138
upon exposure of oestrogenic chemicals such as bisphenol A (BPA) and diethylstilbestrol (DES) led to an increased body weight [15, 19]. Changes in expression of
genes that have their role in the distribution of fat at 19 days of age occur after developmental DES exposure and it is confirmed through various animal studies [13].
EDCs-Induced Diabetes Mellitus
According to evolving evidence, it is proposed that EDCs play a vital role in the
etiology of diabetes and metabolic disorders [3, 20]. From the industry side, the
EDCs’ effects are divided into small-exposure groups; however, the chemicals
which reflect a risk for a much larger group via the food chain are coming from agro
and food products. Diabetogen is defined as any chemical or chemical compound
that can change the endocrine system of pancreas and metabolism of glucose.
According to several epidemiological and experimental studies, it is demonstrated
that a positive association exists between EDCs and hyperglycemia, insulin resistance, and glucose intolerance [3, 21–23]. The suggested mechanisms of action
consist of interactions of EDCs with the aryl hydrocarbon receptor (AhR) and
nuclear hormone receptors which include dysregulated hepatic metabolism, estrogen receptors, induction of oxidative and nitrosative stress, alteration in the ERK/
Akt signaling pathways, and pancreatitis [24]. While accumulating data show that
these molecular modes of action reinforce the effects of endocrine-disrupting chemicals on the development of diabetes. However, their exact mechanism of action is
still not clarified. In the metabolism of drugs and dietary products the role of the gut
microbiota is now well established, and this aspect has been covered by many different reviews [25–28]. Antidiabetic drugs are also well known for the induction of
remarkable changes in the gut microbiota, and this may also suggest their antihyperglycemic effects [29]. Microbial degradation of various chemicals which also
include EDCs with the help of gut microbiota can be associated with microbial
dysbiosis that is a shift in the structure of microbial community, altered microbial
transformation of molecules, and the induction of certain specific bacterial genes
[30, 31]. Moreover, EDCs can also be transported to the liver cells, whereby EDCs
can be conjugated and released into the gut via bile secretion for further microbial
degradation. β-lyases, nitroreductases, azoreductases, lipases, esterases, methylases, β-glucuronidases, and thiolases are all the enzymes which are responsible for
the microbial metabolism of environmental chemicals [25–28, 30, 31].
Heavy Metals
Arsenic (As) is also known as one of the recognized causative factors for metabolic
disorders. According to WHO, As is considered as leading massive poisoning worldwide [32]. Several families of Firmicute (a bacterial phylum) were significantly
F. Fiayyaz et al.
upon exposure of oestrogenic chemicals such as bisphenol A (BPA) and diethylstilbestrol (DES) led to an increased body weight [15, 19]. Changes in expression of
genes that have their role in the distribution of fat at 19 days of age occur after developmental DES exposure and it is confirmed through various animal studies [13].
EDCs-Induced Diabetes Mellitus
According to evolving evidence, it is proposed that EDCs play a vital role in the
etiology of diabetes and metabolic disorders [3, 20]. From the industry side, the
EDCs’ effects are divided into small-exposure groups; however, the chemicals
which reflect a risk for a much larger group via the food chain are coming from agro
and food products. Diabetogen is defined as any chemical or chemical compound
that can change the endocrine system of pancreas and metabolism of glucose.
According to several epidemiological and experimental studies, it is demonstrated
that a positive association exists between EDCs and hyperglycemia, insulin resistance, and glucose intolerance [3, 21–23]. The suggested mechanisms of action
consist of interactions of EDCs with the aryl hydrocarbon receptor (AhR) and
nuclear hormone receptors which include dysregulated hepatic metabolism, estrogen receptors, induction of oxidative and nitrosative stress, alteration in the ERK/
Akt signaling pathways, and pancreatitis [24]. While accumulating data show that
these molecular modes of action reinforce the effects of endocrine-disrupting chemicals on the development of diabetes. However, their exact mechanism of action is
still not clarified. In the metabolism of drugs and dietary products the role of the gut
microbiota is now well established, and this aspect has been covered by many different reviews [25–28]. Antidiabetic drugs are also well known for the induction of
remarkable changes in the gut microbiota, and this may also suggest their antihyperglycemic effects [29]. Microbial degradation of various chemicals which also
include EDCs with the help of gut microbiota can be associated with microbial
dysbiosis that is a shift in the structure of microbial community, altered microbial
transformation of molecules, and the induction of certain specific bacterial genes
[30, 31]. Moreover, EDCs can also be transported to the liver cells, whereby EDCs
can be conjugated and released into the gut via bile secretion for further microbial
degradation. β-lyases, nitroreductases, azoreductases, lipases, esterases, methylases, β-glucuronidases, and thiolases are all the enzymes which are responsible for
the microbial metabolism of environmental chemicals [25–28, 30, 31].
Heavy Metals
Arsenic (As) is also known as one of the recognized causative factors for metabolic
disorders. According to WHO, As is considered as leading massive poisoning worldwide [32]. Several families of Firmicute (a bacterial phylum) were significantly
F. Fiayyaz et al.