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C18 dihydro Ceramide (d18:0/18:0) Sale

(Synonyms: 二羟基神经酰胺,Cer(d18:0/18:0)) 目录号 : GC43048

A bioactive sphingolipid

C18 dihydro Ceramide (d18:0/18:0) Chemical Structure

Cas No.:2304-80-5

规格 价格 库存 购买数量
5mg
¥1,284.00
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10mg
¥2,449.00
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25mg
¥4,814.00
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产品描述

C18 dihydro Ceramide is a bioactive sphingolipid and precursor in the de novo synthesis of C18 ceramide that lacks the 4,5-trans double bond. [1] Increased C18 dihydroceramide lipid levels lead to increased triacylglycerol storage and autophagosome accumulation as well as upregulation of the fibrosis markers α-SMA and FGF2 in Chang and LX-2 liver cells. C18 dihydro Ceramide is elevated in the plasma of pre-diabetics up to 9 years prior to the onset of type 2 diabetes. [2]  It is also elevated in the skin of patients with lesional atopic dermatitis.[3]

Reference:
[1]. Lee, A.Y., Lee, J.W., Kim, J.-E., et al. Dihydroceramide is a key metabolite that regulates autophagy and promotes fibrosis in hepatic steatosis model. Biochem. Biophys. Res. Commun. 494(3-4), 460-469 (2017).
[2]. Wigger, L., Cruciani-Guglielmacci, C., Nicolas, A., et al. Plasma dihydroceramides are diabetes susceptibility biomarker candidates in mice and humans. Cell Rep. 18(9), 2269-2279 (2017).
[3]. Joo, J.-M., Hwang, J.-H., Bae, S., et al. Relationship of ceramide-, and free fatty acid-cholesterol ratios in the stratum corneum with skin barrier function of normal, atopic dermatitis lesional and non-lesional skins. J. Dermatol. Sci. 77(1), 71-74 (2015).

Chemical Properties

Cas No. 2304-80-5 SDF
别名 二羟基神经酰胺,Cer(d18:0/18:0)
化学名 N-[(1S,2R)-2-hydroxy-1-(hydroxymethyl)heptadecyl]-octadecanamide
Canonical SMILES O=C(CCCCCCCCCCCCCCCCC)N[C@@H](CO)[C@H](O)CCCCCCCCCCCCCCC
分子式 C36H73NO3 分子量 568
溶解度 DMSO: Soluble,Ethanol: Warmed 储存条件 Store at -20°C
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1 mg 5 mg 10 mg
1 mM 1.7606 mL 8.8028 mL 17.6056 mL
5 mM 0.3521 mL 1.7606 mL 3.5211 mL
10 mM 0.1761 mL 0.8803 mL 1.7606 mL
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Research Update

Vitamin D Supplementation Enhances C18(dihydro)ceramide Levels in Type 2 Diabetes Patients

Int J Mol Sci 2017 Jul 15;18(7):1532.PMID:28714882DOI:PMC5536020

Sphingolipids are characterized by a broad range of bioactive properties. Particularly, the development of insulin resistance, a major pathophysiological hallmark of Type 2 Diabetes mellitus (T2D), has been linked to ceramide signaling. Since vitamin D supplementation may slow down T2D progression by improving glucose concentrations and insulin sensitivity, we investigated whether vitamin D supplementation impacts on plasma sphingolipid levels in T2D patients. Thus, plasma samples of 59 patients with non-insulin-requiring T2D from a placebo-controlled, randomized, and double-blind study were retrospectively analyzed. Once per week, patients received either 20 drops of Vigantol oil, corresponding to a daily dose of 1904 IU/d vitamin D (verum: n = 31), or a placebo oil consisting of medium chain triglycerides (placebo: n = 28). Blood samples were taken from all of the participants at three different time points: 1) at the beginning of the study (baseline), 2) after 6 months supplementation, and 3) after an additional 6 months of follow-up. Plasma sphingolipids were measured by high-performance liquid chromatography tandem mass spectrometry. At baseline and 6 months follow-up, no significant differences in plasma sphingolipid species were detected between the placebo and verum groups. After 6 months, vitamin D supplementation significantly enhanced plasma C18dihydroceramide (dhCer; N-stearoyl-sphinganine (d18:0/18:0)) and C18ceramide (Cer; N-stearoyl-sphingosine (d18:1/18:0)) levels were observed in the verum group compared to the placebo group. This was accompanied by significantly higher 25-hydroxyvitamin D₃ (25(OH)D₃) blood levels in patients receiving vitamin D compared to the placebo group. Taken together, vitamin D supplementation induced changes of the C18 chain-length-specific dhCer and Cer plasma levels in patients with T2D. The regulation of sphingolipid signaling by vitamin D may thus unravel a novel mechanism by which vitamin D can influence glucose utilization and insulin action. Whether this acts favorably or unfavorably for the progression of T2D needs to be clarified.