Obesogens in Foods

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.

Genetics, epigenetics and transgenerational transmission of obesity in children

“…The endocrine disrupting effects of obesogens may directly or indirectly promote adipogenesis and obesity/obesity related metabolic conditions that drive metabolic syndrome through disturbance of several processes. Studies show that these effects are seen not only in individuals but also in their offspring because of their ability to epigenetically reprogram genetically inherited set points for the control of body weight and body composition at some critical stages of development, such as fetus, early life, and puberty ( 169 , 170 ).…”

Application of In Vitro Models for Studying the Mechanisms Underlying the Obesogenic Action of Endocrine-Disrupting Chemicals (EDCs) as Food Contaminants—A Review

“…Over the past decade, there is considerable evidence that a substantial increase in environmental chemical production may contribute to the rapid increase in human obesity and metabolic syndrome [ 7 , 8 ]. Especially, environmentally existing xenobiotic chemicals, such as endocrine-disrupting chemicals (EDCs) are the main candidates [ 4 , 9 , 10 , 11 , 12 , 13 ]. EDCs are a class of natural or synthetic exogenous chemical substances that may interfere with the function of the endocrine system by mimicking or blocking hormone biosynthesis, metabolism or action [ 4 , 7 , 9 , 10 , 13 ].…”

“…Especially, environmentally existing xenobiotic chemicals, such as endocrine-disrupting chemicals (EDCs) are the main candidates [ 4 , 9 , 10 , 11 , 12 , 13 ]. EDCs are a class of natural or synthetic exogenous chemical substances that may interfere with the function of the endocrine system by mimicking or blocking hormone biosynthesis, metabolism or action [ 4 , 7 , 9 , 10 , 13 ]. Their adverse effects on estrogen, androgen, and thyroid hormone signaling have been well documented [ 14 , 15 , 16 , 17 ].…”

“…(10 nM) proteins related to oxidative stress level of CAT ↓ (10 nM, 100 nM), SOD1 ↓ (10 µM), SOD2 ↓ (10 nM, 100 nM, 1 µM, 10 µM) cellular ROS level ↓ (10 nM, 100 nM, 1 µM, 10 µM) insulin sensitivity, pAKT/AKT ratio ↓ (1 µM) BPB lipid accumulation ↓ (10 nM, 100 nM, 1 µM, 10 µM) binding to PPARγ ↑ (50 µM) PPARγ activity (−) (10 nM, 100 nM, 1 µM, 10 µM) protein level of FABP4, GPD1, LPL, APOE, ADIPOQ ↓ (10 nM, 100 nM, 1 µM, 10 µM) protein level of PNPLA2 ↑ (10 nM), CD36 ↑ (10 nM, 10 µM) release of adiponectin ↓, MCP1 ↑, leptin ↓ (1 µM) proteins related to oxidative stress level of CAT ↓ (10 nM, 100 nM, 1 µM, 10 µM), SOD1 ↓ (10 nM, 100 nM, 1 µM, 10 µM), SOD2 ↓ (10 nM, 100 nM, 1 µM) cellular ROS level ↓ (10 nM, 100 nM, 1 µM, 10 µM) insulin sensitivity, pAKT/AKT ratio ↓ (1 µM) 10 nM, nM, 1 µM, µM, 50 µM Schaffert et al [8] BPF lipid accumulation ↓ (10 nM, 100 nM, 1 µM, 10 µM) binding to PPARγ ↑ (50 µM) PPARγ activity (−) (10 nM, 100 nM, 1 µM, 10 µM) protein level of FABP4, GPD1, LPL, APOE ↓ (10 nM, 100 nM, 1 µM, 10 µM) protein level of LIPE ↑ (1 µM, 10 µM), PNPLA2 ↑ (10 µM), CD36 ↑ (10 nM, 100 nM, 1 µM, 10 µM), ADIPOQ ↑ (10 nM, 10 µM) release of adiponectin ↓ (1 µM), MCP1 ↑ (1 µM), leptin ↑ (10 nM, 1 µM) proteins related to oxidative stress level of CAT ↓ (10 nM, 100 nM, 1 µM, 10 µM), SOD1 ↓ (10 nM, 100 nM, 10 µM), SOD2 ↓ (100 nM, 1 µM, 10 µM) cellular ROS level ↓ (10 nM, 100 nM, 1 µM, 10 µM)…”

Report of the Scientific Committee of the Spanish Agency for Food Safety and Nutrition (AESAN) on the available evidence in relation to the potential obesogenic activity of certain chemical compounds that may be present in foods

“…Obesogens have diverse mechanisms of action and they can act by activating or antagonising the action of nuclear hormone receptors that directly regulate the expression of genes involved in the differentiation of adipocytes, body weight and metabolism, such as oestrogen receptors (ER), androgen and thyroid hormone, and the peroxisome proliferator-activated receptor-γ (PPARγ), among others. They can also act in the regulation of different immune-neuroendocrine metabolic pathways, which can lead to pathophysiological consequences in adipogenesis, lipogenesis, lipolysis, immunity, in the influence on the central regulations of appetite and energy expenditure, and changes in the intestinal microbiota, among other processes (Janesick et al, 2014) (Shahnazaryan et al, 2019) (Kladnicka et al, 2022).…”