Nicotinamide riboside regulates inflammation and mitochondrial markers in AML12 hepatocytes
- Author:
Hee Jae LEE
1
;
Soo Jin YANG
Author Information
- Publication Type:Original Article
- Keywords: Fatty liver; inflammation; mitochondria; niacin
- MeSH: Adiponectin; alpha-2-HS-Glycoprotein; Alzheimer Disease; Animals; Beer; Carnitine O-Palmitoyltransferase; Cell Survival; Cytokines; DNA, Mitochondrial; Fatty Liver; Gene Expression; Hearing Loss; Hepatocytes; Inflammation; Interleukin-6; Mice; Milk; Mitochondria; Mitochondrial Myopathies; Niacin; Niacinamide; Obesity; Organelle Biogenesis; Palmitic Acid; Peroxisomes; Sirtuin 1; Sirtuins; Transcription Factors; Tumor Necrosis Factor-alpha
- From:Nutrition Research and Practice 2019;13(1):3-10
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND/OBJECTIVES: The NAD+ precursor nicotinamide riboside (NR) is a type of vitamin B3 found in cow's milk and yeast-containing food products such as beer. Recent studies suggested that NR prevents hearing loss, high-fat diet-induced obesity, Alzheimer's disease, and mitochondrial myopathy. The objective of this study was to investigate the effects of NR on inflammation and mitochondrial biogenesis in AML12 mouse hepatocytes. MATERIALS/METHODS: A subset of hepatocytes was treated with palmitic acid (PA; 250 µM) for 48 h to induce hepatocyte steatosis. The hepatocytes were treated with NR (10 µM and 10 mM) for 24 h with and without PA. The cell viability and the levels of sirtuins, inflammatory markers, and mitochondrial markers were analyzed. RESULTS: Cytotoxicity of NR was examined by PrestoBlue assay. Exposure to NR had no effect on cell viability or morphology. Gene expression of sirtuin 1 (Sirt1) and Sirt3 was significantly upregulated by NR in PA-treated hepatocytes. However, Sirt1 activities were increased in hepatocytes treated with low-dose NR. Hepatic pro-inflammatory markers including tumor necrosis factor-alpha and interleukin-6 were decreased in NR-treated cells. NR upregulated anti-inflammatory molecule adiponectin, and, tended to down-regulate hepatokine fetuin-A in PA-treated hepatocytes, suggesting its inverse regulation on these cytokines. NR increased levels of mitochondrial markers including peroxisome proliferator-activated receptor γ coactivator-1α, carnitine palmitoyltransferase 1, uncoupling protein 2, transcription factor A, mitochondrial and mitochondrial DNA in PA-treated hepatocytes. CONCLUSIONS: These data demonstrated that NR attenuated hepatic inflammation and increased levels of mitochondrial markers in hepatocytes.
