Type 2 Diabetes: What is It Really?


Type 2 diabetes is recognized as a complication of  metabolic syndrome, which is a cluster that includes hyperlipidemia, hypertension, increased body fat around the waist, and an increased blood sugar, believed to be a result of oxidative stress.

A ketogenic diet decreases glucose tolerance, at least temporarily. Fats do not need insulin to get into tissues nor do they particularly stimulate the mTOR pathway. Hence, like fasting, they stimulate the AMP kinase that promotes autophagy, and so produce a better mitochondrial function.It has been postulated that the inhibition of histone deacetylase is the underlying mechanism for this effect.

 A decreased ATP:AMP ratio is a sign of energy exhaustion or low supplies, and stress, that activate AMPK, comparable to the activation of sirtuins by a decreased NADH:NAD ratio which deacetylates macromolecules post-transcriptionally, thus activating these molecules.These effects activate repairs of worn out cells, including stem cells. AMPK phosphorylates genes involved in autophagy.

mTOR is necessary for muscle function, and is activated during exercise. It is activated in response to increased nutrition, amino acids, leucine, glucose, and oxygen. mTOR matches nutrition to activity. The baseline of mTOR is higher in inflamed tissues, but the muscle equally needs mTOR for repairs, growth and strength. The higher baseline in inflamed tissues means that mTOR cannot be further activated to produce the benefits of exercise in an inflamed muscle. In exercise, nutrients are preferably distributed to the muscles and shunned from the liver and other organs. mTOR in organs not well served by blood flow is low and that promotes autophagy. Muscle mass is important for strength in an increased lifespan, but growth, except for repairs which occur with autophagy, does not do so for liver mass. Exercise also promotes the formation of the brain neurotrophic factor. Exercise activates mTOR. A ketogenic diet, though good for weight loss, is problematic for glucose tolerance.

Type 2 diabetes occurs due to increased amount of fat stored in subcutaneous fat cells that prevents further storage. This leads to insulin resistance and glucose intolerance. Increased fat laydown leads to increased inflammation, and increased inflammation and oxidative stress lead to increased fat deposition.

Another cause of type 2 diabetes is stress, psychological, physical, and disease. It leads to the release of adrenaline and cortisol that cause the release of glucose from glycogen stores, and of adrenaline to mobilize fatty acids from fat stores. Fatty acid release and accumulation in visceral organs, where inflammation is rife, prevent the metabolism of glucose. And this leads to insulin resistance. Inflammation promotes fat accumulation in cells, as the nearest source of energy for inflammatory cells. Lipolysis and free fatty acids produced inhibit glycolysis and this, in turn, causes insulin resistance.

Refined sugars, namely sucrose and fructose overburden the liver as they get converted into fat, leading to a fatty liver, and this  makes it resistant to insulin. More damage by fat to tissue leads to inflammation, and inflammation futher leads to more fat deposition. Fructose does not need insulin to enter the cell, and so it is silently converted into fat at high doses that then overwhelm the cell. Again, this proceeds to insulin resistance.

Dr. Oliver Verbe Binso, MD.

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