Endocrine Disrupting Chemicals, Obesogens, and the Obesity Epidemic
Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss in Nutrition and Cardiometabolic Health, 2017
The “obesogen hypothesis” introduces another level of complexity to the developmental origins of obesity. There is a growing body of research showing that exposure to obesogens during critical windows of development such as in utero development and during lactation lead to obesity later in life (Heindel, Newbold, and Schug 2015).
Mechanism of phthalate esters in the progression and development of breast cancer
Published in Drug and Chemical Toxicology, 2022
Mohd Mughees, Himanshu Chugh, Saima Wajid
Phthalate esters have a profound effect on liver. They cause increase in activity of peroxisome and elevate beta-oxidation of fatty acids with increased level of LDL and decreased levels of HDL. Increased beta-oxidation of fatty acids leads to production of Hydrogen peroxide in peroxisome and decreased activity of catalase (Ganning et al.1984). GU et al in their studies have proved that DEHP is obesogen. They found that mice when treated with DEHP showed increased expression of T-box 15 (Tbx15) and Glypican 4 (Gpc-4) gene. Both the genes are associated with obesity and fat distribution. They also found increased level of serum leptin, insulin, serum total triglycerides, total cholesterol and fasting glucose levels, in mice treated with DEHP (Gu et al.2016). All these findings by Agneta and Gu et al. can be correlated with findings of Badid et al where they have proved that breast cancer patients have high levels of triglycerides, LDL, cholestrol and leptin (Badid et al.2010).
Cadmium: a new risk factor for endometrial cancer?
Published in Expert Review of Anticancer Therapy, 2019
Jane A. McElroy, Mark I. Hunter
The third factor in this trifecta is cadmium exposure. This factor is less definitive. The amount of cadmium found in biospecimens in the general population occurs primarily through smoking and dietary choices. Epidemiologic data on cadmium associated with obesity is suggestive, though inconclusive. These mixed results may be partly explained by both the biomarker used to determine concentration (i.e. blood, urine, hair, nails) as well as differences in the categorization of exposure levels. However, laboratory studies have implicated cadmium in adipose tissue dysfunction, promoting insulin resistance without obesity [23]. With the development of the field of epigenetics, attention has been given to classifying epigenetic alterations associated with this metal. Epigenetics is defined by inherited phenotype changes that are not involved in DNA sequence changes. DNA methylation, histones covalent modifications, chromatin structure, and non-coding RNAs and networking with each other are the elements involved in epigenetic changes [24]. From an epigenetic perspective, Park and colleagues suggest cadmium exposure during development may influence dysregulation of appetite and satiety responses with consequential increased caloric intake in offspring [25]. In the Newborn Epigenetics Study, reported maternal cadmium increased risk of juvenile obesity thereby acting as an obesogen [26].
Related Knowledge Centers
- Appetite
- Chemical Compound
- Nuclear Receptor
- Obesity
- Satiety
- Metabolism
- Lipid
- Adipose Tissue
- Development of The Human Body
- Sex Hormone