Chronic diabetes, including type 1 and type 2 diabetes, means that you have too much glucose (a form of sugar) in your blood. Elevated levels of blood glucose can lead to serious health problems including heart disease, nerve pain, kidney failure, frequent infections, and blindness.
Type 1 diabetes is commonly referred to as “juvenile” diabetes. Type 2 diabetes is often referred to as “adult onset “diabetes and usually occurs later in life. The occurrence of type 2 diabetes has clearly been linked to obesity and a sedentary lifestyle.
Symptoms of type 1 and type 2 diabetes include:
- Chronic fatigue
- Increased thirst
- Frequent urination
- Unexplained weight loss
- Slow-healing sores
- Nerve pain
- Frequent infections
How is Diabetes Linked to Mitochondrial Dysfunction?
Specialized cells located in the pancreas secrete the hormone insulin. Insulin production is an energy-dependent process. If a person’s dietary intake of sugar is too high for a long period of time, the ability of the pancreas to keep up with the demand to produce insulin may begin to fail. The cells that make insulin essentially burn out.
Maintaining normal blood glucose depends on the interplay between glucose-stimulated insulin secretion by pancreatic cells and the absorption of glucose by nerve, muscle and liver cells. Emerging evidence supports the hypothesis that decreased production of insulin as well as its impaired uptake by cells are both promoted by mitochondrial dysfunction [1].
Excess sugar in the bloodstream can damage the body by multiple mechanisms. One mechanism is called “glycosylation.” This process occurs when sugar molecules bind to important cellular proteins rendering them inactive. Another name for these inactivated proteins is “Age-related Glycosylation End Products (AGE’s)”. AGE’s occur as a direct result of elevated sugar levels and promote cellular dysfunction and chronic inflammation, two processes that can damage your mitochondria. Maintaining normal blood glucose depends on the interplay between glucose-stimulated insulin secretion by pancreatic cells and the absorption of glucose by nerve, muscle and liver cells. Emerging evidence supports the hypothesis that decreased production of insulin as well as its impaired uptake by cells are both promoted by mitochondrial dysfunction
When cells are becoming progressively damaged, they send out chemical alarm signals that promote a process called chronic inflammation. Inflammation attracts white blood cells of the immune system in order to clean up and remove the damaged cells. It’s like a fire brigade fighting a fire that’s raging in your tissues.
This is a perfect analogy for how peripheral neuropathy occurs in diabetes. It is essentially an overflow of free radical toxins in the nerves of the hands and feet. The toxins are produced due to chronic inflammation precipitated by the damaging effects too much sugar in the bloodstream. The occurrence of chronic inflammation, and the damaging effects it has on the mitochondria in multiple organs, helps explain why there is an increase in heart disease, kidney failure, blindness, and immune dysfunction in people with diabetes.
References: [1] Sangwung, P., Petersen, K. F., Shulman, G. I., & Knowles, J. W. (2020, April 1). Mitochondrial dysfunction, insulin resistance, and potential genetic implications. Endocrinology. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7341556/