Dietary fructooligosaccharides affect intestinal barrier function in healthy men

In contrast to most expectations, we showed previously that dietary fructooligosaccharides (FOS) stimulate intestinal colonization and translocation of invasive Salmonella enteritidis in rats. Even before infection, FOS increased the cytotoxicity of fecal water, mucin excretion, and intestinal permeability. In the present study, we tested whether FOS has these effects in humans. A double-blind, placebo-controlled, crossover study of 2 x 2 wk, with a washout period of 2 wk, was performed with 34 healthy men. Each day, subjects consumed lemonade containing either 20 g FOS or placebo and the intestinal permeability marker chromium EDTA (CrEDTA). On the last 2 d of each supplement period, subjects scored their gastrointestinal complaints on a visual analog scale and collected feces and urine for 24 h. Fecal lactic acid was measured using a colorimetric enzymatic kit. The cytotoxicity of fecal water was determined with an in vitro bioassay, fecal mucins were quantified fluorimetrically, and intestinal permeability was determined by measuring urinary CrEDTA excretion. In agreement with our animal studies, FOS fermentation increased fecal wet weight, bifidobacteria, lactobacilli, and lactic acid. Consumption of FOS increased flatulence and intestinal bloating. In addition, FOS consumption doubled fecal mucin excretion, indicating mucosal irritation. However, FOS did not affect the cytotoxicity of fecal water and intestinal permeability. The FOS-induced increase in mucin excretion in our human study suggests mucosal irritation in humans, but the overall effects are more moderate than those in rats.     

Dietary fructooligosaccharides increase intestinal permeability in rats

We showed previously that fructooligosaccharides (FOS) decrease the resistance to salmonella infection in rats. However, the mechanism responsible for this effect is unclear. Therefore, we examined whether dietary FOS affects intestinal permeability before and after infection with Salmonella enterica serovar Enteritidis. Male Wistar rats were fed restricted quantities of a purified diet that mimicked the composition of a Western human diet. The diet was supplemented with 60 g/kg cellulose (control) or 60 g/kg FOS and with 4 mmol/kg of the intestinal permeability marker chromium EDTA (CrEDTA) (n = 8 or 10). After an adaptation period of 2 wk, rats were orally infected with 10(8) colony-forming units (cfu) of S. enteritidis. Mucin concentrations in intestinal contents and mucosa were measured fluorimetrically, as markers of mucosal irritation. Intestinal permeability was determined by measuring urinary CrEDTA excretion. Translocation of salmonella was quantified by analysis of urinary nitric oxide metabolites with time. Before infection, FOS increased mucosal lactobacilli and enterobacteria in cecum and colon, but not in the ileum. However, FOS increased cytotoxicity of fecal water and intestinal permeability. Moreover, FOS increased fecal mucin excretion and mucin concentrations in cecal and colonic contents, and in cecal mucosa before infection. After infection, mucin excretion and intestinal permeability in the FOS groups increased even further in contrast to the control group. In addition, FOS increased translocation of salmonella to extraintestinal sites. Thus, FOS impairs the intestinal barrier in rats, as indicated by higher intestinal permeability. Whether these results can be extrapolated to humans requires further investigation.     

Dietary fructo-oligosaccharides dose-dependently increase translocation of salmonella in rats

Prebiotics, such as fructo-oligosaccharides (FOS), stimulate the protective gut microflora, resulting in an increased production of organic acids. This may result in increased luminal killing of acid-sensitive pathogens. However, host defense against invasive pathogens, like salmonella, also depends on the barrier function of the intestinal mucosa. Rapid fermentation of prebiotics leading to high concentrations of organic acids may impair the barrier function. Therefore, we determined the dose-dependent effect of dietary FOS on the resistance of rats to Salmonella enteritidis. Male Wistar rats were fed restricted quantities of a "humanized" purified diet supplemented with 0, 3 or 6 g/100 g of FOS (n = 7 in the 6% FOS group and n = 8 in the other diet groups). After an adaptation period of 2 wk, rats were orally infected with 1.7 x 10(10) colony-forming units of S. enteritidis. Supplement-induced changes in the intestinal microflora and fecal cation excretion were determined before and after infection. Cytotoxicity of fecal water was determined with an in vitro bioassay, and fecal mucins were quantified fluorimetrically. Colonization of S. enteritidis was determined by quantification of salmonella in cecal contents and mucosa. Translocation of S. enteritidis was quantified by analysis of urinary nitric oxide metabolites in time. Before infection, FOS decreased cecal and fecal pH, increased fecal lactic acid concentration and increased bifidobacteria and enterobacteria. FOS also increased cytotoxicity of fecal water and fecal mucin excretion, indicating mucosal irritation. Remarkably, FOS dose-dependently increased salmonella numbers in cecal contents and mucosa and caused a major increase in infection-induced diarrhea. In addition, FOS enhanced translocation of salmonella. Thus, in contrast to most expectations, FOS dose-dependently impairs the resistance to salmonella infection in rats. These results await verification by other controlled animal and human studies.     

Dietary calcium phosphate stimulates intestinal lactobacilli and decreases the severity of a salmonella infection in rats

We have shown recently that dietary calcium phosphate (CaPi) has a trophic effect on the intestinal microflora and strongly protects against salmonella infection. It was speculated that precipitation by CaPi of intestinal surfactants, such as bile acids and fatty acids, reduced the cytotoxicity of intestinal contents and favored growth of the microflora. Because lactobacilli may have antagonistic activity against pathogens, the main purpose of the present study was to examine whether this CaPi-induced protection coincides with a reinforcement of the endogenous lactobacilli. In vitro, Salmonella enteritidis appeared to be insensitive to bile acids and fatty acids, whereas Lactobacillus acidophilus was killed by physiologically relevant concentrations of these surfactants. Additionally, after adaptation to a purified diet differing only in CaPi concentration (20 and 180 mmol CaHPO4. 2H2O/kg), rats (n = 8) were orally infected with S. enteritidis. Besides reducing the cytotoxicity and the concentration of bile acids and fatty acids of ileal contents and fecal water, CaPi notably changed the composition of ileal bile acids in a less cell-damaging direction. Significantly greater numbers of ileal and fecal lactobacilli were detected in noninfected, CaPi-supplemented rats. As judged by the lower urinary NOx excretion, which is a biomarker of intestinal bacterial translocation, dietary CaPi reduced the invasion of salmonella. Additionally, the colonization resistance was improved considering the reduction of excreted fecal salmonella. In accordance, fewer viable salmonella were detected in ileal contents and on the ileal mucosa in the CaPi group. In conclusion, reducing the intestinal surfactant concentration by dietary CaPi strengthens the endogenous lactobacilli and increases the resistance to salmonella.     

Dietary calcium phosphate promotes Listeria monocytogenes colonization and translocation in rats fed diets containing corn oil but not milk fat

Most Gram-positive bacteria are susceptible to the bactericidal action of fatty acids and bile acids. Because dietary calcium phosphate (CaP(i)) lowers the intestinal concentration of these antimicrobial agents, high CaP(i) intake may enhance intestinal colonization of Gram-positive pathogens and the subsequent pathogenesis. In this study, we tested this hypothesis in a rat model using Listeria monocytogenes. Rats were fed diets containing low (20 micromol/g diet) or high (160 micromol/g diet) amounts of CaP(i). Dietary fat was provided as corn oil or milk fat. Rats were orally inoculated with L. monocytogenes. When rats consumed diets containing corn oil, high CaP(i) intake indeed stimulated colonization of L. monocytogenes and increased L. monocytogenes translocation and diarrhea. In addition, supplemental CaP(i) enhanced ex vivo growth of L. monocytogenes in fecal extracts of rats fed corn oil diets, suggesting that high CaP(i) intake decreased a luminal inhibitory factor. The concentrations of bile salts and fatty acids, which were highly listericidal in vitro, were indeed considerably decreased in fecal water of rats in the high calcium corn oil group. Surprisingly, dietary CaP(i) did not affect colonization and translocation of L. monocytogenes in rats fed the milk fat diet, nor did CaP(i) enhance ex vivo growth in fecal extracts. This absence of Listeria stimulation was associated with a lack of effect of dietary CaP(i) on fecal soluble fatty acids. In addition, residual soluble bile salts were higher in rats fed the high CaP(i) milk fat diet compared with the high CaP(i) corn oil diet. These results suggest that the stimulating effect of CaP(i) on L. monocytogenes infection depends on the type of dietary fat consumed.     

Ingestion of (n-3) fatty acids augments basal and platelet activating factor-induced permeability to dextran in the rat mesenteric vascular bed

Loss of intestinal barrier function and subsequent edema formation remains a serious clinical problem leading to hypoperfusion, anastomotic leakage, bacterial translocation, and inflammatory mediator liberation. The inflammatory mediator platelet activating factor (PAF) promotes eicosanoid-mediated edema formation and vasoconstriction. Fish oil-derived (n-3) fatty acids (FA) favor the production of less injurious eicosanoids but may also increase intestinal paracellular permeability. We hypothesized that dietary (n-3) FA would ameliorate PAF-induced vasoconstriction and enhance vascular leakage of dextran tracers. Rats were fed either an (n-3) FA-rich diet (EPA-rich diet; 4.0 g/kg EPA, 2.8 g/kg DHA) or a control diet (CON diet; 0.0 g/kg EPA and DHA) for 3 wk. Subsequently, isolated and perfused small intestines were stimulated with PAF and arterial pressure and the translocation of fluid and macromolecules from the vasculature to lumen and lymphatics were analyzed. In intestines of rats fed the EPA-rich diet, intestinal phospholipids contained up to 470% more EPA and DHA at the expense of arachidonic acid (AA). The PAF-induced increase in arterial pressure was not affected by the EPA-rich diet. However, PAF-induced fluid loss from the vascular perfusate was higher in intestines of rats fed the EPA-rich diet. This was accompanied by a greater basal loss of dextran from the vascular perfusate and a higher PAF-induced transfer of dextran from the vasculature to the lumen (P = 0.058) and lymphatics. Our data suggest that augmented intestinal barrier permeability to fluid and macromolecules is a possible side effect of (n-3) FA-rich diet supplementation.     

Retrograded tapioca starch prevents ovarian hormone deficiency-induced hypercholesterolemia

The purpose of this study was to examine whether retrograded tapioca starch (RS3-tapioca) prevents ovarian hormone deficiency-induced hypercholesterolemia. Six-month-old Wistar female rats were subjected to sham-operation or ovariectomy, and fed a cholesterol-free purified diet with or without RS3-tapioca (150 g/kg diet) instead of digestible cornstarch for 28 d. Body weight gain and food intake increased in ovariectomized rats (OVX-rats). Plasma total cholesterol concentration was lowered by RS3-tapioca in OVX rats, but not in sham-operated rats. Liver lipids increased in OVX-rats, but liver cholesterol concentration was not affected by ovariectomy and RS3-tapioca. CYP7A1 activity, small intestinal and cecal bile acid content, and fecal bile acid excretion were increased by RS3-tapioca. The ratio of cholic acid groups to chenodeoxycholic acid groups in the bile acid of the small intestine was increased by RS3-tapioca. Thus, the preventive effect of RS3-tapioca on the ovarian hormone deficiency-associated increase in plasma cholesterol concentration appears to be mediated by accelerated fecal excretion of bile acid and an increase in the intestinal pool of bile acid.     

微生物酵素预防治疗肠道细菌易位的实验研究

目的探讨微生物酵素对他克莫司(FK506)作用下肠道细菌易位情况的影响。方法健康雄性Wistar大鼠84只,体重180～220g,随机分为对照组、免疫抑制组和预防治疗组;比较3组间肝和肠系膜淋巴结细菌培养阳性率、肠黏膜病理分析。结果免疫抑制组第5、7天脏器细菌培养阳性率分别为28.57%、42.86%,显著高于对照组的0、0(P<0.05);各时间点肠黏膜损伤评分均显著高于对照组(P<0.05);预防治疗组第7天脏器细菌培养阳性率为7.14%,显著低于免疫抑制组的0(P<0.05);第3、5、7天肠黏膜损伤评分均显著低于免疫抑制组(P<0.05)。结论 FK506可以引起肠黏膜上皮损伤,肠道机械屏障功能破坏,肠黏膜通透性增高,发生肠道细菌易位;应用微生物酵素在一定程度上能够减轻FK506引起的肠黏膜上皮损害,保护肠黏膜机械屏障功能,降低肠黏膜通透性,减少肠道细菌易位的发生。     

The hypocholesterolemic effect of high amylose cornstarch in rats is mediated by an enlarged bile acid pool and increased fecal bile acid excretion,not by cecal fermented products

Sham-operated and cecectomized rats were fed for 21 d a cholesterol-free purified diet containing (200 g/kg) either normal cornstarch (CS) or high amylose cornstarch (HACS). In both types of rats, those fed the HACS diet had a significantly lower plasma total cholesterol concentration and a significantly larger intestinal bile acid pool than those fed the CS diet. In cecectomized rats, those fed the HACS diet had significantly lower plasma HDL and LDL cholesterol concentrations, a significantly greater fecal bile acid excretion and a significantly lower hepatic 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase mRNA concentration than those fed the CS diet. The plasma triglyceride concentration and LDL-receptor mRNA concentration were not affected by the diet or cecectomy. In sham-operated rats, the propionate concentration in the cecal contents was significantly greater in those fed the HACS diet than in those fed the CS diet. Compared with sham-operated rats, cecectomized rats had significantly enhanced cholesterol 7alpha-hydroxylase activity. In intact rats, biliary bile acid flux into the small intestine was significantly greater in those fed the HACS diet than in those fed the CS diet. Thus, the hypocholesterolemic effect of HACS appears to be mediated by accelerated fecal excretion of bile acids and increases in the intestinal pool and biliary flux of bile acids, and not by cecal fermentation products.     

Glutamine Supplementation Decreases Intestinal Permeability and Preserves Gut Mucosa Integrity in an Experimental Mouse Model

Background: Glutamine (GLN) is the preferred fuel for enterocytes, and GLN supplementation is critical during stressful conditions. The aim of this study was to evaluate the effect of GLN on intestinal barrier permeability and bacterial translocation in a murine experimental model. Methods: Swiss male mice (25–30 g) were randomized into 3 groups: (1) sham group; (2) intestinal obstruction (IO) group; (3) IO and GLN (500 mg/kg/d) group. Two different experiments were carried out to assess intestinal permeability and bacterial translocation. In the first experiment, the animals were divided into the 3 groups described above and received diethylenetriamine pentaacetate radiolabeled with technetium (^99mTc) on the eighth day. At different time points after intestinal obstruction, blood was collected to determine radioactivity. The animals were killed, and the small intestine was removed for histological analyses. In the bacterial translocation study, on the eighth day all groups received Escherichia coli labeled with ^99mTc. After 90 minutes, the animals underwent intestinal obstruction and were killed 18 hours later. Blood, mesenteric lymph nodes, liver, spleen, and lungs were removed to determine radioactivity. Statistical significance was considered when P ≤ .05. Results: The levels of intestinal permeability and bacterial translocation were higher in the IO group than in the sham and GLN groups (P < .05). GLN decreased intestinal permeability and bacterial translocation to physiologic levels in the treated animals and preserved intestinal barrier integrity. Conclusions: GLN had a positive impact on the intestinal barrier by reducing permeability and bacterial translocation to physiologic levels and preserving mucosal integrity.     

Biochemical changes and essential metals concentration in lead-intoxicated rats pre-exposed to ethanol.

The effects of chronic lead exposure on some hematopoietic and hepatic biochemical indices and urine, feces, and tissue essential metal concentration were investigated in rats pre-exposed to different doses of ethanol. Exposure to ethanol (0.5, 1.0, and 2.0 g/kg intraperitoneally, once daily) for 4 weeks produced an inhibition of blood delta-aminolevulinic acid dehydratase (ALAD) activity and a decrease in hepatic glutathione (GSH) concentration. Ethanol ingestion also produced a dose-dependent elevation of hepatic lipid peroxidation. Blood and hepatic calcium and hepatic magnesium contents decreased and urinary Ca and fecal Ca and Mg contents increased significantly following 4-week exposure to ethanol (2 g/kg). Lead administration (10 mg/kg, orally) for 4 weeks in ethanol pre-exposed (2 g/kg) animals produced a more pronounced inhibition of blood ALAD and elevation of urinary delta-aminolevulinic acid (ALA) excretion and hepatic GSH contents. Hepatic GSH contents decreased and hepatic lipid peroxidation increased significantly in rats given lead and pre-exposed to ethanol (2 g/kg). A more pronounced depletion of blood Ca and Mg and hepatic Mg was observed along with significant elevation of urinary Mg and fecal Ca excretion in animals administered lead and pre-exposed to ethanol (2 g/kg). The results suggest that nutritional deficiencies, particularly depletion of body Ca and Mg levels, play an important role in increasing susceptibility to lead intoxication in the rat.     

Fecal steroid excretion is increased in rats by oral administration of gymnemic acids contained in Gymnema sylvestre leaves.

Gymnemic acids are the saponins with a triterpenoid structure contained in Gymnema sylvestre leaves and have the hypoglycemic effects. In spite of the cholesterol-binding properties of saponins, the effect of gymnemic acids on cholesterol metabolism has not been elucidated to date. We investigated the effects of gymnemic acids on fecal steroid excretion in rats. Three kinds of extracts from Gymnema sylvestre leaves, extract (GSE), acid precipitate (GSA) and column fractionate (GSF), of which the gymnemagenin (an aglycone of gymnemic acids) concentrations are 58.87, 161.6, and 363.3 mg/g respectively, were used for the experiments. These were administered to rats orally at the dose of 0.05-1.0 g/kg for 22 d. Rats were given free access to water and nonpurified diet without cholesterol, and the differences in fecal excretion of steroids and gymnemic acids were investigated. Although there were no significant effects of GSE, GSA and GSF decreased body weight gain and food intakes in a dose-dependent manner (P < 0.01). GSF (1.0 g/kg) significantly increased fecal excretion of neutral steroids and bile acids in a dose-dependent manner (P < 0.05), especially those of cholesterol and cholic acid (CA)-derived bile acids. The increases in fecal steroid excretion of cholesterol, total neutral steroids, total bile acids and CA-related bile acids were acute and significantly correlated with fecal gymnemagenin levels (r2 = 0.2316-0.9861, P < 0. 05). These results demonstrated for the first time that a high dose of gymnemic acids increases fecal cholesterol and CA-derived bile acid excretion. Further studies are needed to clarify the effect of gymnemic acids on cholesterol metabolism.     

Hypocholesterolemic effect of indigestible fraction of Chlorella regularis in cholesterol-fed rats

The effects of Chlorella regularis powder (CP) and Chlorella regularis indigestible fraction (CIF) on serum and liver lipid concentrations and on fecal steroid excretion were estimated in rats fed diets containing 5 g/kg cholesterol and 2.5 g/kg sodium cholate. The ingestion of 12.7% CP or 5.3% CIF did not influence food intake or growth. CP and CIF decreased the levels of serum cholesterol, but had no effect on the levels of serum triacylglycerol and phospholipid. Liver cholesterol contents were lower in the CP and CIF groups than in the control group, but CP and CIF did not affect liver triacylglycerol content. CP and CIF increased the total amount of fecal neutral steroids excreted, but did not modify the total bile acid excretion. However, the soluble bile acid concentrations of reconstituted fecal water in the rats fed CP and CIF diets were lower than the control value. Moreover, CP and CIF had a high bile acid binding capacity in vitro. These results indicated that CIF had a hypocholesterolemic effect and enhanced fecal neutral steroid excretion while decreasing the soluble fecal bile acid concentration.     

Low levels of viscous hydrocolloids lower plasma cholesterol in rats primarily by impairing cholesterol absorption

Hydrocolloids have been proposed as cholesterol-lowering agents, but their viscosity limits their use in human nutrition. A low level (1 %) of hydrocolloids (guar gum, (GG); xanthan gum, (XG); and konjac mannan) was investigated in rats fed 0.2 g/100 g cholesterol diets. Food intake and body weight gain were not altered by the diets. Bile flow and cholesterol bile flux were not modified by diet, whereas the bile acid flux was greater in rats fed hydrocolloid diets. The cecal pool of bile acids was greater than control rats only in rats fed the XG diet (+71%, P<0.001). The fecal excretion of neutral sterols was stimulated in rats fed the hydrocolloid diets; cholesterol apparent digestibility (60% in controls) was reduced to 30-36% in rats fed hydrocolloids. Bile acid fecal excretion was not altered by diet treatment. As a result, apparent steroid balance was about +40 micromol/d in controls and only +10 to +20 micromol/d in rats fed hydrocolloids. Both plasma cholesterol and triglycerides were significantly lower than controls in rats fed XG, but only cholesterol was lower in rats fed the GG diet. These effects were essentially found in the d <1.040 kg/L fraction. Liver cholesterol content was significantly lower than in controls in rats fed the GG or XG diets. Liver HMG CoA reductase was not affected by the hydrocolloid diets. In conclusion, a low percentage of viscous hydrocolloids lowers plasma cholesterol in cholesterol-fed rats. Inhibition of intestinal cholesterol absorption may be the primary mechanism.     

Rat bioassay of wheat bran folate and effects of intestinal bacteria

This study estimates the folate endogenous to a food material (wheat bran) and examines the role of intestinal bacteria in the rat bioassay for folate. After a 4-wk folate depletion period, rats were fed for an additional 4 wk basal diets with or without 0.5% phthalylsulfacetamide and with 100, 200 or 300 g of wheat bran; or 50, 100 or 150 g of xylan; or 0, 0.25, 0.50 or 0.75 mg of folic acid added per kg of basal diet. Xylan increased both liver and fecal folate, and this effect was nearly eliminated by phthalylsulfacetamide. Wheat bran contributed 1.6 micrograms of available folate per g of wheat bran without phthalylsulfacetamide in an apparently valid slope-ratio analysis. With the addition of phthalylsulfacetamide, liver folate increased in rats fed wheat bran diets and decreased in rats fed folic acid diets. The slope-ratio analysis for wheat bran folate with phthalylsulfacetamide became invalid due to a lack of intersection. Phthalylsulfacetamide had no effect on fecal folate excretion from rats fed the wheat bran diets. Further studies are needed on a variety of foods with and without phthalylsulfacetamide to evaluate the effect and importance of intestinal folate synthesis in the rat.     

Reversion by taurine but not by glycine of ovarian hormone deficiency - induced hypercholesterolemia in aged rats is associated with increased fecal bile acids

The effect of taurine and glycine on the ovarian hormone deficiency-associated increase in plasma cholesterol concentration were studied in ovariectomized (ovx) 10-month-old retired breeder female rats. Rats was randomly assigned to four treatment groups: sham-operated+a casein-based cholesterol-free diet (C-diet, sham-C); ovx+C diet (ovx-C); ovx+C diet supplemented by taurine (50 g/kg diet, ovx-T); and ovx+C diet supplemented with glycine (50 g/kg diet, ovx-G). Rats were fed these diets for 28 d and killed at midnight in a fed state. Plasma and liver cholesterol concentrations in ovx-C were significantly higher than in sham-C. Bile flow, biliary bile acid secretion and fecal bile acid excretion were not significantly different between sham-C and ovx-C. Plasma cholesterol concentrations in ovx-T and ovx-G were significantly lower than those in ovx-C. Liver cholesterol concentration in ovx-G was significantly higher than in ovx-C but not in ovx-T. Cholesterol 7a-hydroxylase, bile flow, biliary bile acid secretion and fecal bile acid excretion in ovx-T were significantly higher than in ovx-C, but not in ovx-G. These results indicate that in the case of taurine but not glycine, increased fecal bile acid excretion is one of the factors in the prevention of the ovarian hormone deficiency-associated increase in plasma cholesterol concentration.     

Effect of dietary picolinic acid on the metabolism of exogenous and endogenous zinc in the rat

The excretion of 65Zn was compared by metabolic balance studies in adult male rats fed purified diets containing 0.8 mmol Zn/kg diet, with and without 40 mmol picolinic acid per kilogram diet, after single intragastric (i.g.) and intraperitoneal (i.p.) doses of the isotope. In a third experiment picolinic acid was introduced for 3 d into the diet of rats prelabeled with 65Zn. The urinary excretion of total zinc was increased by the ingestion of picolinic acid in all three experiments. The urinary and fecal outputs of 65Zn were both consistently greater in picolinic acid-fed rats than in the corresponding control animals. This was particularly marked after i.p. injection of the tracer, and the specific activities of urine and feces from the treated rats were both increased. When picolinic acid was introduced into the diet of prelabeled rats there was a delay of 24 h in the urinary response and 48 h in the fecal response. The residual 65Zn levels were reduced in several tissues from the picolinic acid-fed rats, especially after i.p. administration of the isotope. These observations indicate that dietary picolinic acid increases the turnover of endogenous zinc in addition to enhancing the absorption and excretion of ingested metal, and this has implications for its use in cases of zinc deficiency.     

Phytosterol stearate esters elicit similar responses on plasma lipids and cholesterol absorption but different responses on fecal neutral sterol excretion and hepatic free cholesterol in male Syrian hamsters

The dietary impact of specific phytosterols incorporated into phytosterol fatty acid esters has not been elucidated. Therefore, we tested the hypothesis that phytosterol esters containing different sterol moieties (sitosterol, sitostanol, or stigmasterol) but the same fatty acid moiety (stearic acid) produce different effects on cholesterol metabolism. Male Syrian hamsters were fed sitosterol, sitostanol, and stigmasterol stearate esters (25 g/kg diet) in an atherogenic diet containing cholesterol (1.2 g/kg) and coconut oil (80 g/kg). The phytosterol stearates produced no decrease in cholesterol absorption or plasma non-high-density lipoprotein cholesterol despite a reduction in liver free cholesterol in hamsters fed both sitosterol and sitostanol stearate diets. In addition, sitosterol stearate significantly increased fecal esterified and total neutral sterol excretion. Stigmasterol stearate did not differ from control in neutral sterol excretion, plasma lipids, or hepatic lipid concentration. Sitosterol stearate demonstrated the highest level of net intestinal hydrolysis, whereas sitostanol and stigmasterol stearate equivalently demonstrated the lowest. The cholesterol-lowering effect in liver—but not plasma—and the limited presence of fecal free sterols indicate that intact (unhydrolyzed) phytosterol stearates may impact cholesterol metabolism by mechanisms unrelated to the role of free phytosterols. The consumption of phytosterol esters at 2.5% of the diet elicited only modest impacts on cholesterol metabolism, although sitosterol stearate had a slightly greater therapeutic impact by lowering liver free cholesterol and increasing esterified and total neutral sterol fecal excretion, possibly due to a greater level of intestinal hydrolysis.     

57例沙门氏菌感染患者的临床特征及耐药情况分析

目的分析57例沙门氏菌感染患者的临床特征及耐药情况,了解沙门氏菌对常用抗生素的敏感性。方法收集我院2016年1月至2019年2月期间收治的57例沙门氏菌感染患者临床资料,住院后常规行血尿便常规检查,同时行粪便细菌培养及药敏实验。结果57例患者中,临床症状发生率最高为腹痛、腹泻(57例,100.00%),平均(7.46±2.03)次;其他依次为恶心、呕吐(45例,78.95%),发热(43例,75.44%),头痛(34例,59.65%),里急后重(26例,45.61%)及脱水(25例,43.86%)。辅助检查便常规结果显示,粪便白细胞阳性51例(89.47%);粪便隐血试验阳性45例(78.95%)。尿常规结果显示,尿蛋白阳性45例(78.95%);尿潜血试验阳性38例(66.67%)。血常规结果显示白细胞计数平均值为(9.98±4.22)×109/L,中性粒细胞平均占79%,C-反应蛋白平均值为(60.15±32.48)mg/L。药敏结果显示对头孢类和喹诺酮类抗生素耐药菌株所占比例较大。结论本地区沙门氏菌感染以腹痛、腹泻为主,粪便检测及尿常规检测对诊断更有价值。临床治疗过程中应加强对喹诺酮类及头孢类抗生素的耐药检测,为合理化用药提供依据。     

Amino acid-induced hypercalciuria in patients on total parenteral nutrition

Ingestion of protein is known to increase urinary calcium excretion. By studying the effect of intravenous amino acid infusion on calcium excretion, the variables of diets and intestinal absorption are avoided. Five patients on total parenteral nutrition with otherwise constant nutrient infusions containing 240 mg of calcium were randomized to two different levels of amino acid infusion. On 1 g/kg ideal body weight amino acid infusion, two patients excreted more than 240 mg of calcium in the urine, while on 2 g/kg ideal body weight amino acid infusion all five patients lost more calcium in urine than was infused. Mean urinary calcium excretion was increased from 287 to 455 mg/day. On the higher amino acid dose, mean glomerular filtration rate increased from 102 to 143 ml/min. There was no effect of amino acid dose on serum calcium, ionized calcium, parathyroid hormone, and 25 (OH) vitamin D. Calcium excretion corrected for the glomerular filtration rate was increased at the higher amino acid dose, indicating a decrease in renal calcium reabsorption. Daily urinary excretion of sulfate, ammonia, and titratable acidity were increased during the high amino acid infusion. Hypercalciuria induced by high levels of amino acid infusion during total parenteral nutrition may contribute to the development of metabolic bone disease.