β-CM5对离体大鼠小肠葡萄糖吸收的影响

为了探讨β-酪啡肽-5(β-CM5)对大鼠小肠葡萄糖吸收的影响,利用翻转的离体小肠模型,通过测定60 min内β-CM5不同浓度组肠囊内葡萄糖含量及葡萄糖的转运率;测定离体肠道黏膜α-葡萄糖苷酶、Na+-K+-ATP酶活力,分析大鼠小肠钠依赖性葡萄糖共转运载体(SGLT-1)及葡萄糖转运载体2(GLUT-2)mRNA表达水平,揭示β-CM5对葡萄糖吸收影响及机制。结果:不同浓度β-CM5肠囊内葡萄糖的转运量及转运率均显著低于对照组;β-CM5组小肠黏膜中α-葡萄糖苷酶和Na+-K+-ATP酶活力显著低于对照组;β-CM5组小肠黏膜中SGLT-1、GLUT-2 mRNA表达量与对照组相比均显著性下调。结果表明:β-CM5可以通过抑制葡萄糖吸收的相关酶活性,下调葡萄糖转运载体mRNA的表达,从而抑制肠道葡萄糖的吸收,提示β-CM5可能具有降糖作用。     

葡萄糖转运蛋白的研究进展

存在于肠道、肾近端小管的葡萄糖转运载体对葡萄糖的吸收和重吸收具有很重要的作用。其中肠道葡萄糖主要是通过位于肠细胞膜上Na —依赖性葡萄糖转运载体(SGLT1)进行主动转运的。从十二指肠到回肠的肠轴上分布有不同的SGLT亚型,这些转运载体对葡萄糖和半乳糖的转运能力与它们的     

肠道葡萄糖吸收的调节作用

肠道葡萄糖是经过肠粘膜上皮细胞上的Na+-依赖葡萄糖同向转移器 ( SGLI1)而吸收的。借助于基底膜上 Na+/K+ATP酶维持的电化学梯度驱动 ,胃肠道将消耗整个能量的 2 0 % ,其中的大多数是由于 Na+/K+酶作用的结果。肠道葡萄糖的主动转运受大量胃肠肽的调节 ,如表皮生长因子 ( EGF)和肽 YY( PYY)。 EGF和 PYY可将肠道葡萄糖吸收提高 2 0 0 %～ 30 0 % ,值得一提的是肠道组织功能的能耗的改变与转运的葡萄糖量相关 ,这个值定义为“葡萄糖吸收的表观能效率( APEE)”,用于评价各种生理和营养状态下葡萄糖和其它营养物质的能耗值。很少…     

肠道上皮主要葡萄糖转运载体及其作用机制

葡萄糖在肠道的吸收主要通过Na~+依赖性葡萄糖转运载体1(SGLT1)和易化葡萄糖转运载体2(GLUT2)实现。许多影响肠道葡萄糖吸收功能的因素都是通过调控SGLT1和GLUT2转录水平、mRNA稳定性及蛋白水平来实现的。通过对葡萄糖转运载体结构和功能的研究,不仅为人类肥胖症和糖尿病等相关疾病提供潜在药物靶点,还能为调节动物营养物质吸收提供思路。本文综述了肠道上皮主要葡萄糖转运载体SGLT1和GLUT2的功能和影响其在肠道上皮表达的因素,旨在从分子层面揭示葡萄糖在肠道的吸收以及体内葡萄糖平衡的调控。     

妊娠后期营养限制对母羊胃肠道葡萄糖转运载体相关基因表达的影响

本研究旨在研究妊娠后期营养限制对母羊胃肠道葡萄糖转运载体相关基因表达的影响。选取20只同期受孕的湘东黑山羊,随机分为2组,即对照组(自由采食)和限饲组(40%采食量限制),每组10只。预试期15 d(妊娠81~95 d),正试期39 d(妊娠96~135 d)。正试期结束后,屠宰并采取瘤胃、十二指肠、空肠、回肠以及盲肠的黏膜样品,利用实时定量PCR技术,检测Na+-葡萄糖共转运载体1(SGLT1)、Na+-葡萄糖共转运载体3(SGLT3)、易化葡萄糖转运载体2(GLUT2)和易化葡萄糖转运载体5(GLUT5)基因表达量。结果表明:限饲组与对照组相比,SGLT1基因表达量在瘤胃显著降低(P0.05),在空肠和回肠中有降低趋势(0.05≤P0.10);GLUT5基因表达量在盲肠显著降低(P0.05);而其他葡萄糖转运载体基因胃肠道表达量在限饲组和对照组差异均不显著(P0.05)。由此可见,母羊妊娠后期营养限制对胃肠道中葡萄糖转运载体基因表达有不同程度的影响,进而引起母羊机体内葡萄糖转运的改变。     

非反刍动物小肠内葡萄糖的吸收与调控

营养性碳水化合物被非反刍动物摄入后,在消化道内逐渐降解成葡萄糖等单糖以及少量的双糖.小部分葡萄糖在门静脉回流组织(PDV)中进行供能代谢,大部分被小肠绒毛吸收而进入门静脉.葡萄糖吸收是由小肠黏膜上的Na+依赖型葡萄糖协同转运1(SGLT1)、Na+/K+ATP酶、葡萄糖转运子2(GLUT2)以及与吸收有关的调控因子共同完成.     

肠道上皮细胞与菌群的相互作用及益生菌对肠道上皮细胞的保护机制

肠道上皮细胞在肠黏膜的表面形成单细胞屏障,虽然不算真正的免疫细胞,但它们与肠道菌群间的相互作用影响免疫反应,并在维持机体内环境稳态方面起至关重要的作用。对肠道上皮细胞与菌群间的相互作用及益生菌对肠道上皮细胞的保护机制进行综述,旨在为通过改善菌群组成调控黏膜免疫反应,增强肠道上皮屏障功能提供依据。     

精氨酸对仔猪肠道的保护机理及作用

正精氨酸是仔猪的必需氨基酸,可以直接或间接影响仔猪肠道机械屏障,对仔猪肠道黏膜生长、绒毛高、细胞生长、肠道通透性等方面均有重要作用。肠道具有将肠道内物质与机体内环境隔离开的功能,称为肠道屏障功能,主要由肠黏膜屏障实现,可防止肠道内致病抗原及有毒有害物质侵入机体。肠黏膜屏障由机械屏障、化学屏障、免疫屏障与生物屏障共同构成,其中最为关键的是机械屏障和免疫屏障。肠道机械屏障由肠道黏膜上皮细胞,细胞间紧     

肠道屏障功能的测定及其对肠道健康的影响

<正>PIG PROGRESS肠黏膜作为肠腔与机体其他组织的过滤器,不仅可以调节营养物质和分子的通过,还可以防止细菌、毒素和抗原进入黏膜下组织或系统循环。有效的肠道屏障包含多种组分,例如黏液层及其相关的微生物、免疫效应分子和细胞间紧密连接的完整性。已有研究揭示了肠屏障的紊乱如何影响动物的性能和健康。肠黏膜由柱状上皮细胞(也称为上皮)以及下面的固有层和肌肉黏膜组成。存在两种通过上皮的途径,即跨细胞(通     

猪小肠黏膜上皮细胞对不同能源物质的利用和需求特点研究进展

小肠黏膜上皮细胞的能量营养是保障肠道正常发育的基础。葡萄糖、氨基酸和脂肪酸是所有生命活动的初始底物和供能物质,也是为肠黏膜上皮细胞提供营养和维持其生理功能的重要物质。与其他细胞相比,肠黏膜上皮细胞对三大营养物质有不同的代谢特点和需求差异,这些物质通过不同的代谢途径发挥其营养功能,因此明晰肠黏膜上皮细胞对不同营养物质的需求特点,才能为其提供高效利用的营养物质。本文总结了猪小肠黏膜上皮细胞对3种能源物质的代谢、利用及需求特点,以进一步了解肠黏膜上皮细胞对营养物质的代谢和需求规律,为肠道合理高效的能源供给提供理论支撑。     

单胃动物小肠内可消化性碳水化合物的吸收及其调控

本文阐述单胃动物小肠内可消化性碳水化合物的吸收及其调控机制。可消化性碳水化合物在单胃动物体内的降解产物主要为葡萄糖、果糖、半乳糖和双糖。葡萄糖、果糖和半乳糖在小肠内,由小肠内绒毛上皮细胞或细胞间隙直接吸收;双糖在双糖酶的作用下水解成单糖形式,为小肠绒毛上皮细胞吸收。其吸收机制可分为3个途径:主动吸收、被动吸收以及通过细胞间隙直接吸收。其中主动吸收是主要的吸收途径。调控小肠可消化性碳水化合物吸收的因素较多,包括吸收面积、Na 电化学梯度、细胞膜脂质成分、转运细胞与非转运细胞比例、转运子周转速率、亲和系数等因素。通过多种因子的调控作用,能有效地促进碳水化合物的吸收,以满足动物体的生长和发育的需要。     

Nonruminant Nutrition Symposium: intestinal glucose sensing and regulation of glucose absorption: implications for swine nutrition

The Na(+/)glucose cotransporter (SGLT1) is the major route for the transport of dietary sugars from the lumen of the intestine into enterocytes. Regulation of this protein is essential for the provision of glucose to the body and avoidance of intestinal malabsorption. This has important nutritional implications in particular for young and growing animals. It has been demonstrated that dietary sugars and artificial sweeteners increase SGLT1 expression and the capacity of the gut to absorb monosaccharides. Furthermore, diets supplemented with artificial sweeteners have been shown to improve growth and performance of weaning piglets. In this review, after describing the organization of intestinal epithelium, the type of gut hormones released in response to dietary carbohydrates, the mechanism underlying the transcellular transport of glucose in the intestine is outlined. Next, a historical background to the work carried out in various laboratories aimed at identifying molecular mechanisms involved in regulation of intestinal glucose transporter, SGLT1, is described. Subsequently, the more recent data on the role of intestinal glucose, or sweet, sensor T1R2 + T1R3, a G protein-coupled receptor, required for upregulation of SGLT1 by dietary sugars and artificial sweeteners, are presented. The glucose sensor subunits, T1R2 + T1R3, are members of the taste receptor family 1, T1R, and are expressed in the gut enteroendocrine cells. Sensing of dietary sugars and artificial sweeteners by T1R2 + T1R3 activates a pathway in endocrine cells leading to secretion of gut hormones. Finally, after describing molecular mechanisms by which a specific gut hormone released by endocrine cells may regulate SGLT1 expression in the neighboring absorptive enterocytes, the application of these findings to enhancing intestinal capacity to absorb dietary sugars in weaning piglets is presented. A better understanding of the molecular events involved in regulation of SGLT1 will allow the identification of nutritional targets with attendant promise of avoiding nutrient malabsorption and enhancing growth and well-being of species.     

Na(+)-dependent transport of D-xylose by bovine intestinal brush border membrane vesicles (BBMV) is inhibited by various pentoses and hexoses

To detect whether pentoses and hexoses occurring in rumen bacteria or in hemicellulose ingested with feed and partly released in the small intestine have an affinity for the Na(+)-dependent glucose transporter of the bovine intestinal brush border membrane (BBM), we investigated whether these monosaccharides inhibit Na(+)-dependent transport of 14C-labelled D-xylose across the BBM using brush border membrane vesicles (BBMV) isolated from the mid-jejunum of cows. We used D-xylose as the transport substrate, because it has a low affinity for the Na(+)-dependent glucose transporter and thus its uptake into BBMV is more efficiently competitively inhibited by other sugars than that of D-glucose. D-Ribose, D-mannose and L-rhamnose occurring in rumen bacteria significantly inhibited Na(+)-dependent uptake of D-xylose into BBMV, but their inhibitory effect was less than that of D-glucose, D-xylose and phlorizin. This also applied to L-arabinose (and D-arabinose), which is, like D-xylose and D-galactose, a constituent of hemicellulose, and to 2-deoxy-D-glucose. Of all monosaccharides tested, only D-fructose did not affect Na(+)-dependent D-xylose transport. It is concluded that some pentoses and hexoses occurring in rumen bacteria (D-ribose, D-mannose and L-rhamnose) or hemicellulose (L-arabinose and D-xylose) have a low affinity for the Na(+)-dependent glucose transporter of the bovine BBM and may therefore be absorbed from the jejunum when released in the small intestine.     

A proposed mechanism of monensin action in inhibiting ruminal bacterial growth: effects on ion flux and protonmotive force

Streptococcus bovis, a Gram-positive ruminal bacterium, was unable to grow in the presence of monensin. When monensin (5 mg/liter) was added to actively growing cultures, there was an immediate decrease in growth rate, and within 3 h no further growth was observed. Glucose utilization and lactate production continued for another 8 h even though growth had ceased. Monensin caused a decrease (P less than .05) in intracellular K+, a decrease (P less than .05) in intracellular pH and an increase (P less than .05) in intracellular Na+. The net exchange of K+ for Na+ and H+ via monensin was driven by the difference in concentration of K+ and Na+ across the cell membrane. Non-treated cells maintained a 70-fold gradient (inside higher) for K+, while the Na+ gradient was only 2.7-fold (inside higher). Previous models were based on a reverse mechanism whereby monensin would drive an efflux of Na+ from ruminal bacteria, and were not supported by experimental measurements of intracellular Na+ and K+.     

Electrolyte composition of mink (Mustela vison) erythrocytes and active cation transporters of the cell membrane

Red blood cells from mink (Mustela vison) were characterized with respect to their electrolyte content and their cell membranes with respect to enzymatic activity for cation transport. The intra- and extracellular concentrations of Na+, K+, Cl-, Ca2+ and Mg2+ were determined in erythrocytes and plasma, respectively. Plasma and red cell water content was determined, and molal electrolyte concentrations were calculated. Red cells from male adult mink appeared to be of the low-K+, high-Na+ type as seen in other carnivorous species. The intracellular K+ concentration is slightly higher than the extracellular one and the plasma-to-cell chemical gradient for Na+ is weak, though even the molal concentrations may differ significantly. Consistent with the high intracellular Na+ and low K+ concentrations, a very low or no ouabain-sensitive Na+, K(+)-ATPase activity and no K(+)-activated pNPPase activity were found in the plasma membrane fraction from red cells. The Cl- and Mg2+ concentrations expressed per liter cell water were significantly higher in red cells than in plasma whereas the opposite was the case with Ca2+. The distribution of Cl- thus does not seem compatible with an inside-negative membrane potential in mink erythrocytes. In spite of a steep calcium gradient across the red cell membrane, neither a calmodulin-activated Ca(2+)-ATPase activity nor an ATP-activated Ca(2+)-pNPPase activity were detectable in the plasma membrane fraction. The origin of a supposed primary Ca2+ gradient for sustaining of osmotic balance thus seems uncertain.     

Influence of abomasal carbohydrates on small intestinal sodium-dependent glucose cotransporter activity and abundance in steers

Most animals adapt readily to increased supplies of carbohydrate in the intestinal lumen by increasing enzymes for degradation and increasing glucose transporter activity. However, the extent of upregulation of Na+-dependent glucose cotransporter 1 (SGLT1) activity and content in response to increased delivery of carbohydrate to the small intestinal lumen of ruminants is unclear. Therefore, an experiment was conducted to determine the effect of glucose and starch hydrolysate on the activity and abundance of SGLT1 in the small intestine of steers. In a randomized complete block design, 40 crossbred beef steers (243+/-2 kg BW) were fed 0.163 Mcal of ME/(kg BW0.75(d; W), 0.215 Mcal of ME/(kg BW0.75 x d; 2M), or 0.163 Mcal ME/(kg BW0.75 x d) and infused for 35 d into the rumen (R) or abomasum (A) with 12.6 g/(kg BW0.75 x d) of starch hydrolysate (S) or into the abomasum with 14.4 g/(kg BW0.75 x d) of glucose (G). Steers were slaughtered, and brush-border membrane vesicles were prepared from the small intestinal samples obtained from five equidistant sites along the intestine. Maltase activity in vesicles and homogenates differed with intestinal sampling site (quadratic, P < 0.001). Steers on the AG treatment yielded a greater intestinal maltase activity (38 nmol glucose x mg protein(-1) x min(-1)) compared with the AS, RS, W, or 2M treatments (34, 26, 23, and 23 nmol glucose x mg protein(-1) x min(-1) respectively [SEM = 3; P = 0.02]). Sodium-dependent glucose uptake averaged 18.4+/-3.94 pmol glucose/(mg protein x s) and was not affected by treatment, but uptake decreased distally along the intestine (P < 0.001). There was no effect of treatment on SGLT1 protein abundance, but SGLT1 protein abundance increased linearly from the duodenum to the ileum (P = 0.05). The inverse relationship between glucose uptake and SGLT1 abundance suggests that the regulation of brush border Na+-dependent glucose transport capacity is complex, involving factors other than the presence of luminal carbohydrate.     

Age-related intestinal monosaccharides transporters expression and villus surface area increase in broiler and layer chickens

In the chicken small intestine, glucose is mainly transported by the apically located sodium/glucose cotransporter 1 (SGLT1) and the basolaterally located glucose transporter 2 (GLUT2). Fructose is transported by the apically located glucose transporter 5 (GLUT5) and similarly by GLUT2. During the early post-hatching period, the intestinal villus surface area (VSA) should be considered as an important factor related to the monosaccharide absorption capacity. Our objective here was to study intestinal monosaccharide absorption by analyzing the effects of age, diet, and breed on monosaccharide transporters and the VSA. The mRNA expression patterns of SGLT1, GLUT2 and GLUT5 genes in broiler and layer chickens were measured from the day of hatching to day 28 using the absolute quantitative real-time PCR. Both the intestinal mRNA expression levels of these genes and the VSA were affected by age. The mRNA expression levels of SGLT1 and GLUT2 were significantly increased from day 1 to day 3 and then decreased from day 3 to day 28. The expression levels of GLUT5 decreased from day 1 to day 7. The broiler chickens VSAs were significantly larger than those of the layer chickens from days 7 to 28. The effect of diet on the gene expression patterns of these monosaccharide transporters and the VSA were not significant. Our results suggest that the expression levels of these monosaccharide transporters are increased rapidly at the beginning of intestinal growth to meet the demands for monosaccharides to support the fast growth of the chick before day 7. As intestinal maturation and VSA increased, the expression levels of these monosaccharide genes decreased to a certain expression level to maintain the intestinal transport capacity and the absorption balance of all other nutrients.     

Establishment of an in vitro culture model to study milk production and the blood–milk barrier with bovine mammary epithelial cells

This study attempted to establish a culture model to recreate the milk production pathway in bovine mammary epithelial cells (BMECs). BMECs were isolated from Holstein cows (nonlactating, nonpregnant, and parous) and were stored by cryopreservation. To separate the apical and basolateral compartments, BMECs were cultured on a cell culture insert with a collagen gel in the presence of bovine pituitary extract and dexamethasone to induce milk production and tight junction (TJ) formation. The culture model showed the secretion of the major milk components, such as β‐casein, lactose, and triglyceride, and formed less‐permeable TJs in BMECs. Moreover, the TJs were distinctly separated from the apical and basolateral membranes. Glucose transporter‐1, which transports glucose into the cytoplasm through the basolateral membrane, localized in the lateral membrane of BMECs. Toll‐like receptor‐4, which binds to lipopolysaccharide in the alveolar lumen in mastitis, localized in the apical membrane. Beta‐casein was mainly localized near the Golgi apparatus and the apical membrane. Moreover, milk components were almost secreted into the upper chamber of the cell culture insert. These findings indicate that this model has clear cell polarity as well as in vivo and is effective to study of milk production and the blood–milk barrier in lactating BMECs.