Archive for the ‘Obesity’ Category

Weight gain associated with chronic exposure to chlorpyrifos in rats.

Wednesday, January 28th, 2009

J Med Toxicol. 2007 Sep;3(3):89-93

Weight gain associated with chronic exposure to chlorpyrifos in rats.
Meggs WJ, Brewer KL.

Department of Emergency Medicine, Brody School of Medicine at East Carolina University, Greenville, NC 27858, USA. meggsw@ecu.edu

OBJECTIVE: This work exposed rats to low levels of the organophosphate insecticide chlorpyrifos and monitored for toxic effects, including weight gain. METHODS: Rats received either a subcutaneous injection of chlorpyrifos, 5 mg/kg/day, or an equal volume of vehicle daily for 4 months. Subjects were observed for 30 minutes after injection for signs of acute toxicity. Body weights were recorded at baseline, 2 months, 3 months, and 4 months. At the end of the experiment, the weights of hearts, medial lobe of the livers, peri-nephric fat pads, and gastrocnemius muscles were recorded. Effects of chlorpyrifos on adipocyte differentiation in culture were studied. Results were compared using RMANOVA. RESULTS: No signs of acute cholinergic toxicity were observed after injections in any subject. Rats in the 5 mg/kg group were significantly heavier than those in the control group by 2 months (335.7 +/- 16.7 g vs. 318.6 +/- 15.8 g; p = 0.034). This difference increased at 3 months (350.1 +/- 16.4 g vs. 322.3 +/- 21.3 g p = 0.006) and 4 months (374.4 +/- 22.2 g vs. 340.2 +/- 25.2 g p = 0.006). At 4 months, the weights of the perinephric fat pads were significantly increased in the chlorpyrifos group relative to controls (2.867 + 0.516 vs. 1.130 + 0.171, p = 0.0039). The two groups showed no weight differences between hearts, livers, and gastrocnemius muscles. Chlorpyrifos did not affect adipocyte differentiation in tissue culture. CONCLUSIONS: Chronic exposure to chlorpyrifos at 5 mg/kg/day caused an increase in rat body weight when compared to controls. This increase was in adipose tissue. Chlorpyrifos did not induce differentiation of adipocytes in culture.

PMID: 18072142 [PubMed - indexed for MEDLINE]

Effects of endocrine disruptors on obesity

Wednesday, January 28th, 2009

http://www.ncbi.nlm.nih.gov/pubmed/18315718?dopt=AbstractPlus

Int J Androl. 2008 Apr;31(2):201-8.

Effects of endocrine disruptors on obesity

Newbold RR, Padilla-Banks E, Jefferson WN, Heindel JJ.

Developmental Endocrinology and Endocrine Disruptor Section, Laboratory of Molecular Toxicology, Division of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. newbold1@niehs.nih.gov

Environmental chemicals with hormone-like activity can disrupt the programming of endocrine signalling pathways that are established during perinatal life and result in adverse consequences that may not be apparent until much later in life. Increasing evidence implicates developmental exposure to environmental hormone mimics with a growing list of adverse health consequences in both males and females. Most recently, obesity has been proposed to be yet another adverse health effect of exposure to endocrine disrupting chemicals (EDCs) during critical stages of development. Obesity is quickly becoming a significant human health crisis because it is reaching epidemic proportions worldwide, and is associated with chronic illnesses such as diabetes and cardiovascular disease. In this review, we summarize the literature reporting an association of EDCs and the development of obesity, and further describe an animal model of exposure to diethylstilbestrol that has proven useful in studying mechanisms involved in abnormal programming of various oestrogen target tissues during differentiation. Together, these data suggest new targets (i.e. adipocyte differentiation and mechanisms involved in weight homeostasis) of abnormal programming by EDCs, and provide evidence that support the scientific term ‘the developmental origins of adult disease’. The emerging idea of an association of EDCs and obesity expands the focus on obesity from intervention and treatment to include prevention and avoidance of these chemical modifiers.
PMID: 18315718 [PubMed - in process]