Further documentation is available here. There are many ways in which obesogenic the anti estrogenic diet pdf and chemicals can disrupt the body’s adipose tissue biology.
These hormone receptors sense a variety of metabolic ligands including lipophilic hormones, dietary fatty acids and their metabolites, and, depending on the varying levels of these ligands, control transcription of genes involved in balancing the changes in lipid balance in the body. The RXR receptor itself is the second major target of obesogens next to the PPAR receptors. PPARα, typically act to reduce overall serum concentrations of lipids. In contrast, the PPARγ receptor, when complexed with RXR and activated by the binding of fatty acids or their derivatives, promotes lipid biosynthesis and storage of lipids is favored over fatty acid oxidation. RXR complex typically act to increase overall serum concentrations of lipids. RXR complex mimic the metabolic ligands and activate the receptor leading to upregulation of lipid accumulation which explains their obesogenic effects. RXR complex, which when stimulated reduces adipose mass and body weight, there are a few explanations as to how they promote obesity.
Therefore, it may be the case that metabolites of PPARα targeting obesogens are also activating PPARγ, providing the single activation event needed to potentially lead to a pro-adipogenic response. Finally, if PPARα activation occurs during critical periods of development, the resulting decrease in lipid concentration in the developing fetus is recognized by the fetal brain as undernourishment. 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. Sex steroids normally play a significant role in lipid balance in the body.
This alteration in sex steroid levels due to obesogens can vary enormously according to both the sex of the exposed individual as well as the timing of the exposure. If the chemicals are introduced at critical windows of development, the vulnerability of an individual to their effects is much higher than if exposure occurs later in adulthood. It has been shown that obesogenic effects are apparent in female mice exposed to both phytoestrogens and DES during their neonatal periods of development, as they, though born with a lower birth weight, almost always developed obesity, high leptin levels, and altered glucose response pathways. Both phytoestrogen and DES exposed male mice did not develop obesity and, rather, showed decreased body weights with increased exposure confirming the role of gender differences in exposure response. Further studies have shown positive correlations for serum BPA levels with obese females in the human population, along with other xenoestrogen compounds suggesting the parallel roles that these effects may be having on humans. 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.
Many neuropharmaceuticals used to alter behavioral pathways in patients with neurological disorders have shown to have metabolic altering side-effects leading to obesogenic phenotypes as well. These findings give evidence to conclude that an increase in lipid accumulation can result from the targeting of neurotransmitter receptors by foreign chemicals. Such an alteration can lead to induced feelings of hunger and decreased feelings of fullness causing an increase in food intake and inability to feel satisfied, both characteristic of obesity. HPA axis to hormones to become abnormal.
NPY2 receptor expression initially which later is counteracted by neuronal degeneration in lesions causing decrease in signaling ability. While an increase in food intake is often the case after exposure, weight gain involves the body’s maintenance of its metabolic setpoint as well. Given this information, it is particularly important to note that exposure during development and initial programming of these setpoints can be extremely significant throughout the remainder of life. Endocannaboid levels are high in those suffering from obesity due to hyperactivity of cannaboid signalling pathways. 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. These responses are adaptive in that they vary according to the individual’s needs, always working to restore the metabolic setpoint through the increase or decrease of metabolic functions depending on varying energy needs.