Relationship between zinc and cellulose intakes in growing rats

We have studied the effect of cellulose on the intestinal absorption of zinc and its metabolism with weanling male rats. Experimental diets were cellulose (5, 8 or 20%) and noncellulose containing normal zinc (AIN-76 mineral mix., 3.0 mg%) or high zinc (10 times of normal, 30 mg%). Weanling rats fed on these diets ad libitum for 16-42 days. There were no significant differences between noncellulose-feeding and cellulose-feeding groups in body weight gain or protein and DNA concentrations in the liver. The inhibitory effect of 20% cellulose on zinc absorption was observed in the long term experiment, as the concentrations of plasma zinc of the group receiving 20% cellulose were decreased significantly more than that of noncellulose-feeding group.     

Site of zinc absorption in dog small intestine

An in vivo intestinal perfusion technique was used to study the absorption of zinc from the duodenum, proximal jejunum and distal ileum of six dogs (group 1). Net absorption of zinc from the duodenum before and after ligation of the common bile duct averaged 596 and 574 ng.min-1.cm-1, respectively. Zinc absorption was greater (P less than 0.01) from the duodenum than from the jejunum (251 ng.min-1.cm-1) or ileum (404 ng.min-1.cm-1). Four other dogs (group 2) experienced perfusion of approximately equal segments of the duodenum (in two animals the common bile duct was ligated, and in another two it was not), proximal jejunum and distal ileum for 4 h. No change in absorption of zinc with time was noted, nor was any difference in absorption by the duodenum with and without ligation of the common bile duct observed. The data indicate that the duodenum has the greatest capacity for zinc absorption, followed by the distal ileum and proximal jejunum, and that pancreatic secretions do not appear to be necessary for adequate zinc absorption in the dog duodenum.     

Relationship between pre-pregnancy BMI and plasma zinc concentrations in early pregnancy

We previously reported that pregnant women whose plasma Zn concentrations were below the 50th percentile tended to have high pre-pregnancy BMI (kg/m(2)) values. We therefore hypothesized that in pregnant women, plasma Zn concentrations are negatively correlated with BMI. We evaluated the association between BMI values and plasma Zn concentrations in 1474 women whose blood samples were obtained before 15 weeks of gestation. Their mean age was 22.7 years and mean gestational age at blood sampling was 10 weeks. The mean plasma Zn concentration and BMI were 11.6 micromol/l and 26.6 kg/m(2) respectively. Because plasma Zn concentrations decrease as gestational age increases, plasma Zn concentrations were standardized by Z-scores. Z-score distributions were compared among the quartiles of BMI. The highest BMI group had the lowest plasma Zn concentrations, whereas the lowest BMI group had the highest; the differences were significant between the BMI groups (P<0.0001). The interpretation of plasma Zn concentrations to assess Zn nutriture in pregnancy may be complicated not only by the well-established factor of gestational age at blood sampling, but also by a previously unrecognized factor, maternal BMI.     

Dietary zinc deficiency and repletion modulate metallothionein immunolocalization and concentration in small intestine and liver of rats

Metallothionein (MT) functions in zinc (Zn) homeostasis and dietary Zn affects tissue MT concentration. The objective of this study was to investigate the effects of dietary Zn deficiency and 24-h Zn repletion on MT immunolocalization and concentration in the small intestine and liver of growing rats. Three-week-old rats fed Zn-deficient diet (< 1 mg Zn/kg) for 16 d had no MT staining in either small intestine or liver. After 24-h Zn repletion with control diet (30 mg Zn/kg), strong MT staining was observed in intestinal Paneth cells and surface epithelial cells in the proliferative regions of villi. Pair-fed control rats had strong MT staining in liver that was localized around central veins. After 24-h energy repletion, the hepatic MT staining diminished. Furthermore, Zn-deficient rats had significantly reduced intestinal (57%) and hepatic (61%) MT concentrations but unaffected Zn concentrations compared with controls that consumed food ad libitum. Zn repletion for 24 h restored intestinal and hepatic MT concentrations and reduced hepatic Zn concentration. Pair-fed control rats had elevated MT concentration in liver that was normalized by energy repletion. There was a significant positive correlation between tissue Zn and MT concentrations in liver (r = 0.60, P = 0.0001), but not in small intestine. In summary, MT immunolocalization and concentration in rat small intestine and liver were responsive to changes in Zn status, supporting the role of MT in Zn metabolism. Cell-type-specific localization of MT in small intestine after dietary Zn manipulations indicates a function of Zn and MT in gut immunity and intestinal mucosal turnover, and the pattern of hepatic MT distribution with energy restriction may be linked to detoxification processes.     

补锌糖尿病大鼠肝脏糖脂代谢相关基因表达

目的探讨补锌对糖尿病大鼠肝脏糖脂代谢相关基因蛋白磷酸酶2A(PP2A)和磷脂酶D(PLD)表达的调控。方法对补锌糖尿病大鼠差异显示的基因片段进行克隆、测序及同源性分析;设计基因序列引物,RT-PCR检测观察各组大鼠肝脏中基因表达的变化。结果结果显示,片段Zn-4、Zn-8的碱基序列分别与PLD、PP2A同源性为100%,99%。糖尿病对照组PP2A mRNA表达量(0.5072±0.0574)低于正常对照组(1.3303±0.1855),P<0.05;糖尿病补锌组PP2A mRNA的表达量(0.7005±0.1563)与糖尿病对照组比较有所恢复(P<0.05)。糖尿病对照组PLD mRNA表达量(1.0754±0.0312)和糖尿病补锌组PLD mRNA的表达量(1.0130±0.0992)均高于正常对照组(0.7995±0.1040),P<0.05;糖尿病补锌组PLD mRNA的表达量与糖尿病对照组比较无变化(P>0.05)。结论补锌对糖尿病大鼠肝脏PP2A mRNA表达有上调作用,这可能是锌改善糖尿病糖、脂代谢紊乱的分子机制之一。     

吸烟、精浆锌与男性不育患者精子形态的关系

目的:探讨吸烟、精浆锌与不育男性患者精子形态的关系。方法:对115例男性不育患者的吸烟情况进行问卷调查,采用精子形态检测系统下人工修正方法分析共精子形态,以分光光度比色法测定精浆锌含量。结果:不育男性吸烟组精浆锌水平显著低于不吸烟组(P<0.05),且吸烟程度与精浆锌水平呈显著负相关性(r=-0.273,P<0.05);吸烟组正常形态精子百分率显著低于不吸烟组(P<0.05);吸烟精浆锌异常组正常形态精子百分率显著低于吸烟精浆锌正常组(P<0.05),且显著低于不吸烟精浆锌正常和异常组(P<0.01);不吸烟精浆锌异常组正常形态精子百分率与精浆锌正常组差异无统计学意义(P>0.05)。结论:吸烟能使精浆锌水平降低;吸烟对精子形态的影响可能通过降低精浆锌含量,增加氧化应激,使正常形态精子百分率下降。     

Determination of the site of zinc absorption in rat small intestine.

We have studied net uptake of zinc from segments of rat duodenum, jejunum, and ileum using in vivo intestinal perfusion. We have also evaluated the effect of pancreatic and bile secretions on duodenal zinc absorption. Segments of duodenum, jejunum, and ileum and duodenum with bile and pancreatic duct obstruction, 10 cm in length, were studied in six rats each. Percentage absorption of zinc as determined by atomic absorption spectrophotomety was greater from the ileum (60.1%) when compared to duodenum (19.1%) or jejunum (20.2%). Exclusion of bile and pancreatic secretions from the lumen increased zinc absorption in the duodenum (32.0%). Postperfusion mucosal zinc content comprised 29.0% of absorbed zinc from jejunum, 7.4% from ileum, 5.2% from duodenum, and 2.7% from duodenum with bile and pancreatic duct obstructed, indicating rapid transport of zinc across epithelial cells after uptake from the duodenum and ileum. Our data indicate that the ileum has the greatest capacity for zinc absorption.     

血淤症与血浆锌铜的关系

<正> 血瘀症是中医临床常见的病症之一,可见于多种疾病,如冠心病、脑血管疾患、肝硬化、糖尿病、肿瘤等,采用中药活血化瘀治则治疗后,都取得良好的疗效。为了探讨微量元素Zn、Cu与血瘀症之间的关系,我们诱发制作了血瘀症的动物模型,观察血瘀症大鼠血浆中Zn、Cu的变化。     

Effects of prostaglandin modifiers and zinc deficiency on possibly related functions in rats

Experiments were conducted to investigate the role of prostaglandins (PG) in zinc absorption and biological functions (food intake and weight gain, alkaline phosphatase activity, T-cell-mediated immune response). PG levels were modified by administering an inhibitor of their synthesis, aspirin or indomethacin in the diet. Zinc level was modified by controlling the dietary concentration. Weanling rats were fed the assigned diets for 1 month after which they were anesthetized with ether. Samples of blood, gut contents and mucosa, liver, lung and tibia were collected for zinc, PG, lymphocyte stimulation with T-cell mitogen, and alkaline phosphatase assays. There was more than 50% inhibition of PG synthesis by indomethacin and aspirin. This inhibition of PG synthesis, however, did not affect the zinc status of the rats as measured by general appearance, food intake, weight gain, organ weight, zinc concentration in different organs, serum alkaline phosphatase activity, and cell-mediated immune response to T-cell mitogens. It is concluded that under physiological conditions inhibitors of PG synthesis do not alter these zinc metabolic functions.     

The large intestine compensates for insufficient calcium absorption in the small intestine in rats

We previously demonstrated that the large intestine compensated for decreased calcium (Ca) absorption caused by renal failure in rats fed a highly fermentable dietary fiber. In this study, we examined whether the large intestine compensated for insufficient Ca absorption in the rat small intestine without ingestion of a fermentable dietary fiber. Rats were fed one of four test diets containing either insoluble (carbonate) or soluble (gluconate, lactate, or citrate) Ca sources. The dietary Ca level was 2.0 g/kg, which is lower than the minimum requirement for rats (3.0 g/kg), to conduct the present study under a condition in which rats can maximally absorb Ca. To prevent Ca absorption in the small intestine, we replaced a primary phosphate (KH2PO4) with secondary phosphates (K2HPO4 and Na2HPO4) in diets. The apparent Ca absorption in the small intestine was estimated by adding chromic oxide (Cr2O3) as an insoluble and an unabsorbed marker to test diets and by measuring the ratio of Ca:Cr in the cecal content. The apparent Ca absorption in the whole intestine was estimated by the intake and fecal excretion of Ca. The apparent Ca absorption in the small intestine was significantly lower from the Ca carbonate diet than from the Ca gluconate, lactate, or citrate diets. The apparent Ca absorption in the whole intestine was not significantly different among the four groups, and the values were similar to the absorption rates in the small intestines of rats fed diets containing soluble Ca sources. These results show the following: (a) In rats fed 0.2% Ca diets containing soluble Ca salts, Ca is mostly absorbed in the small intestine, even in secondary phosphate intakes; (b) In contrast, in rats fed a 0.2% Ca diet containing an insoluble Ca salt (carbonate), Ca is not sufficiently absorbed in the small intestine. However, the large intestine compensates for the small intestinal Ca absorption decreased by dietary secondary phosphates.     

Anthocyanins are efficiently absorbed from the small intestine in rats

Anthocyanins are natural pigments that possess antioxidant activities and are implicated in various health effects. Recent studies showed that the stomach is a site of anthocyanin absorption. However, the fate of anthocyanins in the small intestine remains unknown. We therefore investigated anthocyanin absorption after in situ perfusion of the jejunum + ileum in rats. The intestine was perfused for 45 min with a physiological buffer supplemented with various anthocyanins. Purified anthocyanin glycosides (9.2 nmol/min) or blackberry (9.0 nmol/min) or bilberry (45.2 nmol/min) anthocyanins were perfused. A high proportion of anthocyanin glycosides was absorbed through the small intestine after perfusion. The rate of absorption was influenced by the chemical structure of the anthocyanin and varied from 10.7 (malvidin 3-glucoside) to 22.4% (cyanidin 3-glucoside). Regardless of the anthocyanins perfused, only glycosides were recovered in the intestinal lumen. After perfusion of a high amount of blackberry anthocyanins (600 nmol/min), native cyanidin 3-glucoside was recovered in urine and plasma from the aorta and mesenteric vein. Methylated and/or glucuronidated derivatives were also identified. Analysis of bile samples revealed that cyanidin 3-glucoside and its methylated derivatives (peonidin 3-glucoside + peonidin glucuronide) quickly appeared in bile. This study demonstrated that anthocyanin glycosides are rapidly and efficiently absorbed from the small intestine. Furthermore, anthocyanins are quickly metabolized and excreted into bile and urine as intact glycosides as well as methylated forms and glucuronidated derivatives.     

Distribution of carnitine and acylcarnitine in small intestine of carnitine-supplemented and fasted rats

Distribution of carnitine and acylcarnitine in lumen flush and tissue of the small intestine was examined in four groups of male Sprague-Dawley rats fed either a nonpurified diet (groups 1, 2) or the same supplemented with 1% DL-carnitine (groups 3, 4). One group of animals under each dietary regimen (groups 2, 4) was fasted for 24 h prior to killing. Carnitine and acylcarnitines were present in higher concentrations in tissue of the small intestine than in the lumen flush. Even though the diets contained only traces of acid-soluble acylcarnitine, it was present in high concentrations both in tissue of the small intestine and lumen flush. Proximal segments of small intestine tended to concentrate carnitine and acylcarnitines under all conditions of treatment. Carnitine supplementation increased the amounts of carnitines in tissue; however, there was only a minor alteration in the pattern of distribution of carnitine and acylcarnitines.     

Bifidobacterium animalis protects intestine from damage induced by zinc deficiency in rats

We investigated the potential beneficial effects of Bifidobacterium animalis on intestinal damage using zinc-deficient (ZD) rats as a model for intestinal alterations. The ZD rats were fed diets containing 1 mg Zn/kg for 20 (ZD(20)) or 40 (ZD(40)) d to induce damage that differed in severity. Subgroups of these rats, the ZD(20) + B and ZD(40) + B groups, received a suspension of B. animalis (3.5 x 10(8) colony forming units) daily for the last 10 d. Another subgroup, the ZD(40) + B + 7 d group, was fed the ZD diet for 7 d after the B. animalis treatment period. Zinc deficiency induced ulcerations, edema, inflammatory cell infiltration and dilatation of blood vessels in duodenum, jejunum and ileum, with increasing severity between 20 and 40 d of zinc deficiency. The mucosa of the ZD(20) + B group was well preserved, and most of the morphologic alterations induced by zinc deficiency were normalized in the ZD(40) + B group. The high fecal concentrations of B. animalis in the ZD(40) + B and ZD(40) + B + 7 d groups indicate that these bifidobacteria survived passage through the gastrointestinal tract and proliferated. Electron microscopy confirmed the elevated numbers of bifidobacteria in cecum. Treatment with B. animalis resulted in greater epithelial cell proliferation and disaccharidase activities in the ZD(40) + B group compared with the ZD(40) group. These findings indicate that B. animalis can protect the intestine from alterations induced by zinc deficiency, suggesting that this bacterium may play a role in intestinal mucosal defense.     

Decrease of lactase activity in the small intestine of jejunum-bypassed rats.

The effect of jejunum-bypass operation on lactase in rat small intestine was examined. Three groups of four or five rats were designated as jejunum-bypassed, sham-operated and normal rats. All animals including normal rats received by pair-feeding 5% glucose/1% NaCl for 5 days following the operation; thereafter they were fed ad libitum the laboratory chow diet. Three weeks after the jejunal bypass operation, the proximal ileum exhibited a hyperplasia as evidenced by a concomitant increase in mucosal contents of both total proteins and DNA. The specific activity of lactase in this segment was significantly lower in the operated rats than sham-operated controls, whereas the specific activity of sucrase in this segment was significantly elevated. The reduction of lactase activity was also evident in the proximal jejunal segment as well as in the distal jejunum which was deprived of luminal nutrition, suggesting that some hormonal factor(s) might be involved in the decrease of lactase activity in jejunum-bypassed animals. Electroimmunoassay revealed that the amount of immunoreactive lactase also declined in the operated rats relative to the sham-operated controls. Our results thus suggest that lactase activity in residual ileum is not only unable to compensate for the loss of digestive-absorptive surface of jejunum, but lactase activity even decreases following jejunum-bypass operation.     

Catechin is metabolized by both the small intestine and liver of rats

Flavan-3-ols are the most abundant flavonoids in the human diet, but little is known about their absorption and metabolism. In this study, the absorption and metabolism of the monomeric flavan-3-ol, catechin, was investigated after the in situ perfusion of the jejunum + ileum in rats. Five concentrations of catechin were studied, ranging from 1 to 100 micromol/L. The absorption of catechin was directly proportional to the concentration, and 35 +/- 2% of the perfused catechin was absorbed during the 30-min period. Effluent samples contained only native catechin, indicating that intestinal excretion of metabolites is not a mechanism of catechin elimination. Catechin was absorbed into intestinal cells and metabolized extensively because no native catechin could be detected in plasma from the mesenteric vein. Mesenteric plasma contained glucuronide conjugates of catechin and 3'-O-methyl catechin (3'OMC), indicating the intestinal origin of these conjugates. Additional methylation and sulfation occurred in the liver, and glucuronide + sulfate conjugates of 3'OMC were excreted extensively in bile. Circulating forms were mainly glucuronide conjugates of catechin and 3'OMC. The data further demonstrate the role of the rat small intestine in the glucuronidation and methylation of flavonoids as well as the role of the liver in sulfation, methylation and biliary excretion.     

Maternal zinc deficiency raises plasma prolactin levels in lactating rats

There is an inverse relation between zinc (Zn) intake and plasma prolactin in men and nonpregnant women. Whether a relation exists in lactating women is unknown, despite the potential consequences of perturbations in prolactin regulation on lactation performance. We examined the effects of low Zn intake on prolactin concentration, the prolactin regulatory pathway in the pituitary gland, and lactation performance in lactating rats. Female rats were fed diets containing 7 (zinc deficient; ZD), 10 (marginally zinc deficient; MZD) or 25 mg Zn/kg (control) from 70 d preconception to lactation d 11. Rats were killed, pituitary glands dissected, and tissues and plasma collected and analyzed for prolactin concentration. Pituitary gland pituitary factor 1 (Pit-1), dopamine 2 receptor (D2R), and prolactin receptor mRNA expression were measured in the pituitary gland. Liver, mammary gland, plasma, and milk Zn were measured. Milk intake of the pups was also recorded. Plasma prolactin concentration was higher in rats fed the ZD (125.9 microg/L) diet compared with control rats (21.7 microg/L). Pituitary gland prolactin concentration was higher in rats fed the ZD diet (69.8 mg/g total protein) compared with controls (29.0 mg/g). Plasma Zn concentration was lower in rats fed the MZD and ZD diets, and mammary gland and milk Zn concentrations were lower in rats fed the ZD diet compared with control rats. Rats fed the ZD diet had lower D2R, prolactin receptor, and Pit-1 mRNA levels, whereas rats fed the MZD diet had lower prolactin receptor and Pit-1 mRNA levels compared with control rats. Milk intake was lower in pups of rats fed the MZD and ZD diets. Our results suggest that marginal Zn nutriture may compromise milk production despite increased prolactin levels. In addition, increased circulating prolactin concentration is not due to altered nursing behavior, but may be due to alterations in the prolactin regulatory pathway in the pituitary gland.     

Influence of prostaglandins on unidirectional zinc fluxes across the small intestine of the rat

1. The regulatory role of prostaglandins (PGs) E2 and F2 alpha on the zinc transport rate across the jejunal segments of rats was examined by employing the Ussing chamber technique. The Zn flux rate from mucosa to serosa across jejunal segments (Jms) was 5.24 (SE 1.54) nmol/h per cm2 (n 48) and that from serosa to mucosa (Jsm) was 15.16 (SE 2.38) nmol/h per cm2 (n 48) when both sides of the segment were bathed with Ringer's bicarbonate solution containing 0.5 mM-zinc chloride and 3 mM-L-histidine. 2. When 5.0 or 50 microM of either PGE2 or PGF2 alpha were added to the serosal side of the tissue, Jsm generally decreased and Jms generally increased, compared with controls. On the other hand, when PGE2 or PGF2 alpha was added to the mucosal side of the tissue, Jms either did not change or increased while Jsm had a tendency to decrease. 3. The Zn uptake capacity of tissue increased significantly when PG was added to the serosal side of the tissue-bathing medium, but not when PG was added to the mucosal side. The uptake capacity of mucosal Zn by jejunal segments was approximately twice that of serosal Zn. 4. When PG was included in the tissue-bathing medium, the short-circuit current, potential difference and conductance between the mucosa- and serosa-bathing media generally decreased. 5. These results suggest that (a) PGs influence Zn flux rate not by chelating Zn and carrying it across the mucosal cell membrane but by interacting with the cytosolic components, (b) it is the serosal PGs which control the Zn flux rate and (c) PGs play a part in triggering a transduction mechanism in the intestinal Zn transport process.