Exposure to alcohol interrupts adipose cell maturation, attenuates adiponectin expression, and contributes to inflammatory markers in 3T3-F442 pre-adipocytes
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Abstract
Drinking alcohol during pregnancy interrupts cellular development, which may have far-reaching health effects on the fetus in its embryonic state and later as a young child. Adipose tissue (AT) is an important target for alcohol action. Alcohol disrupts the synthesis of a wide variety of peptides and adipokines, as well as the endocrine activity of adipose tissue. Adiponectin is an anti-inflammatory and insulin-sensitizing adipokine that is involved in fatty acid breakdown; it is produced in adipose tissue. In this project, it is hypothesized that alcohol disrupts adipose cell development and reduces adiponectin (ApN) expression, concomitant with an elevation of pro-inflammatory cytokines and reduction in anti-inflammatory cytokines. The data suggest that alcohol exposure in 3T3-F442 pre-adipocytes reduces adipocyte proliferation. Pre-adipocytes were exposed to 0.0% (control), 0.25%, 0.5%, 1%, 1.5%, 2%, and 2.5% alcohol solution for 48 hours. Triglycerides and the expression of ApN and several pro- and anti-inflammatory cytokines were measured. Nile Red (NR) staining was used for the detection of adipogenesis and adipocyte differentiation. The results show triglyceride reduction in 3T3-F442 adipocytes and a significant reduction in adipocyte differentiation in comparison with control (non-alcohol-treated) cells. Furthermore, ApN secretion was reduced in 3T3-F442 cells in response to alcohol. The pro-inflammatory cytokines, IL-6, IL-13, IL-1b, TNF-α, and INF-γ were increased, whereas the anti-inflammatory cytokines, including IL-4 and IL-10, IL-12, were reduced. In conclusion, exposure of alcohol reduced differentiation of 3T3-F442 pre-adipocytes to adipocytes. It was demonstrated in this project that alcohol impairs ApN secretion and increases pro-inflammatory cytokines. The results help to establish the potential role of alcohol in promoting inflammation and reducing adiponectin expression in developing pre-adipocytes, suggesting alcohol may be disruptive in metabolism by disruption of adipose cell differentiation.