This product is isolated and purified from the fruits of Garcinia atroviridis
Pentaric acid, 3-C-carboxy-2-deoxy-/Hydroxycitric acid/3-C-Carboxy-2-deoxypentaric acid
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
393.3±42.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
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Hydroxycitric acid, the active ingredient in the herbal compound Garcinia cambogia, competitively inhibits the extramitochondrial enzyme adenosine triphosphate-citrate (pro-3S)-lyase. As a citrate cleavage enzyme that may play an essential role in de novo lipogenesis inhibition, G cambogia is claimed to lower body weight and reduce fat mass in humans.
To evaluate the efficacy of G cambogia for body weight and fat mass loss in overweight human subjects.
Twelve-week randomized, double-blind, placebo-controlled trial.
Outpatient weight control research unit.
Overweight men and women subjects (mean body mass index [weight in kilograms divided by the square of height in meters], approximately 32 kg/m2).
Subjects were randomized to receive either active herbal compound (1500 mg of hydroxycitric acid per day) or placebo, and both groups were prescribed a high-fiber, low-energy diet. The treatment period was 12 weeks. Body weight was evaluated every other week and fat mass was measured at weeks 0 and 12.
MAIN OUTCOME MEASURES:
Body weight change and fat mass change.
A total of 135 subjects were randomized to either active hydroxycitric acid (n = 66) or placebo (n = 69); 42 (64%) in the active hydroxycitric acid group and 42 (61%) in the placebo group completed 12 weeks of treatment (P = .74). Patients in both groups lost a significant amount of weight during the 12-week treatment period (P<.001); however, between-group weight loss differences were not statistically significant (mean [SD], 3.2 [3.3] kg vs 4.1 [3.9] kg; P = .14). There were no significant differences in estimated percentage of body fat mass loss between treatment groups, and the fraction of subject weight loss as fat was not influenced by treatment group. CONCLUSIONS: Garcinia cambogia failed to produce significant weight loss and fat mass loss beyond that observed with placebo.
Garcinia cambogia (hydroxycitric acid) as a potential antiobesity agent: a randomized controlled trial.
Heymsfield SB1, Allison DB, Vasselli JR, Pietrobelli A, Greenfield D, Nunez C.
1998 Nov 11
To evaluate the preventive effects of hydroxycitric acid（HCA） for stone formation in the glyoxylate-induced mouse model.
MATERIALS AND METHODS:
Male C57BL/6J mice were divided into a control group, a glyoxylate(GOX) 100 mg/kg group, a GOX+HCA 100 mg/kg group, and a GOX+HCA 200 mg/kg group. Blood samples and kidney samples were collected on the 8th day. We used Pizzolato staining and polarized light microscope to examine crystal formation and evaluated oxidative stress via the levels of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px). Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) was used to detect the expression of monocyte chemotactic protein-1(MCP-1), nuclear factor-kappa B (NF κ B), interleukin-1 β (IL-1 β) and interleukin-6 (IL-6) messenger RNA (mRNA). The expression of osteopontin (OPN) and cluster of differentiation-44(CD44) was detected by immunohistochemistry and qRT-PCR. In addition, periodic acid Schiff (PAS) staining and TUNEL assay were used to evaluate renal tubular injury and apoptosis.
HCA treatment could reduce markers of renal impairment (Blood Urea Nitrogen and serum creatinine). There was significantly less calcium oxalate crystal deposition in mice treated with HCA. Calcium oxalate crystals induced the production of reactive oxygen species and reduced the activity of antioxidant defense enzymes. HCA attenuated the oxidative stress induced by calcium oxalate crystallization. HCA had inhibitory effects on calcium oxalate-induced inflammatory cytokines, such as MCP-1, IL-1 β, and IL-6. In addition, HCA alleviated tubular injury and apoptosis caused by calcium oxalate crystals.
HCA inhibits renal injury and calcium oxalate crystal deposition in the glyoxylate-induced mouse model through antioxidation and anti-inflammation.
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Hydroxycitric acid; Inflammation; Oxidative stress; Renal lens formation
Hydroxycitric acid inhibits renal calcium oxalate deposition by reducing oxidative stress and inflammation.
Liu X1, Yuan P1, Sun X1, Chen Z1.
2020 Jan 3
Existing spectrophotometric method to quantify hydroxycitric acid (HCA), although is specific and sensitive; finds limited use owing to poor stability of HCA-metavanadate complex. Present study describes improvisation of this method with respect to source of HCA standard and assay parameters. Assay system consisting of HCA and metavanadate reagent was modified to include 1 M NaOH to neutralize excess acidity. Resulting complex showed λmax at 485 nm, obeying Beer-Lambert’s law within concentration range of 33-677 μg/ml, with linear calibration curve showing a good coefficient of determination (R2 = 0.998). Moreover, HCA-metavanadate complex showed enhanced stability retaining up to 70% absorbance even after 60 min of its formation. Similar consistency in scaled-down assay system renders the method suitable for high-throughput screening of HCA-producing microbes. Of the tested metabolites and media components, only tartrate interfered with the spectrophotometric estimation of HCA; a correction factor to eliminate which was also established. Accordingly measured HCA level in the culture supernatant of a bacterial isolate IT6 was comparable to that determined using the standardized HPLC method. The proposed procedure therefore is a convenient, sensitive, accurate and high-throughput method suitable for primary screening of HCA producing microbes; the only ecofriendly alternative source of optically pure HCA.
Copyright © 2019 Elsevier Inc. All rights reserved.
Hydroxycitric acid; Hydroxycitric acid-producing microbes; Improvised spectrophotometric method
Improvisation of a spectrophotometric method to quantify hydroxycitric acid.
Patel D1, Buch A2.
2019 Dec 1