Expression of STING in Women with Morbid Obesity and Nonalcoholic Fatty Liver Disease.
Laia BertranLaia AdalidMercè Vilaró-BlayAndrea Barrientos-RiosalidoCarmen AguilarSalomé MartínezFàtima SabenchDaniel Del CastilloJosé Antonio PorrasAjla AlibalicCristóbal RichartTeresa AuguetPublished in: Metabolites (2023)
Nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic hepatic disease. Although mostly benign, this disease can evolve into nonalcoholic steatohepatitis (NASH). The stimulator of interferon genes (STING) plays an important role in the immune response against stressed cells, but this protein may also be involved in liver lipogenesis and microbiota composition. In this study, the role of STING in NAFLD was evaluated by RT-qPCR to analyze STING mRNA abundance and by immunohistochemical analysis to evaluate protein expression in liver biopsies from a cohort composed of 69 women with morbid obesity classified according to their liver involvement (normal liver, n = 27; simple steatosis (SS), n = 26; NASH, n = 16). The results showed that STING mRNA expression in the liver increases with the occurrence of NAFLD, specifically in the SS stage in which the degree of steatosis is mild or moderate. Protein analysis corroborated these results. Positive correlations were observed among hepatic STING mRNA abundance and gamma-glutamyl transferase and alkaline phosphatase levels, hepatic Toll-like receptor 9 expression and some circulating microbiota-derived bile acids. In conclusion, STING may be involved in the outcome and progression of NAFLD and may be related to hepatic lipid metabolism. However, further studies are needed to confirm these findings.
Keyphrases
- toll like receptor
- insulin resistance
- immune response
- high fat diet induced
- poor prognosis
- bariatric surgery
- metabolic syndrome
- binding protein
- type diabetes
- weight loss
- induced apoptosis
- weight gain
- genome wide
- physical activity
- wastewater treatment
- adipose tissue
- body mass index
- cell cycle arrest
- obese patients
- antibiotic resistance genes
- cell death
- endoplasmic reticulum stress