Pancreas: Do All Roads Lead to Mitochondria.
Over several millions of years of evolution, mitochondria have transformed into specialized organelles. Today, they cannot live outside the cell nor can the host cell live without them, resulting in a symbiotic relationship. Richard Altmann, in 1894, documented them as
cell organelles and called them “bioblasts”.
Later, the term “mitochondria” itself was coined by Carl Benda in 1898. Ever since these findings, we in the field of medicine have learned a
lot about this tiny organelle, but numerous aspects continue to be discovered. In this article, we will
review the significance of this organelle in terms of pancreatic dysfunctions.
Mitochondria are a double membrane organelle and are often considered to
be “the powerhouse of the cell.” This organelle is extremely important to the maintenance of vital biological processes such as the Krebs cycle, Tricarboxylic acid cycle, the generation
of Adenosine Triphosphate, signal transduction, cell growth, cell death and much more.
Due to the many roles that the mitochondrion plays in these
biological processes, it is evident that any type of mitochondrial dysfunction would result in a
myriad of diseases. Over the past decade, we have become aware of several clinical syndromes
that might be associated with mitochondrial DNA mutations.
The increasing recognition of mt-DNA involvement in disease is partially due to the relative ease of sequencing
the mitochondrial genome. Mitochondrial DNA carries only 37 genes that encode
13 polypeptides, 22 transfer RNAs and 2 ribosomal RNAs. A number of the common diseases that
have shown to have possible mt-DNA variations are Alzheimer’s disease, Parkinson’s disease and diabetes.
Pancreas Open J. 2015; 1(1): 1-3. doi: 10.17140/POJ-1-101
