Iron deficiency attenuates catecholamine‑stimulated lipolysis via downregulation of lipolysis‑related proteins and glucose utilization in 3T3‑L1 adipocytes
- Kazuhiko Higashida
- Nodoka Takeuchi
- Sachika Inoue
- Takeshi Hashimoto
- Naoya Nakai
Affiliations: Department of Nutrition, Laboratory of Exercise Nutrition, University of Shiga Prefecture, Hikone, Shiga 522‑8533, Japan, Faculty of Sport and Health Science, Ritsumeikan University, Kusatsu, Shiga 525‑8577, Japan
- Published online on: January 13, 2020 https://doi.org/10.3892/mmr.2020.10929
Copyright: © Higashida
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Iron deficiency has been associated with obesity and related metabolic disorders. The aim of the present study was to evaluate the effect of iron deficiency on fat metabolism, particularly regarding the lipolytic activity, lipolysis‑related protein expression, and glucose utilization of adipocytes. Differentiated 3T3‑L1 adipocytes were incubated with an iron chelator, deferoxamine mesylate (DFO), for 48 h. Subsequently, basal and isoproterenol‑stimulated lipolytic activities, the proteins involved in lipolysis and glucose utilization were compared with a control (CON). The results revealed that treatment with DFO significantly decreased the free iron content but did not affect total protein and lipid contents in adipocytes. Iron deprivation caused a significant reduction in isoproterenol‑stimulated lipolysis, but not basal lipolysis. Lipolysis‑related proteins, including perilipin A, adipose triglyceride lipase, hormone sensitive lipase and comparative gene identification‑58, were decreased in the DFO compared with the CON group. Furthermore, glucose utilization, a major precursor of 3‑glycerol phosphate for micro‑lipid droplet synthesis during lipolysis and the expression of glucose transporter (GLUT) 4 were significantly lower in the DFO group when compared with the CON group. However, hypoxia‑inducible factor‑1α and GLUT1 expressions were upregulated in DFO‑treated adipocytes. In conclusion, the results indicated that low iron availability attenuated catecholamine‑stimulated lipolysis by downregulating lipolytic enzymes and glucose utilization in 3T3‑L1 adipocytes.