Obesogen
Obesogens are certain chemical compounds that are hypothesised to disrupt normal development and balance of lipid metabolism, which in some cases, can lead to obesity.
The three main mechanisms of action include Obesogenic drugs and chemicals have been shown to target transcription regulators found in gene networks that function to control intracellular lipid homeostasis and proliferation and differentiation on adipocytes.
[6][7] The PPARα receptor, when complexed with RXR and activated by the binding of a lipid, promotes peroxisome proliferation leading to increased fatty acid β-oxidation.
However, in the case of obesogens that target the PPARα/RXR complex, which when stimulated reduces adipose mass and body weight, there are a few explanations as to how they promote obesity.
[11][12] A second explanation points to specific PPARα targeters that have been shown to additionally cause abnormal transcriptional regulation of testicular steroidogenesis when introduced during fetal development.
In this case, the developing brain makes what will become permanent changes to the body's metabolic control, leading to long-term upregulation of lipid storage and maintenance.
[22] While hormone receptors tend to be the most obvious candidates for targets of obesogens, central mechanisms that balance and regulate the body's nutritional changes on a day-to-day basis as a whole cannot be overlooked.
The HPA axis (hypothalamic-pituitary-adrenal) is involved in controlling appetite and energy homeostasis circuits which are mediated by a large number of monoaminoergic, peptidergic (use of hormones as neurotransmitters), and endocannabinoid signals that come from the digestive tract, adipose tissues, and from within the brain.
These findings give evidence to conclude that an increase in lipid accumulation can result from the targeting of neurotransmitter receptors by foreign chemicals.
[6][7] Some xenoestrogens such as BPA, nonylphenol, and DEHP have all shown to act is this way, altering NPY expression and significantly shifting the feeding behaviors of exposed mice.
TMT works in a similar but unique way, inducing NPY and NPY2 receptor expression initially which later is counteracted by neuronal degeneration in lesions causing decrease in signaling ability.
It is these high levels that have been found to be closely associated with increased fat stores linking the lipid activator mimics to the actual disease.
[30] [better source needed] A particular study on polybrominated diphenyl ethers (PBDE), a commonly used chemical in flame retardants, made its role in altering the functions of the thyroid hormone axis apparent.
[31][32] This finding leads to increased concern as neonatal thyroid status plays a large role in the integration of maternal environmental signals during development in the womb that is used for long-term body weight programming.
These drugs act as agonists of the PPAR-γ receptor leading to insulin sensitizing effects that can improve glycemic control and serum triglyceride levels.
[34][35] Diethylstilbestrol (DES) is a synthetic estrogen that was once prescribed to women to decrease the risk of miscarriage until it was found to be causing abnormalities in exposed offspring.
Particular members of the organotin class of persistent organic pollutants (POPs), namely tributyltin (TBT) and triphenyltin (TPT) are highly selective and act as very potent agonists of both the retinoid X receptors (RXR α,β, and γ) and PPARγ.
Organotins (tin-based chemicals), used in marine anti-fouling paints, wood catalysts, plasticizers, slimicides, in industrial water systems, and fungicides on food have recently been linked to obesogenic properties when introduced in the body.
[6][7] Phthalates and PFCs in particular have been found to function as agonists for one or more of the PPARs [46] Additionally, metabolites of DHEP such as MEHP also activate PPARγ leading to a proadipogenic response.
[11][12] Although research on endocrine disruptors or "obesogens" is still emerging, the public health implications so far have mainly surrounded obesity, diabetes, and cardiovascular disease.
They are an unnecessary and mostly preventable potential hazard to health,[medical citation needed] which can have a large impact on how individuals gain and lose weight.
It is used in products such as toys, medical devices, plastic food and beverage containers, shower curtains, dental sealants and compounds, and register receipts.
Certain researchers suggest that BPA actually decreases the fat cell count in the body, but at the same time increasing the size of the ones remaining; therefore, no difference in weight is shown, and an individual is even likely to gain more.
[59] Most of the environmental obesogens currently identified are either classified into the category of chemical mimics of metabolic hormones throughout the body or of neurotransmitters within the brain.
Because they fall into these two categories, extensive opportunities for complex interactions and varied sites of action as well as multiple molecular targets are open for consideration.
[6][7] Because the mechanisms behind the different effects of obesogens are so complex and not well understood, the extent to which they play in the current obesity epidemic may be greater than once thought.
Research will be required in order to gain a better understanding of the mechanism of action these chemicals are involved in before the extent of the risk of exposure can be determined and methods of prevention and removal from the environment can be established.
A few ways individuals can proactively reverse the effects would be regularly exercising, maintaining a healthy diet, ensuring quality sleep, and managing stress levels.
