63
increased release of reactive oxygen species in adipose tissues [31]. Interestingly, it
has also been documented that abdominal obesity is generated by mitochondrial
dysfunction such as in rodents and humans [32]. The gene expression is also reduced
in an obese person. So, the obesity can be linked with gene expression of mitofusin
2 lost in skeletal muscle, the mitochondrial dysfunction starts in the tissue [33].
Mitochondrial Involvement in Insulin Resistance
When the level of insulin attains lesser response by cells, the condition is termed as
insulin resistance. There are many factors that contribute to insulin resistance which
include increased age, decreased physical exercise, obesity, and tension. So, it can
say that oxidative stress in mitochondria may be the reason for insulin resistance
[1]. Though it is still not confirmed that metabolic diseases such as insulin are
caused by mitochondrial alterations or disorder, many studies have documented this
fact that alteration in mitochondrial number and morphology cause to generate insulin resistance in skeletal muscle [34]. When glucose level increases from its demand
the reactive species of oxygen also increases which causes mitochondrial alterations
[29]. Similarly, when insulin signaling pathways inhibited, it causes accumulation
of fatty acids and lipids which results in the generation of metabolic syndrome [30].
In various studies, mitochondrial metabolism markers have altered in the person
who is insulin resistant. From the data, it is found that mitochondrial changes in
skeletal muscle cause the increase in deposition of lipids and develop insulin resistance. It is also a well-known fact that lesser fatty acid oxidation results in stopping
insulin signaling which leads to free fatty acid and insulin resistance and also
decreases oxidation and ATP production in these individuals [29]. However, advance
researches are needed to describe the mitochondrial function and insulin sensitivity
via the antioxidant pathway.
Mitochondrial Involvement in Diabetes
Since the past, there is an increased incidence of type 2 diabetes and this number has
become a major problem worldwide. Now diabetes increases up to 382 million individuals and this number is increasing rapidly. Many factors are involved in diabetes
but still, the main reason is not clear. Myocytes, adipocytes, and hepatocytes are the
insulin-sensitive cells when get resistant they are called insulin resistant along with
that abnormal functioning of pancreatic cells is also the main factor that contributes
to insulin resistance. Now, recent studies have proved that the involvement of mitochondrial abnormal functioning causes an excess of reactive species which induce
diabetes [29]. T2DM is the outcome of lesser tissue sensitivity and secretion of insulin [35, 36]. recent study was done on diabetic and obese patients showed decreased
glucose production and impaired lipid homeostasis in skeletal muscle [35]. In obese
3 Mitochondrial Dysfunction in Metabolic Disorders
increased release of reactive oxygen species in adipose tissues [31]. Interestingly, it
has also been documented that abdominal obesity is generated by mitochondrial
dysfunction such as in rodents and humans [32]. The gene expression is also reduced
in an obese person. So, the obesity can be linked with gene expression of mitofusin
2 lost in skeletal muscle, the mitochondrial dysfunction starts in the tissue [33].
Mitochondrial Involvement in Insulin Resistance
When the level of insulin attains lesser response by cells, the condition is termed as
insulin resistance. There are many factors that contribute to insulin resistance which
include increased age, decreased physical exercise, obesity, and tension. So, it can
say that oxidative stress in mitochondria may be the reason for insulin resistance
[1]. Though it is still not confirmed that metabolic diseases such as insulin are
caused by mitochondrial alterations or disorder, many studies have documented this
fact that alteration in mitochondrial number and morphology cause to generate insulin resistance in skeletal muscle [34]. When glucose level increases from its demand
the reactive species of oxygen also increases which causes mitochondrial alterations
[29]. Similarly, when insulin signaling pathways inhibited, it causes accumulation
of fatty acids and lipids which results in the generation of metabolic syndrome [30].
In various studies, mitochondrial metabolism markers have altered in the person
who is insulin resistant. From the data, it is found that mitochondrial changes in
skeletal muscle cause the increase in deposition of lipids and develop insulin resistance. It is also a well-known fact that lesser fatty acid oxidation results in stopping
insulin signaling which leads to free fatty acid and insulin resistance and also
decreases oxidation and ATP production in these individuals [29]. However, advance
researches are needed to describe the mitochondrial function and insulin sensitivity
via the antioxidant pathway.
Mitochondrial Involvement in Diabetes
Since the past, there is an increased incidence of type 2 diabetes and this number has
become a major problem worldwide. Now diabetes increases up to 382 million individuals and this number is increasing rapidly. Many factors are involved in diabetes
but still, the main reason is not clear. Myocytes, adipocytes, and hepatocytes are the
insulin-sensitive cells when get resistant they are called insulin resistant along with
that abnormal functioning of pancreatic cells is also the main factor that contributes
to insulin resistance. Now, recent studies have proved that the involvement of mitochondrial abnormal functioning causes an excess of reactive species which induce
diabetes [29]. T2DM is the outcome of lesser tissue sensitivity and secretion of insulin [35, 36]. recent study was done on diabetic and obese patients showed decreased
glucose production and impaired lipid homeostasis in skeletal muscle [35]. In obese
3 Mitochondrial Dysfunction in Metabolic Disorders