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Obesogens in Foods

Overview
Journal Biomolecules
Publisher MDPI
Date 2022 May 28
PMID 35625608
Authors
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Abstract

Obesogens, as environmental endocrine-disrupting chemicals, are supposed to have had an impact on the prevalence of rising obesity around the world over the last forty years. These chemicals are probably able to contribute not only to the development of obesity and metabolic disturbances in individuals, but also in their progeny, having the capability to epigenetically reprogram genetically inherited set-up points for body weight and body composition control during critical periods of development, such as fetal, early life, and puberty. In individuals, they may act on myriads of neuro-endocrine-immune metabolic regulatory pathways, leading to pathophysiological consequences in adipogenesis, lipogenesis, lipolysis, immunity, the influencing of central appetite and energy expenditure regulations, changes in gut microbiota-intestine functioning, and many other processes. Evidence-based medical data have recently brought much more convincing data about associations of particular chemicals and the probability of the raised risk of developing obesity. Foods are the main source of obesogens. Some obesogens occur naturally in food, but most are environmental chemicals, entering food as a foreign substance, whether in the form of contaminants or additives, and they are used in a large amount in highly processed food. This review article contributes to a better overview of obesogens, their occurrence in foods, and their impact on the human organism.

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References
1.
Li Z, Yu Z, Gao P, Yin D . Multigenerational effects of perfluorooctanoic acid on lipid metabolism of Caenorhabditis elegans and its potential mechanism. Sci Total Environ. 2019; 703:134762. DOI: 10.1016/j.scitotenv.2019.134762. View

2.
Hines E, White S, Stanko J, Gibbs-Flournoy E, Lau C, Fenton S . Phenotypic dichotomy following developmental exposure to perfluorooctanoic acid (PFOA) in female CD-1 mice: Low doses induce elevated serum leptin and insulin, and overweight in mid-life. Mol Cell Endocrinol. 2009; 304(1-2):97-105. DOI: 10.1016/j.mce.2009.02.021. View

3.
Foulds C, Trevino L, York B, Walker C . Endocrine-disrupting chemicals and fatty liver disease. Nat Rev Endocrinol. 2017; 13(8):445-457. PMC: 5657429. DOI: 10.1038/nrendo.2017.42. View

4.
Marti-Cid R, Llobet J, Castell V, Domingo J . Human exposure to polychlorinated naphthalenes and polychlorinated diphenyl ethers from foods in Catalonia, Spain: temporal trend. Environ Sci Technol. 2008; 42(11):4195-201. DOI: 10.1021/es800064p. View

5.
Jackson E, Shoemaker R, Larian N, Cassis L . Adipose Tissue as a Site of Toxin Accumulation. Compr Physiol. 2017; 7(4):1085-1135. PMC: 6101675. DOI: 10.1002/cphy.c160038. View