Acipimox - CAS 51037-30-0
Catalog number:
51037-30-0
Category:
Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C6H6N2O3
Molecular Weight:
154.12
COA:
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Targets:
Others
Description:
Acipimox (trade name Olbetam in Europe) is a niacin derivative used as a hypolipidemic agent. It is used in low doses and may have less marked adverse effects, although it is unclear whether the recommended dose is as effective as are standard doses of nicotinic acid. Acipimox inhibits the production of triglycerides by the liver and the secretion ofVLDL cholesterol, which leads indirectly to a modest reduction in LDL and increase in HDL cholesterol.
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Purity:
>98%
Synonyms:
Olbemox
MSDS:
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1.Free fatty acids, not triglycerides, are associated with non-alcoholic liver injury progression in high fat diet induced obese rats.
Liu J1, Han L2, Zhu L3, Yu Y4. Lipids Health Dis. 2016 Feb 11;15(1):27. doi: 10.1186/s12944-016-0194-7.
BACKGROUND: The incidence of non-alcoholic fatty liver disease (NAFLD), commonly associated with obesity and metabolic syndrome, is increasing worldwide. However, the specific mechanisms that mediate the progression from simple steatosis to non-alcoholic steatohepatitis remain largely unclear. This study aimed to investigate the timedependent changes of triglyceride (TG) and free fatty acid (FFA) levels in the blood and liver over 24 weeks in high-fat diet-induced obese rats with NAFLD and to clarify the role of high FFA levels in the progression of liver injury.
2.Free fatty acid availability is closely related to myocardial lipid storage and cardiac function in hypoglycemia counterregulation.
Winhofer Y1, Krššák M2, Wolf P3, Anderwald CH4, Geroldinger A5, Heinze G5, Baumgartner-Parzer S3, Marculescu R6, Stulnig T7, Wolzt M8, Trattnig S9, Luger A3, Krebs M3. Am J Physiol Endocrinol Metab. 2015 Apr 15;308(8):E631-40. doi: 10.1152/ajpendo.00371.2014. Epub 2015 Feb 10.
Hypoglycemia, a major side effect of intensive glucose-lowering therapy, was recently linked to increased cardiovascular risk in patients with diabetes. Whether increased circulating free fatty acids (FFA) owing to catecholamine-induced lipolysis affect myocardial energy metabolism and thus link hypoglycemia to cardiac vulnerability is unclear. Therefore, this study investigated the impact of hypoglycemia counterregulation (± inhibition of lipolysis) on myocardial lipid content (MYCL) and left ventricular function in healthy subjects. Nine healthy men were studied in randomized order: 1) insulin/hypoglycemia test (IHT; ins+/aci-), 2) IHT during inhibition of adipose tissue lipolysis by acipimox (ins+/aci+), 3) normoglycemia with acipimox (ins-/aci+), and 4) normoglycemia with placebo (ins-/aci-). MYCL and cardiac function were assessed by employing magnetic resonance spectroscopy/imaging at baseline and at 2 and 6 h. In response to acute hypoglycemia, plasma FFA (P<0.
3.Effect of Dapagliflozin With and Without Acipimox on Insulin Sensitivity and Insulin Secretion in T2DM Males.
Merovci A1, Abdul-Ghani M1, Mari A1, Solis-Herrera C1, Xiong J1, Daniele G1, Tripathy D1, DeFronzo RA1. J Clin Endocrinol Metab. 2016 Mar;101(3):1249-56. doi: 10.1210/jc.2015-2597. Epub 2016 Jan 14.
AIM: To investigate the effect of lowering the plasma glucose and free fatty acid (FFA) concentrations with dapagliflozin and acipimox, respectively, on insulin sensitivity and insulin secretion in T2DM individuals.
4.Activation of AMPKα2 in adipocytes is essential for nicotine-induced insulin resistance in vivo.
Wu Y1, Song P2, Zhang W2, Liu J3, Dai X2, Liu Z2, Lu Q2, Ouyang C4, Xie Z2, Zhao Z2, Zhuo X3, Viollet B5, Foretz M5, Wu J6, Yuan Z3, Zou MH4. Nat Med. 2015 Apr;21(4):373-82. doi: 10.1038/nm.3826. Epub 2015 Mar 23.
Cigarette smoking promotes body weight reduction in humans while paradoxically also promoting insulin resistance (IR) and hyperinsulinemia. However, the mechanisms behind these effects are unclear. Here we show that nicotine, a major constituent of cigarette smoke, selectively activates AMP-activated protein kinase α2 (AMPKα2) in adipocytes, which in turn phosphorylates MAP kinase phosphatase-1 (MKP1) at serine 334, initiating its proteasome-dependent degradation. The nicotine-dependent reduction of MKP1 induces the aberrant activation of both p38 mitogen-activated protein kinase and c-Jun N-terminal kinase, leading to increased phosphorylation of insulin receptor substrate 1 (IRS1) at serine 307. Phosphorylation of IRS1 leads to its degradation, protein kinase B inhibition, and the loss of insulin-mediated inhibition of lipolysis. Consequently, nicotine increases lipolysis, which results in body weight reduction, but this increase also elevates the levels of circulating free fatty acids and thus causes IR in insulin-sensitive tissues.
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CAS 51037-30-0 Acipimox

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