Dihydrocapsiate
目录号 : GC67924Dihydrocapsiate 作为二氢 capsinoid 家族的化合物，是一种口服活性 TRPV1 激动剂。Dihydrocapsiate 可用于代谢疾病的研究。
Cas No.:205687-03-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Dihydrocapsiate, as a compound of capsinoid family, is an orally active TRPV1 agonist. Dihydrocapsiate can be used for the research of metabolism disease[1].
Dihydrocapsiate (10, 25 and 50 μM; 48 hours; human preadipocytes) does not affect cell viability[1].
Dihydrocapsiate (10 and 20 μM; 8 days; mature adipocytes) markedly decreases the expression levels of other adipogenic markers (such as SREBP1, FABP4, PLIN1, ADIPOQ and LEPTIN) and inflammatory markers (MCP1 and TNFα), whereas it enhances the expression levels of PGC1α (master regulator of mitochondrial biogenesis) and TBX1 (marker of "brite" cell) [1].
Dihydrocapsiate (25~200 μM; RAW 264.7 cells) prevents NO release and intracellular ROS generation[1].
Cell Viability Assay[1]
| Cell Line: | Human preadipocytes |
| Concentration: | 10, 25 and 50 μM |
| Incubation Time: | 48 hours |
| Result: | Did not affect cell viability. |
RT-PCR[1]
| Cell Line: | Mature adipocytes |
| Concentration: | 10 and 20 μM |
| Incubation Time: | 8 days |
| Result: | Markedly decreased the expression levels of other adipogenic markers (such as SREBP1, FABP4, PLIN1, ADIPOQ and LEPTIN) and inflammatory markers (MCP1 and TNFα), whereas it enhanced the expression levels of PGC1α (master regulator of mitochondrial biogenesis) and TBX1 (marker of "brite" cell). |
Dihydrocapsiate (2 and 10 mg/kg; p.o.) improves morphometric parameters and insulin levels, prevents high fat diet (HFD)-induced adipocyte size and enhances energy expenditure-related genes in WAT, alleviates HFD-induced hepatic steatosis, prevents HFD-induced fat deposition and enhances mitochondrial biogenesis genes in BAT and improves intestinal morphology and modulates SCFA availability.
| Animal Model: | HFD-fed mice[1] |
| Dosage: | 2 and 10 mg/kg |
| Administration: | P.o. |
| Result: | Improved morphometric parameters and insulin levels, prevented HFD-induced adipocyte size and enhanced energy expenditure-related genes in WAT, alleviated HFD-induced hepatic steatosis, prevented HFD-induced fat deposition and enhanced mitochondrial biogenesis genes in BAT and improved intestinal morphology and modulates SCFA availability. |
[1]. Baboota RK, et al. Dihydrocapsiate supplementation prevented high-fat diet-induced adiposity, hepatic steatosis, glucose intolerance, and gut morphological alterations in mice. Nutr Res. 2018;51:40-56.
| Cas No. | 205687-03-2 | SDF | Download SDF |
| 分子式 | C18H28O4 | 分子量 | 308.41 |
| 溶解度 | 储存条件 | Store at -20°C, protect from light | |
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.2424 mL | 16.2122 mL | 32.4244 mL |
| 5 mM | 0.6485 mL | 3.2424 mL | 6.4849 mL |
| 10 mM | 0.3242 mL | 1.6212 mL | 3.2424 mL |
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动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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Dihydrocapsiate supplementation prevented high-fat diet-induced adiposity, hepatic steatosis, glucose intolerance, and gut morphological alterations in mice
Nutr Res 2018 Mar;51:40-56.PMID:29673543DOI:10.1016/j.nutres.2017.11.006.
Despite the lipolytic and thermogenic properties of capsaicin, its putative use as a weight-lowering dietary supplement has been limited because of the burning sensation caused by capsaicin when it comes in contact with mucous membranes. A potential alternative to capsaicin are the capsinoids, nonpungent capsaicin analogs that exhibit effects similar to capsaicin. Whereas the antiobesity properties of capsinoids have been reported, the effectiveness of FDA-approved synthetic Dihydrocapsiate has not yet been investigated. In the present study, we hypothesized that Dihydrocapsiate might ameliorate high-fat diet (HFD)-induced metabolic disorders in a manner similar to capsaicin and therefore can be its nonpungent alternative. To test this hypothesis, HFD-fed mice were orally administered Dihydrocapsiate (2 and 10mg/kg body weight) for 12weeks. Dihydrocapsiate modestly reduced the HFD-induced weight gain and significantly prevented the associated hyperglyceridemia and hyperinsulinemia while improving glucose tolerance. Histological and gene expression analysis showed that Dihydrocapsiate significantly prevented the lipid accumulation in white adipose tissue and brown adipose tissue via targeting genes involved in energy expenditure and mitochondrial biogenesis, respectively. Dihydrocapsiate corrected hepatic triglyceride concentrations and normalized expression of genes regulating hepatic lipid and glucose metabolism. Moreover, Dihydrocapsiate administration significantly improved gut morphology and altered gut microbial composition, resulting in reduced host energy availability. Collectively, these results indicate that Dihydrocapsiate administration improved glucose tolerance, prevented adiposity and hepatic steatosis, as well as improved HFD-induced gut alterations, positing Dihydrocapsiate as a potential food ingredient for the dietary management of HFD-induced metabolic alterations.
Dihydrocapsiate does not increase energy expenditure nor fat oxidation during aerobic exercise in men with overweight/obesity: a randomized, triple-blinded, placebo-controlled, crossover trial
J Int Soc Sports Nutr 2022 Jul 19;19(1):417-436.PMID:35875695DOI:10.1080/15502783.2022.2099757.
Background: Prior evidence suggests that capsinoids ingestion may increase resting energy expenditure (EE) and fat oxidation (FATox), yet whether they can modulate those parameters during exercise conditions remains poorly understood. We hypothesized that Dihydrocapsiate (DHC) ingestion would increase EE and specifically FATox during an acute bout of aerobic exercise at FATmax intensity (the intensity that elicits maximal fat oxidation during exercise [MFO]) in men with overweight/obesity. Since FATmax and MFO during aerobic exercise appear to be indicators of metabolic flexibility, whether DHC has an impact on FATox in this type of population is of clinical interest. Methods: A total of 24 sedentary men (age = 40.2 ± 9.2 years-old; body mass index = 31.6 ± 4.5 kg/m2 [n = 11 overweight, n = 13 obese]) participated in this randomized, triple-blinded, placebo-controlled, crossover trial (registered under ClinicalTrials.gov Identifier no. NCT05156697). On the first day, participants underwent a submaximal exercise test on a cycle ergometer to determine their MFO and FATmax intensity during exercise. After 72 hours had elapsed, the participants returned on 2 further days (≥ 72 hours apart) and performed a 60 min steady-state exercise bout (i.e. cycling at their FATmax, constant intensity) after ingesting either 12 mg of DHC or placebo; these conditions were randomized. Respiratory gas exchange was monitored by indirect calorimetry. Serum marker concentrations (i.e. glucose, triglycerides, non-esterified fatty acids (NEFAs), skin temperature, thermal perception, heart rate, and perceived fatigue) were assessed. Results: There were no significant differences (P > 0.05) between DHC and placebo conditions in the EE and FATox during exercise. Similarly, no significant changes were observed in glucose, triglycerides, or NEFAs serum levels, neither in the skin temperature nor thermal perception across conditions. Heart rate and perceived fatigue did not differ between conditions. Conclusions: DHC supplementation does not affect energy metabolism during exercise in men with overweight/obesity.
Quantitation of capsiate and Dihydrocapsiate and tentative identification of minor capsinoids in pepper fruits (Capsicum spp.) by HPLC-ESI-MS/MS(QTOF)
Food Chem 2019 Jan 1;270:264-272.PMID:30174045DOI:10.1016/j.foodchem.2018.07.112.
A highly sensitive, selective method has been developed and validated for determination of capsiate and Dihydrocapsiate for the first time using HPLC-ESI/MS(QTOF). For both capsinoids, LODs and LOQs were 0.02 and 0.05 µmol/l, respectively. The intra- and interday repeatability values (RSD %) were 0.26-0.41% for retention time, and 2.25-2.11% for peak area. Recoveries were up to 98% and 97% for capsiate and Dihydrocapsiate, respectively. This method was successfully applied to quantify capsiate and Dihydrocapsiate in eight pepper fruit accessions. Capsinoids were found in the range of 1.21-544.59 μg/g DW for capsiate and of 0.61-81.95 μg/g DW for Dihydrocapsiate. In the 'Tabasco' accession, capsiate and Dihydrocapsiate were quantified for the first time, ranging from 3.09 to 58.76 and 1.80 to 6.94 μg/g DW, respectively. Additionally, the ESI-MS/MS(QTOF) analysis has allowed the tentative identification of two other minor capsinoids by exact mass and fragmentation pattern, in the 'Bhut Jolokia' accession.
Dihydrocapsiate improved age-associated impairments in mice by increasing energy expenditure
Am J Physiol Endocrinol Metab 2017 Nov 1;313(5):E586-E597.PMID:28811294DOI:10.1152/ajpendo.00132.2017.
Metabolic dysfunction is associated with aging and results in age-associated chronic diseases, including type 2 diabetes mellitus, cardiovascular disease, and stroke. Hence, there has been a focus on increasing energy expenditure in aged populations to protect them from age-associated diseases. Dihydrocapsiate (DCT) is a compound that belongs to the capsinoid family. Capsinoids are capsaicin analogs that are found in nonpungent peppers and increase whole body energy expenditure. However, their effect on energy expenditure has been reported only in young populations, and to date the effectiveness of DCT in increasing energy expenditure in aged populations has not been investigated. In this study, we investigated whether DCT supplementation in aged mice improves age-associated impairments. We obtained 5-wk-old and 1-yr-old male C57BL/6J mice and randomly assigned the aged mice to two groups, resulting in a total of three groups: 1) young mice, 2) old mice, and 3) old mice supplemented with 0.3% DCT. After 12 wk of supplementation, blood and tissue samples were collected and analyzed. DCT significantly suppressed age-associated fat accumulation, adipocyte hypertrophy, and liver steatosis. In addition, the DCT treatment dramatically suppressed age-associated increases in hepatic inflammation, immune cell infiltration, and oxidative stress. DCT exerted these suppression effects by increasing energy expenditure linked to upregulation of both the oxidative phosphorylation gene program and fatty acid oxidation in skeletal muscle. These results indicate that DCT efficiently improves age-associated impairments, including liver steatosis and inflammation, in part by increasing energy expenditure via activation of the fat oxidation pathway in skeletal muscle.
Effect of Dihydrocapsiate on resting metabolic rate in humans
Am J Clin Nutr 2010 Nov;92(5):1089-93.PMID:20826626DOI:10.3945/ajcn.2010.30036.
Background: Dihydrocapsiate is a capsinoid found in chili peppers. Dihydrocapsiate is similar to capsaicin, which is known for its thermogenic properties. Objective: The objective was to determine the acute and chronic effect of Dihydrocapsiate on resting metabolic rate (RMR). Design: Seventy-eight healthy subjects in a double-blind, parallel-arm trial were randomly assigned to 3 groups receiving 0 (placebo), 3, or 9 mg Dihydrocapsiate/d for 28 d. After a 10-h overnight fast, RMR was measured by indirect calorimetry for 30 min before and 120 min after ingestion of Dihydrocapsiate. Results: RMR was similar in the 3 groups before dosing on day 1 [1714 ± 41 kcal/d (0 mg), 1760 ± 41 kcal/d (3 mg), and 1694 ± 38 kcal/d (9 mg)] and after acute dosing (41 ± 17, 55 ± 17, and 3 ± 24 kcal/d for 3-mg, 9-mg, and placebo groups, respectively). When the chronic effect of Dihydrocapsiate on RMR was calculated from the average 2-h RMR on day 28 minus the 30-min preingestion RMR at baseline, a borderline effect in subjects receiving 3 mg Dihydrocapsiate/d compared with placebo was observed (61 ± 24 kcal/d compared with -1 ± 12 kcal/d, P = 0.054), whereas no significant increase in RMR in comparison with placebo was noted for the 9-mg/d dose (48 ± 23 kcal/d compared with -1 ± 12 kcal/d, P = 0.12). When data from both groups were combined, the thermic effect of Dihydrocapsiate reached significance (53 ± 9 kcal/d compared with -1 ± 12 kcal/d in the placebo group, P = 0.04). Fat oxidation was unaffected by Dihydrocapsiate. Conclusion: After 1 mo of supplementation, Dihydrocapsiate had a small thermogenic effect of ≈50 kcal/d, which is in the range of day-to-day RMR variability. This trial was registered at clinicaltrials.gov as NCT00999297.