What is mitochondria in simple words?

Mitochondria (sing. mitochondrion) are organelles, or parts of a eukaryote cell. They are in the cytoplasm, not the nucleus. They make most of the cell's supply of adenosine triphosphate (ATP), a molecule that cells use as a source of energy. Their main job is to convert energy.

Present in nearly all types of human cell, mitochondria are vital to our survival. They generate the majority of our adenosine triphosphate (ATP), the energy currency of the cell. Mitochondria are also involved in other tasks, such as signaling between cells and cell death, otherwise known as apoptosis.

If your mitochondria are not working properly then you are less able to convert food into ATP. For cells that require a lot of ATP, for example your muscles, this is a problem and they may become weaker and get tired faster.

Adult-onset mitochondrial disease often presents in more subtle ways. The disease may manifest for the first time in adulthood or may be first recognized in adulthood after a history of symptoms dating back to childhood. Adult-onset mitochondrial disease is typically a progressive multisystem disorder.

What causes mitochondrial dysfunction? On a physiological level, mitochondrial dysfunction is caused by exposure to certain environmental factors (such as certain pharmaceutical drugs, occupational chemicals and cigarette smoke) or genetic abnormalities (of both mitochondrial and nuclear DNA).

Mitochondrial disease can cause a vast array of health concerns, including fatigue, weakness, metabolic strokes, seizures, cardiomyopathy, arrhythmias, developmental or cognitive disabilities, diabetes mellitus, impairment of hearing, vision, growth, liver, gastrointestinal, or kidney function, and more.

It has been determined that to counteract damage, mitochondria possess well-defined repair pathways quite similar to those of the nucleus, among which are: base excision repair (BER), mismatch repair (MMR), single-strand break repair (SSBR), microhomology-mediated end joining (MMEJ), and probably homology recombination ...

Diabetes mellitus is a common feature of mitochondrial disease, but rarely occurs in isolation; other clinical features depend largely on the underlying mtDNA or nuclear DNA mutation. This association was appreciated in families with either a large-scale mtDNA rearrangement (duplication) or the m.

The symptoms of mitochondrial myopathies include muscle weakness or exercise intolerance, heart failure or rhythm disturbances, dementia, movement disorders, stroke-like episodes, deafness, blindness, droopy eyelids, limited mobility of the eyes, vomiting, and seizures.

A small study in children with mitochondrial disease examined the patient records of 221 children with mitochondrial disease. Of these, 14% died three to nine years after diagnosis. Five patients lived less than three years, and three patients lived longer than nine years.

INTRODUCTION. Type 2 diabetes is a multifactorial disorder in which variants in mitochondrial DNA (mtDNA) could play a role. While diabetes is a major feature in certain mtDNA diseases, pathogenic mtDNA mutations have only been identified in a tiny minority of diabetics.

Mitochondrial diabetes is caused by poor functioning of insulin-producing cells in the pancreas and/or by the emergence of insulin resistance as part of a mitochondrial disorder.

One of the suggested benefits of intermittent fasting is the optimization of mitochondrial health, potentially leading to improved energy production and overall function.

Various genetic and environmental factors can cause mitochondrial dysfunction. Mitochondrial dysfunction is a culprit defect that leads to type 2 diabetes by affecting β‐cell dysfunction and insulin resistance.

Glucagon works along with the hormone insulin to control blood sugar levels and keep them within set levels. Glucagon is released to stop blood sugar levels dropping too low (hypoglycaemia), while insulin is released to stop blood sugar levels rising too high (hyperglycaemia).