Abstract
Adipocyte differentiation is regulated by intracellular reactive oxygen species (ROS) generation and mitochondrial fission and fusion processes. However, the correlation between intracellular ROS generation and mitochondrial remodeling during adipocyte differentiation is still unknown. Here, we investigated the effect on adipocyte differentiation of 3T3-L1 cells of intracellular ROS inhibition using N-acetyl cysteine (Nac) and Mito-TEMPO and of mitochondrial fission inhibition using Mdivi-1. Differentiated 3T3-L1 adipocytes displayed an increase in mitochondrial fission, ROS generation, and the expression of adipogenic and mitochondrial dynamics-related proteins. ROS scavenger (Nac or Mito-TEMPO) treatment inhibited ROS production, lipid accumulation, the expression of adipogenic and mitochondrial dynamics-related proteins, and mitochondrial fission during adipogenesis of 3T3-L1 cells. On the other hand, treatment with the mitochondrial fission inhibitor Mdivi-1 inhibited mitochondrial fission but did not inhibit ROS production, lipid accumulation, or the expression of adipogenic and mitochondrial dynamics-related proteins, with the exception of phosphorylated Drp1 (Ser616), in differentiated 3T3-L1 adipocytes. The inhibition of mitochondrial fission did not affect adipocyte differentiation, while intracellular ROS production decreased in parallel with inhibition of adipocyte differentiation. Therefore, our results indicated that ROS are an essential regulator of adipocyte differentiation in 3T3-L1 cells.
Highlights
Obesity increases the number and size of adipocyte cells [1, 2]
Expression of adipogenic, mitochondrial dynamics, and antioxidant gene proteins induced during adipocyte differentiation
We investigated the altered expression of adipogenic, mitochondrial dynamics, and antioxidant genes during adipocyte differentiation
Summary
Obesity increases the number (hyperplasia) and size (hypertrophy) of adipocyte cells [1, 2]. It can lead to many health problems, such as type 2 diabetes, insulin resistance, coronary heart disease, and cancer [3]. Adipocytes are responsible for lipid uptake, synthesis, and storage in the form of triglyceride (TG). Abnormal accumulation of stored TG in adipocytes causes. Inhibition of insulin-stimulated lipid accumulation by ROS scavengers but not by a Drp inhibitor no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
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