Deinoxanthin, a Carotenoid from the Radioresistant Bacterium Deinococcus radiodurans, Inhibits Lipogenesis in Liver

Creative Commons License

Kuzucu M., Çiçek B.

9th Drug Chemistry Conference, Antalya, Türkiye, 8 - 11 Nisan 2021, ss.68

  • Yayın Türü: Bildiri / Özet Bildiri
  • Basıldığı Şehir: Antalya
  • Basıldığı Ülke: Türkiye
  • Sayfa Sayıları: ss.68
  • Erzincan Binali Yıldırım Üniversitesi Adresli: Evet

Özet

Lipogenesis is an important defining feature of overweight and obesity. These conditions, particularly in the presence of excess fat are in some visceral area or in the ectopic locations, are associated with health risk factors such as dyslipidemia, insulin resistance, or hypertension [1]. Hepatic steatosis refers to excessive lipid accumulation in the liver and ectopic area. CCAAT/enhancer-binding protein alpha (CEBPA) and Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1 Alpha (PGC1A) is a transcription factor that plays a vital role in hepatic de novo lipogenesis, thermogenesis, mitochondrial biogenesis and cholesterol metabolism. PGC1A interacts with Peroxisome proliferator-activated receptor gamma (PPAR-γ), which permits the interaction of this protein with multiple transcription factors. The genes activated by PPAR-γ induce lipid uptake and adipogenesis by fat cells [2]. In the last few years, Anti-lipogenesis activities of carotenoids have been shown in a number of preclinical studies, and its metabolic interactions have begun to be explained, suggesting these compounds may help obesity prevention and treatment. The keto-carotenoid deinoxanthin is a unique xanthophyll that provides greater antioxidant effects compared to other carotenoids due to its superior scavenging activity against reactive oxygen species can only derived from Deinococcus spp [3, 4]. This study was designed to investigate the effect of deinoxanthin on hepatic steatosis in male Wistar rats. Animals were randomly divided into three groups (n=8/group) and treated orally with distilled water (0.25 ml-group 1) or deinoxanthin (50 μg/day-group 2, 100μg/day-group 3) for 56 days. Thereafter, blood and liver samples were collected and have been examined for level of CEBPA and PGC-1α. The effect of deinoxanthin on the mRNA and protein expression of PGC-1α and CEBPA were analyzed by RT-qPCR and ELISA. Deinoxanthin treatment also decreased expression of PGC-1α and CEBPA.