57
© The Editor(s) (if applicable) and The Author(s), under exclusive license
to Springer Nature Switzerland AG 2021
M. S. H. Akash et al. (eds.), Endocrine Disrupting Chemicals-induced
Metabolic Disorders and Treatment Strategies, Emerging Contaminants
and Associated Treatment Technologies,
https://doi.org/10.1007/978-3-030-45923-9_3
Chapter 3
Mitochondrial Dysfunction in Metabolic
Disorders
Ghulam Murtaza, Muhammad Tariq, and Ramzi Shawahna
Abstract Mitochondria are the energy houses of cells. Cell functioning and stability are critical responsibilities of mitochondria. The other functioning of cells
includes ATP production, intracellular calcium ion regulation, production of reactive oxygen species, radical scavenging property, regulation of the cell survival and
death, and caspase family of protease stimulation. Mitochondrial dysfunction can
be described as abnormality in functioning in addition to the production of reactive
species. Mitochondrial dysfunction leads to the development of metabolic syndromes such as obesity, diabetes, and neurodegenerative disorders. Since the past,
many studies have been done on morphology, physiology, and pharmacology of
mitochondria involved in metabolic diseases. By adopting interventions that include
lifestyle intervention, pharmacologic approaches, and the targeted-mitochondrial
methodologies, the progression of metabolic disease decelerates. These approaches
are involved in maintaining mitochondrial number and morphology, eliminate dysfunctional mitochondria, and reduce oxidative stress in metabolic disorders. The
aim of the study is to illuminate the role of mitochondria in the metabolic disorder
and sum up the process of the targeted mitochondrial molecule to treat metabolic
syndrome.
Keywords Mitochondria · Metabolic disorders · Oxidative stress
G. Murtaza
Department of Pharmacy, COMSATS University Islamabad, Lahore, Pakistan
M. Tariq
Department of Pharmacology, Lahore Pharmacy College, Lahore, Pakistan
R. Shawahna (*)
Department of Physiology, Pharmacology, and Toxicology, An-Najah National University,
Nablus, Palestine
© The Editor(s) (if applicable) and The Author(s), under exclusive license
to Springer Nature Switzerland AG 2021
M. S. H. Akash et al. (eds.), Endocrine Disrupting Chemicals-induced
Metabolic Disorders and Treatment Strategies, Emerging Contaminants
and Associated Treatment Technologies,
https://doi.org/10.1007/978-3-030-45923-9_3
Chapter 3
Mitochondrial Dysfunction in Metabolic
Disorders
Ghulam Murtaza, Muhammad Tariq, and Ramzi Shawahna
Abstract Mitochondria are the energy houses of cells. Cell functioning and stability are critical responsibilities of mitochondria. The other functioning of cells
includes ATP production, intracellular calcium ion regulation, production of reactive oxygen species, radical scavenging property, regulation of the cell survival and
death, and caspase family of protease stimulation. Mitochondrial dysfunction can
be described as abnormality in functioning in addition to the production of reactive
species. Mitochondrial dysfunction leads to the development of metabolic syndromes such as obesity, diabetes, and neurodegenerative disorders. Since the past,
many studies have been done on morphology, physiology, and pharmacology of
mitochondria involved in metabolic diseases. By adopting interventions that include
lifestyle intervention, pharmacologic approaches, and the targeted-mitochondrial
methodologies, the progression of metabolic disease decelerates. These approaches
are involved in maintaining mitochondrial number and morphology, eliminate dysfunctional mitochondria, and reduce oxidative stress in metabolic disorders. The
aim of the study is to illuminate the role of mitochondria in the metabolic disorder
and sum up the process of the targeted mitochondrial molecule to treat metabolic
syndrome.
Keywords Mitochondria · Metabolic disorders · Oxidative stress
G. Murtaza
Department of Pharmacy, COMSATS University Islamabad, Lahore, Pakistan
M. Tariq
Department of Pharmacology, Lahore Pharmacy College, Lahore, Pakistan
R. Shawahna (*)
Department of Physiology, Pharmacology, and Toxicology, An-Najah National University,
Nablus, Palestine