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Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

The endocrine disruptor 4-nonylphenol promotes adipocyte differentiation and induces obesity in mice.


PMID 22739433

Abstract

The environmental obesogen hypothesis proposes that exposure to endocrine disruptors during developmental "window" contributes to adipogenesis and the development of obesity. Implication of environmental endocrine disruptor such as 4Nonylphenol (4-NP) on adipose tissue development has been poorly investigated. 3T3-L1 preadipocytes were incubated with different doses of 4-NP. Six-week-old C57BL/6J male mice received an intraperitoneal injection of vehicle, troglitazone or 4-NP (0.5 mg/kg). Gene expression of adipogenic regulators was analyzed. Pregnant mice were dosed by gavage with vehicle or 4-NP (0.05, 0.25 or 0.5 mg/kg) from day 12 of gestation until day 7 of lactation. The body weight, liver weight, fat mass, and serum lipids and glucose levels were measured in offspring at postnatal day 60. Low concentration of 4-NP induced adipocyte differentiation, glycerol-3-phosphate dehydrogenase activity, and expression of peroxisome proliferator-acivated receptor γ as well as its target genes required for adipogenesis. 4-NP perturbed key regulators of adipogenesis and lipogenic pathway in vivo. Perinatal exposure to 4-NP increased body weight, fat mass, and serum total cholesterol and glucose levels in offspring. 4-NP may be expected to increase the incidence of obesity and can act as a potential chemical stressor for obesity and obesity-related disorders.

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