65
injury [44], this oxidative stress then evolves abnormality in mitochondria, so mitochondrial dysfunction is also indirectly the cause of brain stroke. As the mitochondrial disorder causes decreased supply of oxygen and glucose to the tissues, it
decreases the production of ATP and also the pathway of cell death change [45].
There are a series of experimentation done on the stroke model, to generate a stroke
model the oxygen supply of the stroke model is stopped and also the glucose source
is terminated which results in decreased oxidative metabolism. There are series of
events generated in a nutrient-deprived stroke model which causes high storage of
reduced material and accumulation of reactive oxygen species [44]. The tissue damage starts in the form of necrosis and apoptosis when the heart muscle gets focal
ischemia due to oxidative stress [46, 47]. Thus, peroxynitrite radical is the causative
agent of brain stroke. Thus it is proved that in the ischemic brain, oxidative metabolism is the result of the overproduction of reactive species brain [45].
Concluding Remarks
Mitochondria, the membranous organelle is involved in cell death and survival [47].
The main functions of mitochondria include the production of energy. Also, it hosts
many cellular functions including metabolism of energy, generation of reactive species, and Ca
2+
homeostasis along with cell integrity. Alteration in the morphology and
function of mitochondria produces metabolic disorders in humans. Mitochondrial dysfunctions in metabolic syndrome that were reported in recent studies were impaired
dynamics of mitochondria, deformity of synthesis of mitochondria, abnormal functioning of mitochondria, and production of reactive oxygen species. Furthermore, the
researchers showed that maintaining mitochondrial dynamics and functions is mandatory to treat metabolic diseases. If we want to slow down the progression of metabolic
disease, many interventions and approaches are helpful to make life better. These
include lifestyle intervention, pharmaceutical plans to treat the patient in better ways,
and mitochondrial-targeted molecules for the treatment of patients. However, the link
between metabolic syndrome and mitochondrial function has not been fully elucidated. Similarly, genetics and its susceptibility with metabolic syndromes and the role
of epigenetics are unclear. Additionally, the treatments related to metabolic syndromes
are not so beneficial as the body physiology varies from population to population.
Conflict of Interest Nothing to declare.
References
1. Kim JA, Wei Y, Sowers JR. Role of mitochondrial dysfunction in insulin resistance. Circ Res.
2008;102:401–14.
2. Halliwell B, Gutteridge JMC. Free radicals in biology and medicine. 4th ed. Oxford: Oxford
University Press; 2007.
3 Mitochondrial Dysfunction in Metabolic Disorders
injury [44], this oxidative stress then evolves abnormality in mitochondria, so mitochondrial dysfunction is also indirectly the cause of brain stroke. As the mitochondrial disorder causes decreased supply of oxygen and glucose to the tissues, it
decreases the production of ATP and also the pathway of cell death change [45].
There are a series of experimentation done on the stroke model, to generate a stroke
model the oxygen supply of the stroke model is stopped and also the glucose source
is terminated which results in decreased oxidative metabolism. There are series of
events generated in a nutrient-deprived stroke model which causes high storage of
reduced material and accumulation of reactive oxygen species [44]. The tissue damage starts in the form of necrosis and apoptosis when the heart muscle gets focal
ischemia due to oxidative stress [46, 47]. Thus, peroxynitrite radical is the causative
agent of brain stroke. Thus it is proved that in the ischemic brain, oxidative metabolism is the result of the overproduction of reactive species brain [45].
Concluding Remarks
Mitochondria, the membranous organelle is involved in cell death and survival [47].
The main functions of mitochondria include the production of energy. Also, it hosts
many cellular functions including metabolism of energy, generation of reactive species, and Ca
2+
homeostasis along with cell integrity. Alteration in the morphology and
function of mitochondria produces metabolic disorders in humans. Mitochondrial dysfunctions in metabolic syndrome that were reported in recent studies were impaired
dynamics of mitochondria, deformity of synthesis of mitochondria, abnormal functioning of mitochondria, and production of reactive oxygen species. Furthermore, the
researchers showed that maintaining mitochondrial dynamics and functions is mandatory to treat metabolic diseases. If we want to slow down the progression of metabolic
disease, many interventions and approaches are helpful to make life better. These
include lifestyle intervention, pharmaceutical plans to treat the patient in better ways,
and mitochondrial-targeted molecules for the treatment of patients. However, the link
between metabolic syndrome and mitochondrial function has not been fully elucidated. Similarly, genetics and its susceptibility with metabolic syndromes and the role
of epigenetics are unclear. Additionally, the treatments related to metabolic syndromes
are not so beneficial as the body physiology varies from population to population.
Conflict of Interest Nothing to declare.
References
1. Kim JA, Wei Y, Sowers JR. Role of mitochondrial dysfunction in insulin resistance. Circ Res.
2008;102:401–14.
2. Halliwell B, Gutteridge JMC. Free radicals in biology and medicine. 4th ed. Oxford: Oxford
University Press; 2007.
3 Mitochondrial Dysfunction in Metabolic Disorders