from cereals may reduce postprandial lipemia in humans to a variable extent.

Effects of moderate amounts of emulsified dietary fat on postprandial lipemia and lipoproteins in normolipidemic adults.

Eight normolipidemic males ingested a meal containing either 42 g fat or 31 g fat in the form of emulsions (9.0 and 9.2 m2) and a fixed amount of retinyl palmitate. Fasting and postmeal blood samples were obtained for 7 h. Serum and chylomicron triglyceride responses were related to the amount of fat ingested and peaked after 2-3 h. The chylomicron retinyl palmitate response was lower (P < or = 0.05) with the 31-g fat supply. After the 42-g fat intake, but not after the 31-g fat intake, serum free cholesterol and phospholipids increased and esterified cholesterol decreased postprandially. Significantly different responses were observed after both meals for low-density-lipoprotein (LDL) free cholesterol, very-low-density-lipoprotein (VLDL) and LDL esterified cholesterol, and high-density-lipoprotein (HDL) phospholipids. These data show that ingesting 31 g instead of 42 g fat in a meal reduces postmeal lipoprotein variations and suggest that a threshold level of dietary fat should be overcome to promote significant postprandial changes in lipoprotein particles.

Chronic oat bran intake alters postprandial lipemia and lipoproteins in healthy adults.

This study evaluates the possible interaction between chronic oat bran intake and the postmeal metabolic response. Six normolipidemic men consumed three different diets for 14 d, at the end of which they consumed a test meal. The diets were C (control), basal low-fiber diet (15.6 g fiber/d) and a low-fiber (2.8 g fiber) test meal; OB (oat bran), basal low-fiber diet and a 40-g oat bran-enriched test meal (12.8 g fiber); and OB-A (oat bran-adaptation), 14-d oat bran (40 g/d) supplemented diet (23.8 g fiber/d) and an oat bran test meal (12.8 g fiber). The diets were fed in a random order. Fasting and postmeal blood samples were obtained for 7 h and lipoproteins were isolated. Adding oat bran to the test meals markedly reduced the postmeal insulin rise (P < 0.05). Compared with the low-fiber control diet, the effects elicited postprandially by adding oat bran to a single meal were enhanced after 14 d of oat bran feeding, ie, increased plasma triglycerides, phospholipids, and free cholesterol; decreased plasma esterified cholesterol; increased chylomicron and small-sized triglyceride-rich lipoprotein triglycerides; increased LDL and HDL free cholesterol; and decreased HDL esterified cholesterol. Thus, chronic oat bran feeding alters the postmeal response in human subjects.

Dietary cholesterol is secreted in intestinally derived chylomicrons during several subsequent postprandial phases in healthy humans.

BACKGROUND: The process of intestinal absorption and chylomicron resecretion of dietary cholesterol in humans is poorly understood. OBJECTIVE: The present study aimed to test the hypothesis that dietary cholesterol ingested during a given meal is resecreted into chylomicrons (and plasma) during several subsequent postprandial periods. DESIGN: Seven healthy subjects ingested 3 comparable mixed test meals (at 0, 8, and 24 h) containing a given amount of fat (49 g) and cholesterol (157 mg); blood samples were taken 3 and 6 h after each test meal and 48 and 72 h after the beginning of the experiment. Heptadeuterated dietary cholesterol was present in the first test meal only, enabling its specific determination with use of gas chromatography-mass spectrometry. Chylomicrons, LDL, and HDL were isolated and lipids were quantified. RESULTS: In apolipoprotein B-48-containing chylomicrons, deuterated cholesterol concentrations were moderate after the first meal (1.3 x 10(-4) mmol/L), reached a maximum after the second meal (2.4 x 10(-4) mmol/L), and were still elevated after the third meal (1.7 x 10(-4) mmol/L). In plasma, LDL and HDL cholesterol enrichment in deuterated cholesterol was lower than in chylomicrons and plateaued after 24--48 h. Estimates of newly secreted exogenous deuterated cholesterol in chylomicrons indicate that 30.7%, 55.2%, and 14.1% of the total was secreted after the first, second, and third meals, respectively. CONCLUSION: Ingested dietary cholesterol is secreted by the small intestine in chylomicrons into the circulation during > or =3 subsequent postprandial periods in healthy humans. This likely results from a complex multistep intestinal processing of cholesterol with dietary fat as a driving force.

Effects of lowering fat and increasing dietary fiber on fasting and postprandial plasma lipids in hypercholesterolemic subjects consuming a mixed Mediterranean-Western diet.

The aim of this study was to evaluate the cholesterol-lowering effects of reducing fat and increasing or not increasing dietary fiber in subjects consuming a mixed Mediterranean-Western diet. Thirty-one free-living, mildly hypercholesterolemic subjects were randomly allocated to two groups. Subjects in both groups first shifted for 4 wk to a low-fat, low-fiber diet (LFLFD). For an additional 4-wk period, subjects in group 1 continued consuming the LFLFD whereas subjects in group 2 consumed a low-fat, high-fiber diet (LFHFD). Most dietary fatty acids were monounsaturated (38-41%) and fibers, when provided (up to 35 g/d), came from unrefined cereals, legumes, and soluble-fiber-enriched ready-to-eat cereals. After period 1 of the LFLFD, mean serum and low-density-lipoprotein (LDL)-cholesterol concentrations of subjects in groups 1 (-12.5% and -15.5%, respectively) and 2 (-10.5% and -15.5%, respectively) decreased significantly from baseline (P < 0.05). After period 2, mean serum and LDL-cholesterol concentrations of subjects consuming the LFLFD (group 1) were still lower (by 8.8% and 9.2%, respectively, from baseline) whereas in subjects consuming the LFHFD (group 2) these values decreased further to significantly lower values (14.2% and 17.6% from baseline, respectively). Fasting high-density-lipoprotein (HDL) cholesterol, apolipoprotein A-I, glycemia, and insulinemia did not change significantly. In seven men, postprandial lipemia transiently increased more after a breakfast test meal at the completion of the LFHFD period than after the LFLFD period. In conclusion, an LFHFD more comparable with the traditional Mediterranean diet may improve the dietary management of moderate hypercholesterolemia.

Effects of graded amounts (0-50 g) of dietary fat on postprandial lipemia and lipoproteins in normolipidemic adults.

Eight normolipidemic males ingested on separate days and in a random order five mixed meals containing 0, 15, 30, 40, or 50 g fat. Fasting and postprandial blood samples were obtained for 7 h and chylomicrons and lipoproteins were isolated. The nonfat and 15-g fat meals did not generate noticeable postprandial variations except for HDL phospholipids (P < 0.05). The serum and chylomicron triacylglycerol responses obtained after the meals correlated positively with the amount of fat ingested and peaked after 2-3 h. Serum free cholesterol and phospholipids increased and esterified cholesterol decreased postprandially in a dose-response manner. At the same time, triacylglycerol-rich-lipoprotein triacylglycerols, esterified cholesterol, LDL free cholesterol, HDL triacylglycerols, phospholipids, and free cholesterol increased whereas LDL and HDL esterified cholesterol decreased when the amount of ingested fat increased. The data showed that increasing the amount of fat in the usual range of ingestion (0-50 g) led to stepwise increases in the postprandial rise of chylomicron and serum triacylglycerols and induced marked changes in serum lipoproteins postprandially. The existence of a no-effect level of dietary fat (15 g) on postprandial lipemia and lipoproteins in healthy adults was shown.

Postprandial appearance of dietary deuterated cholesterol in the chylomicron fraction and whole plasma in healthy subjects.

This study examined the appearance of dietary cholesterol in the chylomicron fraction (chylomicrons plus chylomicron remnants) and whole plasma in healthy normolipidemic subjects during a 0-7-h postprandial period. Six adult males were given two diet sequences in random order: a low-fiber diet (standard Western diet for 14 d) followed by a labeled low-fiber test meal or a fiber-supplemented diet (40 g oat bran/d for 14 d) followed by a labeled oat bran (40 g) test meal. The test meals provided 192.5 mg cholesterol, including 80.1 mg octadeuterated cholesterol. Fasting and hourly postmeal blood samples were obtained for 7 h. Isotopic cholesterol ratios [tracer:(tracer+native cholesterol)] were determined by gas chromatography-mass spectrometry. Chylomicron triacylglycerol and cholesterol concentrations peaked after 2-3 h and returned to baseline after 7 h. After the low-fiber test meal, the isotopic cholesterol ratio continuously increased until 7 h in the chylomicron fraction (4.2 +/- 1.2 x 10(-3)) and whole plasma (1.04 +/- 0.39 x 10(-3)). At 7 h postprandial, the maximum dietary cholesterol concentration in the chylomicron fraction and plasma cholesterol was 1 in 99 and 1 in 397 cholesterol molecules, respectively. No marked differences were obtained after the high-fiber sequence compared with the low-fiber one; there was a comparable isotopic cholesterol ratio and concentration in the chylomicron fraction and a slightly lower (-44%, P < 0.10) 0-7 h area under the curve whole-plasma deuterated cholesterol concentration. Thus, dietary cholesterol supplied as a single meal does not simultaneously appear in the chylomicron fraction postprandially with endogenous cholesterol and triacylglycerols and fiber feeding does not markedly alter this process in healthy normolipidemic humans.

Digestion and absorption of 2 fat emulsions with different droplet sizes in the human digestive tract.

BACKGROUND: The extent of fat emulsification affects the activity of digestive lipases in vitro and may govern digestion and absorption of dietary fat. OBJECTIVE: We investigated the effect of the fat globule size of 2 enteral emulsions on fat digestion and assimilation in humans. DESIGN: Healthy subjects received intragastrically a coarse (10 microm) and a fine (0.7 microm) lipid emulsion of identical composition in random order. Gastric and duodenal aspirates were collected throughout digestion to measure changes in fat droplet size, gastric and pancreatic lipase activities, and fat digestion. Blood lipids were measured postprandially for fat assimilation. RESULTS: Despite an increase in droplet size in the stomach (2.75-6.20 microm), the fine emulsion retained droplets of smaller size and its lipolysis was greater than that of the coarse emulsion (36.5% compared with 15.8%; P < 0.05). In the duodenum, lipolysis of the fine emulsion was on the whole higher (73.3% compared with 46.3%). The overall 0-7-h plasma and chylomicron responses given by the areas under the curve were not significantly different between the emulsions, but the triacylglycerol peak was delayed with the fine emulsion (3 h 56 min compared with 2 h 50 min). CONCLUSIONS: Fat emulsions behave differently in the digestive tract depending on their initial physicochemical properties. A lower initial fat droplet size facilitates fat digestion by gastric lipase in the stomach and duodenal lipolysis. Overall fat assimilation in healthy subjects is not affected by differences in initial droplet size because of efficient fat digestion by pancreatic lipase in the small intestine. Nevertheless, these new observations could be of interest in the enteral nutrition of subjects suffering from pancreatic insufficiency.

Postprandial studies on dietary cholesterol in human subjects using stable isotopes and gas chromatography-mass spectrometry analysis.

We hypothesized that intestinal absorption and postprandial re-secretion of dietary cholesterol may be a particularly complex process in humans. To test this hypothesis, we used deuterium-enriched cholesterol to specifically label meal cholesterol and developed an improved method for quantitative measurement of traces of deuterated cholesterol as well as cholesterol with reference to two different internal standards by gas chromatography-mass spectrometry (GC-MS) measurement. In the first study, a group of healthy subjects ingested a single test meal containing deuterated cholesterol with a 7 h postprandial follow-up. In the second one, a group of healthy subjects ingested a first test meal containing deuterated cholesterol and a follow-up was performed during three consecutive test meals and later until 72 h. The most striking observations were that the occurrence of dietary cholesterol in chylomicrons is not concomitant to triglycerides and is very low after a single meal while most dietary cholesterol is re-secreted in chylomicrons after a second, and even a third, fat test meal. The data obtained show that the re-secretion of dietary cholesterol from the small intestine is a slow and complex process in humans.