166
different MRC complexes, which could take part in mitochondrial ROS production
[39–41]. However, TCDD caused excessive mitochondrial ROS production appears
to be the factor that activates AhR [42]. It also promotes liver fibrosis development
in high fat diet obese mice [43].
Obesity
Chronic exposure to PCBs causes obesity; the possible effects are endocrine disruptors on body weight. The exposure of PCBs also causes obesity in children [44].
PCBs act by altering the AhR expression of principal genes correlated to adipogenesis, lipid metabolism, and inflammatory factors [45]. Leptin Receptor (LEPR),
Ras-Related Associated with Diabetes (RRAD), Aryl hydrocarbon receptor nuclear
translocator (ARNT), and Paraoxonase 1 (PON1) are the most common receptor
and genes that plays significant role in the obesity. Abnormality of these receptors
is observed among highly exposed subjects [46]. PCBs readily cross the placental
barrier. It can harm developing neonates. Prenatal exposure of the PCBs can also
cause obesity in children [5, 47]. Prenatal exposure of certain PCBs can be the reason of smaller size at birth [48]. Early exposure of PCBs in pregnant women can be
a predisposing factor for the development of obesity in future [49].
Diabetes Mellitus
PCBs have the potential to directly alter glucose homeostasis and cause diabetes
[50]. In the US, it is observed that PCBs exposure is linked with an escalation in
β-cell function, resulting in hyperinsulinemia and insulin resistance [51]. Beta-cells
of the pancreas lack the antioxidant potential. This oxidant stress mediates the reactive oxygen and nitrogen species that ruin their function by modifying metabolism
and/or ATP sensitive potassium channel activity while inducing apoptosis [52].
Chronic exposure to the PCBs causes insulin resistance and hyperinsulinemia leading to diabetes mellitus [53]. Increased serum concentrations can lead to type II
diabetes [54]. The exposure of PCBs in the elderly age increased the likelihood of
diabetes [55].
TCDD reduces glucose-stimulation and insulin release in animal models, similar
effects were observe in AhR knock-out mice [56]. TCDD exposed rats had depleted
islets of langerhans [57], similarly the depletion of islets is detected during the long
lasting exposure to PCBs [58]. Due to the depletion of islets, the insulin secretory
effects resulted in a diminution of cellular insulin level [59] and TCDD anticipated
to promote β-cell “exhaustion” [60]. This recommends that chronic extended exposure of these compounds could result in deficit of insulin.
W. Hassan et al.
different MRC complexes, which could take part in mitochondrial ROS production
[39–41]. However, TCDD caused excessive mitochondrial ROS production appears
to be the factor that activates AhR [42]. It also promotes liver fibrosis development
in high fat diet obese mice [43].
Obesity
Chronic exposure to PCBs causes obesity; the possible effects are endocrine disruptors on body weight. The exposure of PCBs also causes obesity in children [44].
PCBs act by altering the AhR expression of principal genes correlated to adipogenesis, lipid metabolism, and inflammatory factors [45]. Leptin Receptor (LEPR),
Ras-Related Associated with Diabetes (RRAD), Aryl hydrocarbon receptor nuclear
translocator (ARNT), and Paraoxonase 1 (PON1) are the most common receptor
and genes that plays significant role in the obesity. Abnormality of these receptors
is observed among highly exposed subjects [46]. PCBs readily cross the placental
barrier. It can harm developing neonates. Prenatal exposure of the PCBs can also
cause obesity in children [5, 47]. Prenatal exposure of certain PCBs can be the reason of smaller size at birth [48]. Early exposure of PCBs in pregnant women can be
a predisposing factor for the development of obesity in future [49].
Diabetes Mellitus
PCBs have the potential to directly alter glucose homeostasis and cause diabetes
[50]. In the US, it is observed that PCBs exposure is linked with an escalation in
β-cell function, resulting in hyperinsulinemia and insulin resistance [51]. Beta-cells
of the pancreas lack the antioxidant potential. This oxidant stress mediates the reactive oxygen and nitrogen species that ruin their function by modifying metabolism
and/or ATP sensitive potassium channel activity while inducing apoptosis [52].
Chronic exposure to the PCBs causes insulin resistance and hyperinsulinemia leading to diabetes mellitus [53]. Increased serum concentrations can lead to type II
diabetes [54]. The exposure of PCBs in the elderly age increased the likelihood of
diabetes [55].
TCDD reduces glucose-stimulation and insulin release in animal models, similar
effects were observe in AhR knock-out mice [56]. TCDD exposed rats had depleted
islets of langerhans [57], similarly the depletion of islets is detected during the long
lasting exposure to PCBs [58]. Due to the depletion of islets, the insulin secretory
effects resulted in a diminution of cellular insulin level [59] and TCDD anticipated
to promote β-cell “exhaustion” [60]. This recommends that chronic extended exposure of these compounds could result in deficit of insulin.
W. Hassan et al.