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| HCA is a naturally occurring compound primarily known for its potential effects on appetite and lipid metabolism via inhibition of ATP citrate lyase. Derivative of citric acid that is found in a variety of tropical plants including Garcinia cambogia and Hibiscus sabdariffa Hydroxycitric acid (HCA) is a plant‐derived hydroxycinnamic acid derivative best known for inhibiting ATP citrate lyase (ACLY), a key enzyme that generates cytosolic acetyl-CoA from citrate for lipid and cholesterol synthesis. By reducing ACLY activity and downstream lipogenesis, HCA shifts cellular metabolism and can activate energy-sensing pathways (such as AMPK) in some models. Evidence for direct anticancer cytotoxicity is modest and often linked to metabolic stress rather than primary cytotoxic mechanisms. Oral exposure is influenced by rapid metabolism and conjugation, with systemic bioavailability often limited compared to levels used in many in vitro studies. • Hydroxy-Citric Acid (HCA) is a compound extracted from Garcinia cambogia, primarily recognized for its potential effects on lipid metabolism and appetite suppression. • It has been proposed to inhibit the enzyme ATP citrate lyase, which is involved in converting citrate into acetyl-CoA—a key step in fatty acid synthesis. • By modulating lipid synthesis pathways, HCA has been studied in the context of obesity and metabolic disorders, with some exploratory research considering its implications in cancer metabolism. • Inhibition of ATP Citrate Lyase (ACLY)****** ACLY converts citrate into acetyl-CoA, a building block for fatty acid and cholesterol synthesis. Many cancer cells upregulate lipid synthesis to support membrane production and energy storage; hence, inhibiting ACLY presents a potential strategy to disrupt cancer cell metabolism. • Impact on Lipogenesis Reduced acetyl-CoA production can impair de novo lipogenesis, potentially limiting the proliferation of rapidly dividing cells that have high lipid demands. • Interactions with Other Metabolic Pathways (modulation of citrate levels may affect the TCA cycle) -Dosages used in weight loss studies typically ranging from 500 mg to 1500 mg per day Human cyclists: 3.1 mL/kg body wt of an HCA solution (19 g/L) --> 248mg "Studies have shown that humans can safely ingest 13.5 g of hydroxycitrate per day with plasma levels of 82 mg/L (0.39 mM) achieved". Appetite suppression and weight loss effects are mixed. Typically, HCA used in dietary weight loss supplement is bound to calcium, which results in a poorly soluble (<50%) and less bioavailable form. Conversely, the structural characteristics of a novel Ca2+/K+ bound (-)-HCA salt (HCA-SX or Super CitriMax) make it completely water soluble as well as bioavailable. -HydroxyCitrate (HCA) typically used in a dose of about 1.5g/day or more for cancer (inhibition of the Melavonate Pathway?)
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| Glycolysis is a metabolic pathway that converts glucose into pyruvate, producing a small amount of ATP (energy) in the process. It is a fundamental process for cellular energy production and occurs in the cytoplasm of cells. In normal cells, glycolysis is tightly regulated and is followed by aerobic respiration in the presence of oxygen, which allows for the efficient production of ATP. In cancer cells, however, glycolysis is often upregulated, even in the presence of oxygen. This phenomenon is known as the Warburg Mutations in oncogenes (like MYC) and tumor suppressor genes (like TP53) can alter metabolic pathways, promoting glycolysis and other anabolic processes that support cell growth.effect. Acidosis: The increased production of lactate from glycolysis can lead to an acidic microenvironment, which may promote tumor invasion and suppress immune responses. Glycolysis is a hallmark of malignancy transformation in solid tumor, and LDH is the key enzyme involved in glycolysis. Pathways: -GLUTs, HK2, PFK, PK, PKM2, LDH, LDHA, PI3K/AKT/mTOR, AMPK, HIF-1a, c-MYC, p53, SIRT6, HSP90α, GAPDH, HBT, PPP, Lactate Metabolism, ALDO Natural products targeting glycolytic signaling pathways https://pmc.ncbi.nlm.nih.gov/articles/PMC9631946/ Alkaloids: -Berberine, Worenine, Sinomenine, NK007, Tetrandrine, N-methylhermeanthidine chloride, Dauricine, Oxymatrine, Matrine, Cryptolepine Flavonoids: -Oroxyline A, Apigenin, Kaempferol, Quercetin, Wogonin, Baicalein, Chrysin, Genistein, Cardamonin, Phloretin, Morusin, Bavachinin, 4-O-methylalpinumisofavone, Glabridin, Icaritin, LicA, Naringin, IVT, Proanthocyanidin B2, Scutellarin, Hesperidin, Silibinin, Catechin, EGCG, EGC, Xanthohumol. Non-flavonoid phenolic compounds: Curcumin, Resveratrol, Gossypol, Tannic acid. Terpenoids: -Cantharidin, Dihydroartemisinin, Oleanolic acid, Jolkinolide B, Cynaropicrin, Ursolic Acid, Triptolie, Oridonin, Micheliolide, Betulinic Acid, Beta-escin, Limonin, Bruceine D, Prosapogenin A (PSA), Oleuropein, Dioscin. Quinones: -Thymoquinone, Lapachoi, Tan IIA, Emodine, Rhein, Shikonin, Hypericin Others: -Perillyl alcohol, HCA, Melatonin, Sulforaphane, Vitamin D3, Mycoepoxydiene, Methyl jasmonate, CK, Phsyciosporin, Gliotoxin, Graviola, Ginsenoside, Beta-Carotene. |
| 5791- | CRMs, | HCA, | NAD, | Sper, | RES | Caloric Restriction Mimetics in Nutrition and Clinical Trials |
| - | Review, | Nor, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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