Nicotinic Acid GPCR Assays
Background of Nicotinic Acid Receptors
Nicotinic acid, also known as niacin, is the first orally available drug for the treatment of high cholesterol levels and the improvement of the balance between low-density lipoprotein (LDL) and high-density lipoprotein (HDL). The developed nicotinic acid receptor agonists may result in adipocyte TG accumulation and increased flushing.
Fig.1 Model of the physiological function of GPR109A and GPR109B. (Ahmed, 2009)
Distribution and Functions of Nicotinic Acid Receptors
The nicotinic acid receptors are mainly distributed in adipose tissue, spleen, and macrophages. Nicotinic acid receptors have served as potential therapeutic targets for the treatment of neuroimmune disorders, such as multiple sclerosis and Parkinson's disease.
Subtypes and Mechanisms of Nicotinic Acid Receptors
In humans, there are two nicotinic acid receptor isoforms, including niacin receptor 1 (NIACR1) and niacin receptor 2 (NIACR2). NIACR1 is a high-affinity Gi/o-coupled G protein-coupled receptor (GPCR). Activation of NIACR1 can inhibit lipolytic and atherogenic activity, induce vasodilation, and is responsible for mediating niacin-induced flushing. NIACR2 is also a Gi/o-coupled GPCR but with low affinity.
| Receptor | Gene | Mechanism | Agonists | Antagonists |
| Niacin receptor 1 | NIACR1 |
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| Niacin receptor 2 | NIACR2 |
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Assay List of Nicotinic Acid Receptors
Creative Biolabs can provide a range of assays of nicotinic acid receptors. You can choose the assay in the list or contact us for more information:
Published Data
| Paper Title |
Nicotinic acid suppresses sebaceous lipogenesis of human sebocytes via activating hydroxycarboxylic acid receptor 2 (HCA2) |
| Journal |
Journal of cellular and molecular medicine |
| Published | 2018 |
| Abstract |
Due to the ability to activate hydroxycarboxylic acid receptor 2 (HCA2), niacin (NA) has been widely used in the treatment of dyslipidemia but is accompanied by a series of side effects. Using human immortalized SZ95 sebocytes, we found that non-cytotoxic (≤100 μmol/L) concentrations of NA had no effect on steady-state sebaceous lipogenesis. Furthermore, it exerted a marked antiproliferative effect and increased [Ca2+]IC. Although NA was unable to inhibit LPS-induced pro-inflammatory response in sebocytes, our experimental data allowed us to conclude that NA might be effective in inhibiting sebum production in vivo. During the study, we also found that sebocytes expressed HCA2 and siRNA-mediated silencing prevented NA-induced Ca2+ signaling and fat suppression. Collectively, we described the possible anti-acne potential of NA and HCA2 activators. |
| Result |
In the present study, we have initially demonstrated that NA is able to normalize acne-mimicking, excessive sebaceous lipogenesis (SLG) induced by various acne-promoting drugs without affecting the basal, homeostatic lipid synthesis or viability of human sebocytes. These effects are achieved through the activation of HCA2 receptors. Thus, our data not only highlight the possibility of NA for dermatology, but also that the HCA2 receptor is an attractive pharmacological target for the development of future sebum-suppressive and anti-acne drugs. Clinical trials and further development of its therapeutic potential by delivering NA directly to the sebaceous glands using appropriate topical formulations are then required.
Fig.2 Overview of the anti-acne potential of NA and HCA2-agonism. (Markovics, 2022) |
References 
- Ahmed, K.; et al. GPR109A, GPR109B and GPR81, a family of hydroxy-carboxylic acid receptors. Trends in pharmacological sciences. 2009, 30(11): 557-562.
- Markovics, A.; et al. Nicotinic acid suppresses sebaceous lipogenesis of human sebocytes via activating hydroxycarboxylic acid receptor 2 (HCA2). Journal of cellular and molecular medicine. 2019, 23(9): 6203-6214.
