312
insulin resistance and maintain everyday glucose tolerance. However, if β-cellular
dysfunction happens because of genetic causes, environmental perturbations, or
both, then the individual is greater at risk of developing impaired glucose tolerance,
excessive fasting glucose stages, and ultimately types 2 diabetes.
Environmental Contributions to Obesity, T2DM,
and Dyslipidemia
The mark changes in diet and lifestyle that includes consumption of high energy
diet, increase in dietary intake, and decrease in physical activity are secondarily
linked to the global epidemic of obesity, T2DM, and MetS. Moreover, it is obvious
that the possibility of these diseases is not that simple. Certainly, various environmental factors play role in the occurrence of metabolic diseases such as childhood
antibiotics, lack of sleep, adenoviruses and stress [108–110], and exposure to environmental chemicals [111]. Although all the environmental factors play a role in the
epidemic of metabolic diseases we have focused on EDCs (PFASs). Indeed, the
current increase in metabolic diseases associates with considerable rises in environmental chemical production and exposures over the past four eras [112–114].
PAFSs Association with Obesity
Rising evidence suggests that raised BMI is not associated only with a diet rich in
calories and sedentary lifestyle, but also coupled with extensive environmental
exposure to “obesogens,” such as perfluoroalkyl substances (PFASs) [115]. PFASs
are extensively used in various products due to their high chemical and thermal
stability [116]. A variety of animal studies has suggested that exposure to PFASs
can impair lipids and carbohydrates homeostasis, change in the composition of fatty
acid, and alter adipocyte differentiation [117], although results have been conflicting [118]. Similarly, findings of human epidemiological are various. A number of
epidemiological investigations reported links between high level of PFOS or PFOA
in maternal serum and enhanced BMI of offspring, the possibility of being obese,
and low level of serum leptin levels in kids or adults [119]. Particularly, females are
more pronounced to these effects [120]. Comparatively, other researchers have not
found any association between adiposity and PFASs exposure [121]. PFASs show
some endocrine-disrupting properties as they halt the metabolism of fatty acids,
promote adipogenesis, change lipid homeostasis, and disturb energy balance
through different pathways [122], together with peroxisome proliferator-activated
receptors α/γ (PPAR-α/γ) activation [123], homeostatic disruption of thyroid hormones [124], and changes in level of estrogen and androgen [125]. Moreover,
branched isomers of PFASs can more efficiently cross the placenta as compared to
S. G. Niazi et al.
insulin resistance and maintain everyday glucose tolerance. However, if β-cellular
dysfunction happens because of genetic causes, environmental perturbations, or
both, then the individual is greater at risk of developing impaired glucose tolerance,
excessive fasting glucose stages, and ultimately types 2 diabetes.
Environmental Contributions to Obesity, T2DM,
and Dyslipidemia
The mark changes in diet and lifestyle that includes consumption of high energy
diet, increase in dietary intake, and decrease in physical activity are secondarily
linked to the global epidemic of obesity, T2DM, and MetS. Moreover, it is obvious
that the possibility of these diseases is not that simple. Certainly, various environmental factors play role in the occurrence of metabolic diseases such as childhood
antibiotics, lack of sleep, adenoviruses and stress [108–110], and exposure to environmental chemicals [111]. Although all the environmental factors play a role in the
epidemic of metabolic diseases we have focused on EDCs (PFASs). Indeed, the
current increase in metabolic diseases associates with considerable rises in environmental chemical production and exposures over the past four eras [112–114].
PAFSs Association with Obesity
Rising evidence suggests that raised BMI is not associated only with a diet rich in
calories and sedentary lifestyle, but also coupled with extensive environmental
exposure to “obesogens,” such as perfluoroalkyl substances (PFASs) [115]. PFASs
are extensively used in various products due to their high chemical and thermal
stability [116]. A variety of animal studies has suggested that exposure to PFASs
can impair lipids and carbohydrates homeostasis, change in the composition of fatty
acid, and alter adipocyte differentiation [117], although results have been conflicting [118]. Similarly, findings of human epidemiological are various. A number of
epidemiological investigations reported links between high level of PFOS or PFOA
in maternal serum and enhanced BMI of offspring, the possibility of being obese,
and low level of serum leptin levels in kids or adults [119]. Particularly, females are
more pronounced to these effects [120]. Comparatively, other researchers have not
found any association between adiposity and PFASs exposure [121]. PFASs show
some endocrine-disrupting properties as they halt the metabolism of fatty acids,
promote adipogenesis, change lipid homeostasis, and disturb energy balance
through different pathways [122], together with peroxisome proliferator-activated
receptors α/γ (PPAR-α/γ) activation [123], homeostatic disruption of thyroid hormones [124], and changes in level of estrogen and androgen [125]. Moreover,
branched isomers of PFASs can more efficiently cross the placenta as compared to
S. G. Niazi et al.