350
Smoking-Induced Insulin Resistance and Impaired Insulin
Secretion
The incidence of diabetes is increasing worldwide and has become a considerable
health concern globally. Although in the previous era, several studies have found the
associations between tobacco/cigarette smoke and disturbance in the metabolism of
glucose. Insulin sensitivity and secretion both are the principal features that responsible for glucose tolerance [37]. Tobacco smoke can injure the pancreatic β-cells
that lead to the impaired insulin secretion and hence, the overall metabolic pathway
becomes impaired [38].
Mitochondria plays a key role in metabolic syndrome and insulin resistance.
Tobacco smoking has been considered as mitochondrial function disrupter.
Mitochondria are individual intracellular energy houses that generate power in the
form of ATP. Mitochondrial dysfunction might be the reason of impairment of insulin secretion, glucose intolerance, and insulin resistance. The decline in the density
of mitochondrial DNA in circulating blood led to the development of T2DM [39,
40]. Mitochondrial dysfunction decreases the fatty acid oxidation which results in
the accumulation of intracellular fat, improved serine phosphorylation of insulin
receptor by augmented production of lipid metabolites, giving rise to insulin resistant. Moreover, numerous genetic and environmental factors are involved in mitochondrial dysfunction [41, 42]. The maintenance of energy metabolism depends on
the combined action of a huge count of hormones functioning that liable to maintain
and control glycemia, secretion of insulin from pancreas, and insulin resistance.
EDCs can interact with hormones receptors and activate the impairment of insulin
secretion and resistance [43].
Tobacco smoke has influential role and pathophysiological role in the prevalence
of metabolic syndrome. These factors also play a pivotal role to interrupt the insulin
signaling in adipose tissue, muscle, and liver, resulting in epigenetic alterations
leading to resistance of insulin and impairment of β-cells. Accordingly, metabolic
distress may also accelerate the actions of EDCs. For example, excess of fat and
calories in food and lack of walk may lead to the onset of obesity which is a primary
for the progression of insulin resistance and impaired insulin secretion [44].
Smoking-Induced Oxidative Stress in Metabolic Disorders
Oxidative stress has been broadly recognized as potential mediator of metabolic
disorders and obesity. Oxidative stress is typically defined as an imbalance between
the antioxidant and oxidant species within an organism when exposed to dissimilar
sources of environmental stress. Exposures of cigarette smoking as an EDC are
responsible to generate inflammatory response and oxidative stress, which have
been linked with insulin resistance, metabolic syndrome, obesity, cardiovascular
diseases, and diabetes. Smoking can cause increased production of reactive oxygen
K. Jabeen et al.
Smoking-Induced Insulin Resistance and Impaired Insulin
Secretion
The incidence of diabetes is increasing worldwide and has become a considerable
health concern globally. Although in the previous era, several studies have found the
associations between tobacco/cigarette smoke and disturbance in the metabolism of
glucose. Insulin sensitivity and secretion both are the principal features that responsible for glucose tolerance [37]. Tobacco smoke can injure the pancreatic β-cells
that lead to the impaired insulin secretion and hence, the overall metabolic pathway
becomes impaired [38].
Mitochondria plays a key role in metabolic syndrome and insulin resistance.
Tobacco smoking has been considered as mitochondrial function disrupter.
Mitochondria are individual intracellular energy houses that generate power in the
form of ATP. Mitochondrial dysfunction might be the reason of impairment of insulin secretion, glucose intolerance, and insulin resistance. The decline in the density
of mitochondrial DNA in circulating blood led to the development of T2DM [39,
40]. Mitochondrial dysfunction decreases the fatty acid oxidation which results in
the accumulation of intracellular fat, improved serine phosphorylation of insulin
receptor by augmented production of lipid metabolites, giving rise to insulin resistant. Moreover, numerous genetic and environmental factors are involved in mitochondrial dysfunction [41, 42]. The maintenance of energy metabolism depends on
the combined action of a huge count of hormones functioning that liable to maintain
and control glycemia, secretion of insulin from pancreas, and insulin resistance.
EDCs can interact with hormones receptors and activate the impairment of insulin
secretion and resistance [43].
Tobacco smoke has influential role and pathophysiological role in the prevalence
of metabolic syndrome. These factors also play a pivotal role to interrupt the insulin
signaling in adipose tissue, muscle, and liver, resulting in epigenetic alterations
leading to resistance of insulin and impairment of β-cells. Accordingly, metabolic
distress may also accelerate the actions of EDCs. For example, excess of fat and
calories in food and lack of walk may lead to the onset of obesity which is a primary
for the progression of insulin resistance and impaired insulin secretion [44].
Smoking-Induced Oxidative Stress in Metabolic Disorders
Oxidative stress has been broadly recognized as potential mediator of metabolic
disorders and obesity. Oxidative stress is typically defined as an imbalance between
the antioxidant and oxidant species within an organism when exposed to dissimilar
sources of environmental stress. Exposures of cigarette smoking as an EDC are
responsible to generate inflammatory response and oxidative stress, which have
been linked with insulin resistance, metabolic syndrome, obesity, cardiovascular
diseases, and diabetes. Smoking can cause increased production of reactive oxygen
K. Jabeen et al.