Too much Enzymes and acids

[sciencesimon]

I have been reading about diabetes and types and how it is functionally regulated by the body.

 

The only logical conclusion i can theory is:

 

Diabetes is a result of enzymes and acids that destroy skeletal tissue or re-regulate and the normal hormonal processes that regulate the endocrine system. Excess Sugar and fats in a diet void of meat(creatine) Vitamin c, calcium, phosphorus, magnesium, vitamin d, high biological value proteins, complex carbs, change the endocrine system to a new mode of survival regulation. The excess sugar and unhealthy fats are the predominant energy supply for the anaerobic system and aerobic system, any stored skeletal nutrients become used up to an extent and not replaced when they should, so the body changes to regulate survival.

 

What is your opinion on my own evaluation?

[Greippi]

Exactly what experimental evidence do you have for that? The more classical explanations (while we don't fully understand it - especially type 2 and 3) have masses of empirical "evidence".

 

Type 1 diabetes is autoimmune. Lymphocytes infiltrate the pancreas, and destroy pancreatic beta cells (those that sense glucose levels and produce insulin). Therefore you get a loss of insulin production.

 

For type 2 and MODY (maturity onset diabetes of the young), are not autoimmune, but both have very strong genetic factors as well as environmental factors. From the genes that have a strong link to disease susceptibility, one can determine the biochemical pathways that are involved in these types of diabetes.

 

For example, genes linked to disease susceptability in:

tpe 2:

CAPN10 - protease associated with insulin release from pancreatic cells.

GCK - a hexokinase that increases metabolism of glucose

GLUT2 - transports glucose into the cell, gene variants may disrupt glucose regulation.

 

MODY:

Most identified genes are transcription factors

MODY1 - HNF4A - caauses abnormal regulation of transcription in beta cells, leading to a defect in the signalling of insulin secretion, beta cell mass or both.

Glucokinase (MODY2) - decreases phosphorylation of glucose, leading to a defect in sensitivity of beta cells to glucose and defect in storage of flucose as glucogen in liver.

Plus other genes involved in gene regulation.