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the activation of glucose transporter which enhances the uptake of glucose in the
adipocytes [51]. Another study shows that perinatal exposure of BPA in male rat
offspring in later life reduces the gene expression and production of adiponectin.
Exposure to a high concentration of BPA causes metabolic dysfunction [52].
Exposure of low concentration of BPA to human adipocytes in vitro causes dysregulation of the functions of adipocytes by impairing the utilization of glucosestimulated by insulin and pathway of insulin signaling [51].
Impairment in Glucose Metabolism
BPA has the potential to exhibit its role as an obesogen and diabetogenic. Only diet
and lifestyles are not sufficient to elaborate on the incidence of obesity. Many
endocrine- disrupting chemicals can disturb the homeostasis of glucose in the various organs such as the liver, pancreas, adipocytes, and neuroendocrine cells [53].
BPA influences the glucose homeostasis in liver, adipose tissues, skeletal muscles,
pancreas, and central nervous system.
Impairment in Insulin Secretion from Pancreatic Islets
The pancreas produces hormones, insulin, and glucagon, for the regulation of glucose homeostasis [54]. Β-cells of pancreatic islets are responsible for producing
and releasing the insulin while α cells of pancreatic islets are responsible for producing and releasing of glucagon. Any abnormality in pancreatic function leads
to the disruption in the production and release of hormones; insulin and glucagon,
which may lead to the development of T2DM and insulin resistance that are the
major contributing factors for obesity and metabolic syndrome [55]. Estrogen has
also a role in maintaining the function of the pancreas by binding with the estrogen
receptor that is present on the pancreas. It has the potential for maintaining the
functions of β-cells and the sensitivity of insulin. If there is a low level of estrogen
in the body, then intolerance of glucose and resistance to insulin is developed in
the body [54]. BPA is considered a xenoestrogen substance, which mimics the
action of estrogen in the pancreatic cells. BPA is responsible for the overproduction of insulin as 17-β estradiol by binding with estrogen receptor and activating
extracellular signaling kinase [56]. BPA exposure cause fasting hyperglycemia,
hyperinsulinemia, and intolerance of glucose in animals [57]. Another study shows
that BPA has an opposite effect on the production of insulin when using the insulinoma cells of a rat as β-cells. BPA exposure induced apoptosis in the rat insulinoma cells, reduction in the viability of cells that are triggered by defects in
mitochondria and decreased insulin production and secretion by stimulation of
glucose [58].
K. Irshad et al.
the activation of glucose transporter which enhances the uptake of glucose in the
adipocytes [51]. Another study shows that perinatal exposure of BPA in male rat
offspring in later life reduces the gene expression and production of adiponectin.
Exposure to a high concentration of BPA causes metabolic dysfunction [52].
Exposure of low concentration of BPA to human adipocytes in vitro causes dysregulation of the functions of adipocytes by impairing the utilization of glucosestimulated by insulin and pathway of insulin signaling [51].
Impairment in Glucose Metabolism
BPA has the potential to exhibit its role as an obesogen and diabetogenic. Only diet
and lifestyles are not sufficient to elaborate on the incidence of obesity. Many
endocrine- disrupting chemicals can disturb the homeostasis of glucose in the various organs such as the liver, pancreas, adipocytes, and neuroendocrine cells [53].
BPA influences the glucose homeostasis in liver, adipose tissues, skeletal muscles,
pancreas, and central nervous system.
Impairment in Insulin Secretion from Pancreatic Islets
The pancreas produces hormones, insulin, and glucagon, for the regulation of glucose homeostasis [54]. Β-cells of pancreatic islets are responsible for producing
and releasing the insulin while α cells of pancreatic islets are responsible for producing and releasing of glucagon. Any abnormality in pancreatic function leads
to the disruption in the production and release of hormones; insulin and glucagon,
which may lead to the development of T2DM and insulin resistance that are the
major contributing factors for obesity and metabolic syndrome [55]. Estrogen has
also a role in maintaining the function of the pancreas by binding with the estrogen
receptor that is present on the pancreas. It has the potential for maintaining the
functions of β-cells and the sensitivity of insulin. If there is a low level of estrogen
in the body, then intolerance of glucose and resistance to insulin is developed in
the body [54]. BPA is considered a xenoestrogen substance, which mimics the
action of estrogen in the pancreatic cells. BPA is responsible for the overproduction of insulin as 17-β estradiol by binding with estrogen receptor and activating
extracellular signaling kinase [56]. BPA exposure cause fasting hyperglycemia,
hyperinsulinemia, and intolerance of glucose in animals [57]. Another study shows
that BPA has an opposite effect on the production of insulin when using the insulinoma cells of a rat as β-cells. BPA exposure induced apoptosis in the rat insulinoma cells, reduction in the viability of cells that are triggered by defects in
mitochondria and decreased insulin production and secretion by stimulation of
glucose [58].
K. Irshad et al.