Sphingomyelins (buttermilk)
(Synonyms: SMs (buttermilk)) 目录号 : GC48088
A sphingolipid
Cas No.:475662-40-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Sphingomyelins (SMs) are bioactive sphingolipids found in mammalian cell membranes.1 SMs make up 2-15% of the total organ phospholipid population but are found at higher concentrations in the brain and myelin sheaths surrounding peripheral nerves. They interact with cholesterol to control its distribution within cellular membranes and maintain cholesterol homeostasis in cells. SMs undergo hydrolysis by sphingomyelinase to form ceramides, which are sphingolipid mediators of intracellular signaling.2 This product is a mixture of SMs, with variable fatty acyl chain lengths, isolated from buttermilk. [Matreya, LLC. Catalog No. 1329]
1.Slotte, J.P., and Ramstedt, B.The functional role of sphingomyelin in cell membranesEur. J. Lipid Sci. Technol.109(10)977-981(2007) 2.Shayman, J.A.SphingolipidsKidney Int.58(1)11-26(2000)
| Cas No. | 475662-40-9 | SDF | |
| 别名 | SMs (buttermilk) | ||
| Canonical SMILES | [R]C(N[C@@H](COP(OCC[N+](C)(C)C)([O-])=O)[C@H](O)/C=C/CCCCCCCCCCCCC)=O | ||
| 分子式 | C46H93N2O6P (for tricosanoyl) | 分子量 | 801.2 |
| 溶解度 | Chloroform: soluble,Ethanol: soluble | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.2481 mL | 6.2406 mL | 12.4813 mL |
| 5 mM | 0.2496 mL | 1.2481 mL | 2.4963 mL |
| 10 mM | 0.1248 mL | 0.6241 mL | 1.2481 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Feeding Buttermilk-Derived Choline Forms During Gestation and Lactation Modulates Ex Vivo T-Cell Response in Rat Dams
J Nutr 2020 Jul 1;150(7):1958-1965.PMID:32271922DOI:10.1093/jn/nxaa089.
Background: buttermilk contains a mixture of choline forms; it is high in phosphatidylcholine (PC) and sphingomyelin (SM), which could have an impact on immune system development and function. Objectives: We aimed to determine the effect of feeding buttermilk-derived choline forms during pregnancy and lactation on maternal immune function. Methods: Sprague Dawley dams (n = 8 per diet) were randomly assigned midway through pregnancy (10 d of gestation) to 1 of 3 experimental diets, containing 1.7 g/kg choline: control [100% free choline (FC)]; buttermilk [37% PC, 34% SM, 17% glycerophosphocholine (GPC), 7% FC, 5% phosphocholine]; or placebo (50% PC, 25% FC, 25% GPC). Dams consumed the same diet until the end of the lactation period (21 d after parturition). Cell phenotypes and cytokine production by mitogen-stimulated splenocytes were measured and compared using 1-factor ANOVA test in order to asses the effect of diet on immune fuction of lactating dams (main outcome). Results: After ConA stimulation, splenocytes from dams in the buttermilk group produced more IL-2 (30%), TNF-α (30%), and IFN-γ (42%) compared with both the placebo and control diets. Placebo-fed dams had a higher proportion of CD8+ cells expressing CD152+ (22%) in spleen, and splenocytes from dams that were fed the buttermilk and the placebo diets produced about 50% and 53% more IL-10 after LPS and OVA stimulation, respectively, compared with the control group. Conclusions: Feeding buttermilk-derived choline forms during pregnancy and lactation had a beneficial impact on the immune system of Sprague Dawley rat dams, especially on T-cell function.
Evolution of phospholipid contents during the production of quark cheese from buttermilk
J Dairy Sci 2016 Jun;99(6):4154-4159.PMID:27060823DOI:10.3168/jds.2016-10861.
We report the evolution of phosphatidylethanolamine (PE), phosphatidylinositol (PI), phosphatidylcholine (PC), phosphatidylserine (PS), and sphingomyelin (SM) contents during the production of quark cheese from buttermilk by successive ultrafiltration concentration, enrichment with cream, concurrent homogenization and pasteurization, fermentative coagulation, and separation of quark from whey by further ultrafiltration. buttermilk is richer than milk itself in phospholipids that afford desirable functional and technological properties, and is widely used in dairy products. To investigate how phospholipid content is affected by end-product production processes such as ultrafiltration, homogenization, pasteurization or coagulation, we measured the phospholipids at several stages of each of 5 industrial-scale quark cheese production runs. In each run, 10,000L of buttermilk was concentrated to half volume by ultrafiltration, enriched with cream, homogenized, pasteurized, inoculated with lactic acid bacteria, incubated to coagulation, and once more concentrated to half volume by ultrafiltration. Phospholipid contents were determined by HPLC with evaporative light scattering detection in the starting buttermilk, concentrated buttermilk, ultrafiltrate, cream-enriched concentrated buttermilk (both before and after concurrent homogenization and pasteurization), coagulate, and quark, and also in the rinsings obtained when the ultrafiltration equipment was washed following initial concentration. The average phospholipid content of buttermilk was approximately 5 times that of milk, and the phospholipid content of buttermilk fat 26 to 29 times that of milk fat. Although phospholipids did not cross ultrafiltration membranes, significant losses occurred during ultrafiltration (due to retention on the membranes) and during the homogenization and pasteurization process. During coagulation, however, phospholipid content rose, presumably as a consequence of the proliferation of the inoculated lactic acid bacteria. In spite of these changes in total phospholipid content, the relative proportions of the phospholipids studied remain fairly stable throughout quark production (PE>PC>SM>PS>PI) and similar to those found in the milk of the region, except that SM content was lower than in milk.
Impact of buttermilk consumption on plasma lipids and surrogate markers of cholesterol homeostasis in men and women
Nutr Metab Cardiovasc Dis 2013 Dec;23(12):1255-62.PMID:23786821DOI:10.1016/j.numecd.2013.03.003.
Background and aims: Sphingolipids (SL) are important components of the milk fat globule membrane (MFGM) found in buttermilk. While studies in animal models suggest that dietary SL may have cholesterol-lowering properties, data in human are lacking. The aim of this study was to investigate the impact of buttermilk consumption on plasma lipids and surrogate markers of cholesterol (C) homeostasis in humans. Methods and results: Men and women (n = 34) with serum LDL-C <5.0 mmol/L at screening (mean LDL-C = 3.8 mmol/L) were recruited in this double-blinded randomized crossover placebo controlled study. Their diets were supplemented with 45 g/d of buttermilk and with 45 g/d of a macro/micronutrient matched placebo (4 weeks each in random order). Serum lipid concentrations and surrogate markers of cholesterol homeostasis were measured post diet and compared using mixed models for repeated measures. Consumption of buttermilk led to reduction in serum cholesterol (-3.1%, P = 0.019), LDL-C (-3.1%, P = 0.057) and triacylglycerol (-10.7%, P = 0.007). buttermilk consumption increased plasma lathosterol concentrations (+12.1%, P = 0.001), but multiple regression analysis indicated that variations in β-sitosterol concentrations (P = 0.002) were the only significant predictor of the LDL-C response to buttermilk consumption. Conclusion: buttermilk consumption may be associated with reduced cholesterol concentrations in men and women, primarily through inhibition of intestinal absorption of cholesterol. Registration number: This trial is registered at clinicaltrials.gov as NCT01248026.
Sweet buttermilk intake reduces colonisation and translocation of Listeria monocytogenes in rats by inhibiting mucosal pathogen adherence
Br J Nutr 2012 Dec 14;108(11):2026-33.PMID:22370235DOI:10.1017/S0007114512000165.
The bovine milk fat globule membrane (MFGM) contains several antimicrobial components with proven efficacy in vitro, but in vivo evidence is scarce. The present study was performed to determine the efficacy of the bovine MFGM in vivo. Rats were fed diets based on bovine skimmed milk powder (low in MFGM) or bovine sweet buttermilk powder (high in MFGM). After dietary adaptation, rats were orally infected with Salmonella enteritidis or Listeria monocytogenes. Whereas sweet buttermilk powder did not protect rats against infection with S. enteritidis, it protected against L. monocytogenes, as shown by a lower colonisation and translocation of this pathogen. Protection coincided with higher listericidal capacity of gastric and caecal contents. The digestion products of phosphoglycerides and sphingomyelin are bactericidal in vitro. To study their role, rats were fed diets containing either 0·1 % phosphatidylcholine or sphingomyelin, or a control diet. After dietary adaptation, rats were infected with L. monocytogenes. Since Listeria colonisation was not affected by these diets, phosphoglycerides and sphingomyelin are not involved in the protective effect of sweet buttermilk. Additional in vitro experiments were performed to further explore the mechanism of the beneficial effects of sweet buttermilk. Inhibition of the adherence of L. monocytogenes to the intestinal mucosa is the most likely explanation, since sweet buttermilk powder inhibited the binding of L. monocytogenes in both a haemagglutination assay and a Caco-2 cell adherence assay. In conclusion, sweet buttermilk powder, which is rich in MFGM, protects against L. monocytogenes infection in rats, probably by preventing adherence of this pathogen to the intestinal mucosa.
buttermilk: an important source of lipid soluble forms of choline that influences the immune system development in Sprague-Dawley rat offspring
Eur J Nutr 2021 Aug;60(5):2807-2818.PMID:33416979DOI:10.1007/s00394-020-02462-3.
Purpose: To determine the effect of feeding buttermilk-derived choline metabolites on the immune system development in Sprague-Dawley rat pups. Methods: Sprague-Dawley dams were randomized to one of the three diets containing 1.7 g/kg choline: 1-Control (100% free choline (FC)), 2-Buttermilk (BM, 37% phosphatidylcholine (PC), 34% sphingomyelin (SM), 17% glycerophosphocholine (GPC), 7% FC, 5% phosphocholine), and 3-Placebo (PB, 50% PC, 25% FC, 25% GPC) until the end of the lactation period. At weaning, pups continued on the same diet as their mom. Cell phenotypes and cytokine production by mitogen-stimulated splenocytes isolated from 3- and 10-week-old pups were measured. Results: At 3 weeks, BM-pups had a higher proportion of cytotoxic T cells (CTL; CD3 + CD8 +) while both BM- and PB-pups had an increased proportion of cells expressing CD28 + , CD86 + and CD27 + (all p > 0.05). Following ConA stimulation, splenocytes from BM- and PB-pups produced more TNF-α and IFN-γ and after LPS stimulation produced more IL-10 and TNF-α (all p > 0.05). Starting at week 6 of age, BM-pups had a higher body weight. At 10 weeks, both the BM- and PB-pups had a higher proportion of CTL expressing CD27 + . After ConA stimulation, splenocytes from BM- and PB-pups produced more IL-2, IFN-γ and IL-6 and more IL-10 after LPS stimulation (all p > 0.05). Conclusion: The proportion of lipid soluble forms of choline in the diet during lactation and weaning periods influence the immune system development in rat offspring.