137
products which contain hair dyes, cleaning products, air fresheners, cosmetics, and
sunscreens. Some heavy metals even like arsenic were also shown to possess EDCs
like properties. A large number of observations suggest that EDCs show a contribution to obesity, diabetes, cancer, infertility, and the metabolic syndrome [7]. In this
chapter our main focus is on the metabolic disorders that are because of exposure
to endocrine-disrupting chemicals. This chapter will also provide data on the alteration of gut microbiota as a result of exposure of EDCs and it will ultimately lead
to metabolic disorders like obesity, diabetes, and non-alcoholic fatty liver disease.
EDCs-Induced Obesity
Obesity is accompanied by other metabolic disorders and severe health related problems which include type II diabetes, certain types of cancer, and hence, mortality
[8]. Change in diet and lack of physical activity may trigger the increase in body
weight although certain other factors may also have their role [9]. Furthermore,
sedentary behavior in humans which involve prolonged sitting can change the endocrine and other mechanisms of chemical signaling which may promote constant
weight gain in a person [10, 11]. Exposure to EDCs also has a significant contribution in the weight gain or obesity [9]. EDCs are the chemicals that produce alteration
in the hormonal and other chemical signaling functions in the body [3]. Reproductive
and carcinogenic effects of EDCs are mainly focused on too much exposure to endocrine-disrupting chemicals. More recent researches had emerged a hypothesis that
these chemicals have their effect on weight homeostasis. However, from the investigations in the past, the adipose tissues were considered as inert storage depots, but
in the 1990s, hormone leptin was discovered which suggested that adipose tissues
itself are considered as active endocrine organ, releasing various adipokines and
hormones and also responsible for the expression of many receptors [12, 13].
Moreover, numerous reports started to evolve that are describing excessive gain of
body weight in those animals who are treated developmentally with certain EDCs
which involve bisphenol A (BPA) and diethylstilbestrol (DES) [14, 15]. The exact
mechanisms of EDCs-induced obesity are still under investigation because there are
many potential targets of EDCs on weight homeostasis. Many of the chemicals have
the ability to bind with peroxisome proliferator activated receptors (PPARs) which
perform the critical roles in lipid metabolism and adipogenesis [16]. PPAR-gamma
(PPARɣ), a subtype of PPARs, is a master regulator of the development of fat cells,
with activation required for adipocyte maturation and differentiation [17]. The thiazolidinediones are well known as PPARɣ agonist medications that can improve insulin resistance, but they also induced obesity. Some organotin [16] and phthalates
[18], which are the environmental contaminants, are PPARɣ agonists and have been
associated with increased body weight in animal studies. Alteration in the adipose
tissue’s development itself in terms of size, number, and distribution of adipocytes
formed occurs upon the in utero exposure of EDCs and it may also affect the largest
regulatory systems responsible for body weight homeostasis. In animal studies,
9 Alteration of Gut Microbiota in EDCs-Induced Metabolic Disorders
products which contain hair dyes, cleaning products, air fresheners, cosmetics, and
sunscreens. Some heavy metals even like arsenic were also shown to possess EDCs
like properties. A large number of observations suggest that EDCs show a contribution to obesity, diabetes, cancer, infertility, and the metabolic syndrome [7]. In this
chapter our main focus is on the metabolic disorders that are because of exposure
to endocrine-disrupting chemicals. This chapter will also provide data on the alteration of gut microbiota as a result of exposure of EDCs and it will ultimately lead
to metabolic disorders like obesity, diabetes, and non-alcoholic fatty liver disease.
EDCs-Induced Obesity
Obesity is accompanied by other metabolic disorders and severe health related problems which include type II diabetes, certain types of cancer, and hence, mortality
[8]. Change in diet and lack of physical activity may trigger the increase in body
weight although certain other factors may also have their role [9]. Furthermore,
sedentary behavior in humans which involve prolonged sitting can change the endocrine and other mechanisms of chemical signaling which may promote constant
weight gain in a person [10, 11]. Exposure to EDCs also has a significant contribution in the weight gain or obesity [9]. EDCs are the chemicals that produce alteration
in the hormonal and other chemical signaling functions in the body [3]. Reproductive
and carcinogenic effects of EDCs are mainly focused on too much exposure to endocrine-disrupting chemicals. More recent researches had emerged a hypothesis that
these chemicals have their effect on weight homeostasis. However, from the investigations in the past, the adipose tissues were considered as inert storage depots, but
in the 1990s, hormone leptin was discovered which suggested that adipose tissues
itself are considered as active endocrine organ, releasing various adipokines and
hormones and also responsible for the expression of many receptors [12, 13].
Moreover, numerous reports started to evolve that are describing excessive gain of
body weight in those animals who are treated developmentally with certain EDCs
which involve bisphenol A (BPA) and diethylstilbestrol (DES) [14, 15]. The exact
mechanisms of EDCs-induced obesity are still under investigation because there are
many potential targets of EDCs on weight homeostasis. Many of the chemicals have
the ability to bind with peroxisome proliferator activated receptors (PPARs) which
perform the critical roles in lipid metabolism and adipogenesis [16]. PPAR-gamma
(PPARɣ), a subtype of PPARs, is a master regulator of the development of fat cells,
with activation required for adipocyte maturation and differentiation [17]. The thiazolidinediones are well known as PPARɣ agonist medications that can improve insulin resistance, but they also induced obesity. Some organotin [16] and phthalates
[18], which are the environmental contaminants, are PPARɣ agonists and have been
associated with increased body weight in animal studies. Alteration in the adipose
tissue’s development itself in terms of size, number, and distribution of adipocytes
formed occurs upon the in utero exposure of EDCs and it may also affect the largest
regulatory systems responsible for body weight homeostasis. In animal studies,
9 Alteration of Gut Microbiota in EDCs-Induced Metabolic Disorders