Mitochondria and Type 2 Diabetes

I'll start with the conclusion. This is a reprinted abstract from the ncbi dot gov website (the National Library of Medicine) (http://www.ncbi.nlm.nih.gov/pubmed/22399425) and states:

"Mitochondria play a key role in energy metabolism and ATP production in many tissues, including skeletal muscle, cardiac muscle, brain and liver. Inherent disorders of mitochondria such as mDNA deletions cause major disruption of metabolism and can result in severe disease phenotypes. However, the incidence of such mDNA based disorders is extremely rare and cannot account for the dramatic rise in human metabolic diseases, which are characterised by defects in energy metabolism. Mitochondrial dysfunction characterized by reduced ATP generation and reduced mitochondrial number in skeletal muscle or reduced ATP generation and mitochondrial stimulus-secretion coupling in the pancreatic beta cell has been implicated in the pathology of chronic metabolic disease associated with type 2 diabetes mellitus and also with aging. Additionally the generation of ROS from mitochondria and other cellular sources may interfere in insulin signaling in muscle, contributing to insulin resistance. Reduced mitochondrial oxidative capacity coupled with increased ROS generation underlies the accumulation of intramuscular fat, insulin resistance and muscle dysfunction in aging. We will review the molecular basis for optimal mitochondrial function or mechanisms of dysfunction and correlate with pathology of identified diseases and aging."

To break that paragraph down and to bring in a small historical perspective, the Mitochondria in especially muscle cells has long been thought to be important to the development of type 2 DM (Diabetes Millitus). The reason that Mitochondria is implicated is that it is the primary agent in the transformation of blood sugar into energy. Type 2 DM is, basically, when the body forgets how to use its glycogen/sucrose and therefore the little Mitochondria are at the forefront of suspicion (since they are the main "users"). For some time science believed that a mutation in the DNA of Mitochondria was the culprit, as stated above: "Inherent disorders of mitochondria such as mDNA deletions cause major disruption of metabolism and can result in severe disease phenotypes. However, the incidence of such mDNA based disorders is extremely rare and cannot account for the dramatic rise in human metabolic diseases, which are characterised by defects in energy metabolism." As you can read in this snippet, the huge rise in metabolic disease cannot be accounted for by the extremely rare occurrence of the DNA mutation. The only other player in the card game is the dwindling amount of Mitochondria in possible concert with a large sugar intake.

To simplify, when we increase the amount of Mitochondria in muscle cells then we enhance the body's ability to handle sugar and the incidence of type 2 DM decreases. It is just that simple. Am I saying that a lifestyle of aerobic exercise through a lifetime can prevent type 2 DM? Well, I'm afraid to make that statement of course. However, the overwhelming consensus in the scientific community supports that thought:

1. University of New Mexico Dr. Len Kravitz: "Mitochondria . . . improve insulin sensitivity (and thus help to manage or prevent pre-diabetes or diabetes)
2. The Endocrine Society, in their study published at NCBI: "The pathophysiology of type 2 diabetes mellitus (DM) is varied and complex. However, the association of DM with obesity and inactivity indicates an important, and potentially pathogenic, link between fuel and energy homeostasis and the emergence of metabolic disease. Given the central role for mitochondria in fuel utilization and energy production, disordered mitochondrial function at the cellular level can impact whole-body metabolic homeostasis. Thus, the hypothesis that defective or insufficient mitochondrial function might play a potentially pathogenic role in mediating risk of type 2 DM has emerged in recent years."
3. The above paragraph from the National Library of Medicine
4. From the Diabetes Learning Center at Medpage (http://www.medpagetoday.com/resource-center/diabetes/Mitochondrial-Mechanisms-Disease-Diabetes-Mellitus/a/31636): "Mitochondria are found in every cell in the human body. Known as the "power plant of the cell," mitochondria are central to the conversion of fatty acids and glucose to usable energy in the form of ATP (adenosine triphosphate). A growing body of evidence now demonstrates a link between various disturbances in mitochondrial functioning and type 2 diabetes. In patients with type 2 diabetes, the size, number, and efficiency of mitochondria are reduced."
5. From Nature Reviews Endocrinology (http://www.nature.com/nrendo/journal/v8/n2/abs/nrendo.2011.138.html), in an article entitled "The role of mitochondria in insulin resistance and type 2 diabetes mellitus": "Type 2 diabetes mellitus (T2DM) has been related to alterations of oxidative metabolism in insulin-responsive tissues. Overt T2DM can present with acquired or inherited reductions of mitochondrial oxidative phosphorylation capacity, submaximal ADP-stimulated oxidative phosphorylation and plasticity of mitochondria and/or lower mitochondrial content in skeletal muscle cells and potentially also in hepatocytes. Acquired insulin resistance is associated with reduced insulin-stimulated mitochondrial activity as the result of blunted mitochondrial plasticity. Hereditary insulin resistance is frequently associated with reduced mitochondrial activity at rest, probably due to diminished mitochondrial content. Lifestyle and pharmacological interventions can enhance the capacity for oxidative phosphorylation and mitochondrial content and improve insulin resistance in some (pre)diabetic cases. Various mitochondrial features can be abnormal but are not necessarily responsible for all forms of insulin resistance. Nevertheless, mitochondrial abnormalities might accelerate progression of insulin resistance and subsequent organ dysfunction via increased production of reactive oxygen species. This Review discusses the association between mitochondrial function and insulin sensitivity in various tissues, such as skeletal muscle, liver and heart, with a main focus on studies in humans, and addresses the effects of therapeutic strategies that affect mitochondrial function and insulin sensitivity."

And there are plenty more. Google away, folks!

My conclusion: Actively increasing Mitochondria in muscle cells, especially through a lifestyle of aerobic exercise, severely diminishes a person's chances of contracting Type 2 DM.

See you on the bike!!