CMPF
目录号 : GC40478An endogenous furan fatty acid metabolite and inhibitor of serum T4 transport and deiodination
Cas No.:86879-39-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Furan fatty acids are unique, naturally occurring lipids that are found in significant amounts in dietary phospholipids, such as in salmon roe. [1] CMPF is an endogenous metabolite of furan fatty acids in humans. CMPF is highly albumin-bound and accumulates in the serum of uremic patients to concentrations in excess of 0.2 mM. Its primary effect is to inhibit cellular transport and subsequent deiodination of thyroxine (T4). [2] [3] CMPF is tightly bound to albumin but only moderately inhibits T4 binding in a direct manner (10-14% at 0.3 mM). However, CMPF effectively displaces competitive T4 binding molecules from albumin, such as acidic drugs and free fatty acids. [3] Therefore, CMPF may indirectly influence T4 binding to albumin by increasing the serum concentration of competitive binding molecules, particularly free fatty acids such as oleic acid.[3]
Reference：
[1]. Ishii, K., Okajima, H., Okada, Y., et al. Studies on furan fatty acids of salmon roe phospholipids. Journal of Biochemistry 103(5), 836-839 (1988).
[2]. Lim, C.F., Bernard, B.F., De Jong, M., et al. A furan fatty acid and indoxyl sulfate are the putative inhibitors of thyroxine hepatocyte transport in uremia. Journal of Clinical Endocrinology and Metabolism 76(2), 318-324 (1993).
[3]. Lim, C.F., Stockigt, J.R., Curtis, A.J., et al. A naturally occuring furan fatty acid enhances drug inhibition of thyroxine binding in serum. Metabolism 42(11), 1468-1474 (1993).
| Cas No. | 86879-39-2 | SDF | |
| 化学名 | 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid | ||
| Canonical SMILES | CCCc1oc(CCC(=O)O)c(C(=O)O)c1C | ||
| 分子式 | C12H16O5 | 分子量 | 240.3 |
| 溶解度 | 30 mg/ml in DMF, 30 mg/ml in DMSO, 30 mg/ml in Ethanol | 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 | 4.1615 mL | 20.8073 mL | 41.6146 mL |
| 5 mM | 0.8323 mL | 4.1615 mL | 8.3229 mL |
| 10 mM | 0.4161 mL | 2.0807 mL | 4.1615 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。
The association between TMAO, CMPF, and clinical outcomes in advanced chronic kidney disease: results from the European QUALity (EQUAL) Study
Am J Clin Nutr 2022 Dec 19;116(6):1842-1851.PMID:36166845DOI:10.1093/ajcn/nqac278.
Background: Trimethylamine N-oxide (TMAO), a metabolite from red meat and fish consumption, plays a role in promoting cardiovascular events. However, data regarding TMAO and its impact on clinical outcomes are inconclusive, possibly due to its undetermined dietary source. Objectives: We hypothesized that circulating TMAO derived from fish intake might cause less harm compared with red meat sources by examining the concomitant level of 3-carboxy-4-methyl-5-propyl-2-furanpropionate (CMPF), a known biomarker of fish intake, and investigated the association between TMAO, CMPF, and outcomes. Methods: Patients were recruited from the European QUALity (EQUAL) Study on treatment in advanced chronic kidney disease among individuals aged ≥65 y whose estimated glomerular filtration rate (eGFR) had dropped for the first time to ≤20 mL/min per 1.73 m2 during the last 6 mo. The association between TMAO, CMPF, and outcomes including all-cause mortality and kidney replacement therapy (KRT) was assessed among 737 patients. Patients were further stratified by median cutoffs of TMAO and CMPF, suggesting high/low red meat and fish intake. Results: During a median of 39 mo of follow-up, 232 patients died. Higher TMAO was independently associated with an increased risk of all-cause mortality (multivariable HR: 1.46; 95% CI: 1.17, 1.83). Higher CMPF was associated with a reduced risk of both all-cause mortality (HR: 0.79; 95% CI: 0.71, 0.89) and KRT (HR: 0.80; 95% CI: 0.71, 0.90), independently of TMAO and other clinically relevant confounders. In comparison to patients with low TMAO and CMPF, patients with low TMAO and high CMPF had reduced risk of all-cause mortality (adjusted HR: 0.49; 95% CI: 0.31, 0.73), whereas those with high TMAO and high CMPF showed no association across adjusted models. Conclusions: High CMPF conferred an independent role in health benefits and might even counteract the unfavorable association between TMAO and outcomes. Whether higher circulating CMPF concentrations are due to fish consumption, and/or if CMPF is a protective factor, remains to be verified.
CMPF does not associate with impaired glucose metabolism in individuals with features of metabolic syndrome
PLoS One 2015 Apr 15;10(4):e0124379.PMID:25874636DOI:10.1371/journal.pone.0124379.
Objective: 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF) is a metabolite produced endogenously from dietary sources of furan fatty acids. The richest source of furan fatty acids in human diet is fish. CMPF was recently shown to be elevated in fasting plasma in individuals with gestational diabetes and type 2 diabetes, and mechanistically high level of CMPF was linked to β cell dysfunction. Here we aimed to study the association between plasma CMPF level and glucose metabolism in persons with impaired glucose metabolism. Methods: Plasma CMPF concentration was measured from plasma samples of the study participants in an earlier controlled dietary intervention. All of them had impaired glucose metabolism and two other characteristics of the metabolic syndrome. Altogether 106 men and women were randomized into three groups for 12 weeks with different fish consumption (either three fatty fish meals per week, habitual fish consumption or maximum of one fish meal per week). Associations between concentration of CMPF and various glucose metabolism parameters at an oral glucose tolerance test at baseline and at the end of the study were studied. Results: Fasting plasma CMPF concentration was significantly increased after a 12-week consumption of fatty fish three times per week, but the concentration remained much lower compared to concentrations reported in diabetic patients. Increases of plasma CMPF concentrations mostly due to increased fish consumption were not associated with impaired glucose metabolism in this study. Instead, elevated plasma CMPF concentration was associated with decreased 2-hour insulin concentration in OGTT. Conclusions: Moderately elevated concentration of CMPF in plasma resulting from increased intake of fish is not harmful to glucose metabolism. Further studies are needed to fully explore the role of CMPF in the pathogenesis of impaired glucose metabolism. Trial registration: ClinicalTrials.gov NCT00573781.
CMPF: A Biomarker for Type 2 Diabetes Mellitus Progression?
Trends Endocrinol Metab 2016 Jul;27(7):439-440.PMID:27132217DOI:10.1016/j.tem.2016.04.010.
The factors that precipitate the transition from insulin resistance to type 2 diabetes mellitus (T2DM) remain elusive. A recent study showed that circulating levels of the furan fatty acid (FA) metabolite 3-Carboxy-4-Methyl-5-Propyl-2-Furanopropanoic Acid (CMPF) increase in individuals who progress from prediabetes to T2DM. CMPF increases oxidative stress and impairs insulin granule maturation and secretion.
CMPF, a Metabolite Formed Upon Prescription Omega-3-Acid Ethyl Ester Supplementation, Prevents and Reverses Steatosis
EBioMedicine 2018 Jan;27:200-213.PMID:29290411DOI:10.1016/j.ebiom.2017.12.019.
Prescription ω-3 fatty acid ethyl ester supplements are commonly used for the treatment of hypertriglyceridemia. However, the metabolic profile and effect of the metabolites formed by these treatments remain unknown. Here we utilized unbiased metabolomics to identify 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF) as a significant metabolite of the ω-3-acid ethyl ester prescription Lovaza™ in humans. Administration of CMPF to mice before or after high-fat diet feeding at exposures equivalent to those observed in humans increased whole-body lipid metabolism, improved insulin sensitivity, increased beta-oxidation, reduced lipogenic gene expression, and ameliorated steatosis. Mechanistically, we find that CMPF acutely inhibits ACC activity, and induces long-term loss of SREBP1c and ACC1/2 expression. This corresponds to an induction of FGF21, which is required for long-term steatosis protection, as FGF21KO mice are refractory to the improved metabolic effects. Thus, CMPF treatment in mice parallels the effects of human Lovaza™ supplementation, revealing that CMPF may contribute to the improved metabolic effects observed with ω-3 fatty acid prescriptions.
Rapid Elevation in CMPF May Act As a Tipping Point in Diabetes Development
Cell Rep 2016 Mar 29;14(12):2889-900.PMID:26997281DOI:10.1016/j.celrep.2016.02.079.
Prediabetes, a state of mild glucose intolerance, can persist for years before a sudden decline in beta cell function and rapid deterioration to overt diabetes. The mechanism underlying this tipping point of beta cell dysfunction remains unknown. Here, the furan fatty acid metabolite CMPF was evaluated in a prospective cohort. Those who developed overt diabetes had a significant increase in CMPF over time, whereas prediabetics maintained chronically elevated levels, even up to 5 years before diagnosis. To evaluate the effect of increasing CMPF on diabetes progression, we used obese, insulin-resistant models of prediabetes. CMPF accelerated diabetes development by inducing metabolic remodeling, resulting in preferential utilization of fatty acids over glucose. This was associated with diminished glucose-stimulated insulin secretion, increased ROS formation, and accumulation of proinsulin, all characteristics of human diabetes. Thus, an increase in CMPF may represent the tipping point in diabetes development by accelerating beta cell dysfunction.