may also have dysregulation of the afferent signals, central nervous system integration, and efferent signals. Many of these factors are influenced by genetic predispositions in different populations.
The occurrence of obesity and its pathogenesis as described above is influenced by both environmental and genetic components. In previous sections the environmental aspect was discussed, here the genetics behind obesity will be reviewed. Within the genetic component, there are degrees of variability where obesity can be due to a single gene mutation or via complex interactions between several genes. [Bray, UpToDate].
The monogenic polymorphisms that influence obesity can be seen in the Agouti gene, leptin gene, the leptin receptor gene, and others. …show more content…
BPA was introduced in the plastic industry and used as the base compound for the manufacture of polycarbonate plastic and the resin lining of food and beverage cans. BPA is also used an additive in other widely used plastics such as plyvinyl chloride and polyethylene terephthalate. BPA can leach from these polycarbonate containers under heat and either acidic or basic conditions, as these environmental factors accelerate the hydrolysis of the ester bond linking BPA monomers, leading to the release of BPA with the concomitant potential for human exposure. It can also be absorbed through the skin by handling paper receipts and money (Trasande). Though BPA accumulates in adipose tissue, it can also be detected in 93% of urine samples, as well as amniotic fluid, neonatal blood, placenta, cord blood, and human breast milk. According to the Environmental Protection Agency, the lowest adverse effect level for BPA was established at 50 micrograms/kg/d. These effects include alteration of mammary gland development, behavioral effects, abnormalities in the prostate growth, alterations of sexual maturation, altered immune system function, and detrimental effects on glucose homeostasis and insulin sensitivity. Experimental research conducted in animals has shown that exposure to BPA during critical developmental stages can influence lipid and energy balance, promoting adipogenesis (Alonso-Magdalena). Exposure to low doses of BPA during critical periods of development has been shown to increase body weight (obesogenic action), alter glucose homeostasis (diabetogenic action), or both (diabetogenic action). The current theories on the underlying mechanisms of BPA’s obesogenic/diabetogenic effects include BPA’s adverse estrogenic effect and consequent DNA modification; BPA’s adverse effect on the hunger and satiety hormones of adiponectin,
The occurrence of obesity and its pathogenesis as described above is influenced by both environmental and genetic components. In previous sections the environmental aspect was discussed, here the genetics behind obesity will be reviewed. Within the genetic component, there are degrees of variability where obesity can be due to a single gene mutation or via complex interactions between several genes. [Bray, UpToDate].
The monogenic polymorphisms that influence obesity can be seen in the Agouti gene, leptin gene, the leptin receptor gene, and others. …show more content…
BPA was introduced in the plastic industry and used as the base compound for the manufacture of polycarbonate plastic and the resin lining of food and beverage cans. BPA is also used an additive in other widely used plastics such as plyvinyl chloride and polyethylene terephthalate. BPA can leach from these polycarbonate containers under heat and either acidic or basic conditions, as these environmental factors accelerate the hydrolysis of the ester bond linking BPA monomers, leading to the release of BPA with the concomitant potential for human exposure. It can also be absorbed through the skin by handling paper receipts and money (Trasande). Though BPA accumulates in adipose tissue, it can also be detected in 93% of urine samples, as well as amniotic fluid, neonatal blood, placenta, cord blood, and human breast milk. According to the Environmental Protection Agency, the lowest adverse effect level for BPA was established at 50 micrograms/kg/d. These effects include alteration of mammary gland development, behavioral effects, abnormalities in the prostate growth, alterations of sexual maturation, altered immune system function, and detrimental effects on glucose homeostasis and insulin sensitivity. Experimental research conducted in animals has shown that exposure to BPA during critical developmental stages can influence lipid and energy balance, promoting adipogenesis (Alonso-Magdalena). Exposure to low doses of BPA during critical periods of development has been shown to increase body weight (obesogenic action), alter glucose homeostasis (diabetogenic action), or both (diabetogenic action). The current theories on the underlying mechanisms of BPA’s obesogenic/diabetogenic effects include BPA’s adverse estrogenic effect and consequent DNA modification; BPA’s adverse effect on the hunger and satiety hormones of adiponectin,