Abstract
In the member countries of the Organization for Economic Co-operation and Development (OECD), overweight and obesity affect the majority of the population. The use of environmental chemicals, such as the plasticizer DEHP, has largely increased simultaneously with this development. DEHP is an "obesogen" that interferes with normal adipocyte differentiation and energy homeostasis. Obesity in turn is accompanied by chronic low-grade adipose tissue inflammation, leading to metabolic disorders such as type II diabetes. The main actors in adipose tissue inflammation are adipocytes and macrophages. However, the impact of DEHP on adipose tissue inflammation and the crosstalk between adipocytes and macrophages are unknown and the subjects of the current study. The influence of DEHP on inflammation was investigated in human Simpson–Golabi–Behmel syndrome (SGBS)-derived adipocytes and human THP-1 macrophages. The proinflammatory markers IL8, MCP1, IL1β, TNFα and others were measured (qRT-PCR, ELISA) in SGBS-derived adipocytes treated with DEHP [day 0 (d0)–d4; 50 µg/ml] and THP-1 macrophages cultured with conditioned medium (CM) from DEHP-treated adipocytes (SGBS-CM) (from d4 and d8). DEHP exposure led to a proinflammatory state in SGBS-derived adipocytes (e.g., increased secretion of IL8 and MCP1). Surprisingly, exposure of THP-1 macrophages to SGBS-CM did not show DEHP-induced effects. However, we demonstrated that medium containing (pre)adipocyte-secreted factors had a significant impact on the expression and secretion of macrophage and inflammatory markers in THP-1 macrophages in general and led to the significantly increased accumulation of intracellular lipid droplets.
Highlights
Obesity and its comorbidities, such as type 2 diabetes, are symptoms of metabolic syndrome, a clinical condition that has become a major health issue in developed countries
We aimed to investigate whether DEHP alters the expression of inflammatory markers such as IL8 and MCP1 in adipocytes and whether conditioned medium (CM) from these adipocytes would influence the expression of macrophage and inflammatory markers in THP-1 macrophages
Exposure of Simpson–Golabi–Behmel syndrome (SGBS)-derived cells to DEHP during adipogenic induction from day 0 (d0) to d4 led to an eightfold increase in secreted IL8 and a 1.6-fold increase in MCP1 at d8, supporting the hypothesis that DEHP exposure had a proinflammatory effect on differentiating SGBS-derived cells (Fig. 1)
Summary
Obesity and its comorbidities, such as type 2 diabetes, are symptoms of metabolic syndrome, a clinical condition that has become a major health issue in developed countries. According to the World Health Organization (WHO), most of the world’s population lives in countries where overweight and obesity kill more people than underweight The reasons for this development are the increased intake of energy-dense foods and a decrease in physical activity due to fundamental changes in forms of work and changing modes of t ransportation[2]. Over the last 2–3 decades, the prevalence of obesity and diseases of metabolic syndrome and environmental pollution with so-called endocrine disruptors such as di-(2-ethylhexyl)-phthalate (DEHP), TBT, BPA and others have increased 3 These endocrine-disrupting chemicals are suspected to act as obesogens on the basis of the Developmental Origins of Health and Disease hypothesis[4,5,6]. To the best of our knowledge, this is the first study to investigate the correlation between DEHP exposure and human adipocyte inflammation as well as the crosstalk between DEHP-treated differentiating human adipocytes and THP-1 macrophages in vitro
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