HOW IS DIABETES caused A technical view

HOW IS DIABETES caused A technical view

I had posted earlier last week on the topicLipodystrophy and leptin harmone treatment for A small group of thin patients who develop disorders typically tied to obesity and Diabetes2 (see linkbelow)

Obesity is not widely considered a protective mechanism. Quite the opposite is true.. It’s usually considered one of the causal factors of the metabolic syndrome and insulin resistance. Obesity is a marker of disease, but ultimately it serves to protect the body from the effects of hyperinsulinemia.

Claire Johnson a patient with a rare case of lipodystrophy, a genetic disorder characterized by the lack of fat. She was skinny but always ravenously hungry and could never get fat, because she lacked fat cells.

She was finally diagnosed in 1996 with lipodystrophy by Dr. Simeon Taylor, who was chief of diabetes at the National Institute of Diabetes, Digestive and Kidney Diseases. The above case signifies thatwe need to understand the new paradigm of insulin resistance how insulin resistance, obesity, fatty liver, and fatty pancreas are actually all the different forms of protection our body uses.

The basic problem is hyper-insulinemia. There are many possible causes of too-much-insulin, but one of the major ones is excessive dietary intake of food particularly sugar. However, this is not the only cause.

Insulin has several roles. One is to allow glucose into cells. Another is to stop glucose production and fat burning in the liver (gluconeogenesis). After this stops, then it stores glycogen in the liver and turns excessive carbohydrates and protein into fat via de novo lipogenesis. Insulin is basically a hormone to signal the body to store some of the incoming food energy, either as glycogen or fat.

When insulin falls, during fasting, the reverse happens. The body releases some of this stored food energy to power the body. If feeding and fasting are relatively balanced, then it all works as planned.

However, if insulin becomes excessive, then the body is always trying to store glycogen and fat. Since there’s not much room for glycogen, it produces fat. (Note – this is normal. This process reverses during fasting) The liver exports this fat out as triglycerides along with very low density lipoprotein (VLDL) to other organs but particularly to fat cells called adipocytes

which are specialized cells to store fat. Having more fat cells is not particularly dangerous. The fat cell is designed to hold fat, so you don’t get sick from it. Obesity itself is not the cause of the problem. The critical problem occurs when you get fat where it’s not supposed to be.

It’s usually first noticed in the liver. Fat is not supposed to be stored in the liver. But under conditions of hyperinsulinemia and excessive carbohydrates, it can.. Glucose get turned into fat and too much of it ends up in the liver instead of the fat cells. The fat cells (adipocytes) are trying to protect the body by holding the fat in a safe place. Fat inside the fat cell is OK. Fat inside the liver is not.

The fat cells actually have a secondary protective mechanism. The expansion of the fat cells encourages the release of leptin, which will cause us to stop eating. However, over time chronic excessive release of leptin will create leptin resistance, which is what we find in common obesity.

So the liver tries really, hard not to get anymore fat. But insulin is pushing really hard to shove more fat into the liver. In Claire Johnson’s case, there are no adipocytes to hold this excess fat so it must remain in the liver and other organs. Develop insulin resistance of course! . So the glucose piles up outside in the blood. The insulin resistance is not a bad thing, it’s a protective mechanism. to resist insulin.

the liver in trying to pump out as much of the fat as it can. It’s pumping out triglycerides d triglyceride levels go up (a classic sign of metabolic syndrome). It’s trying to relieve the fat-engorged liver by exporting it out. So muscles get fat, and you get fatty muscle.

The pancreas also gets some fat and you get fatty pancreas. As the pancreas becomes distended with fat, it produces less insulin. because it’s trying to protect the body from the effects of too much insulin! Both the fatty liver creating insulin resistance and fatty pancreas, creating lowering insulin levels results in the same thing. Increase glucose in the blood, but organ protection against this excessive insulin. This high blood glucose causes the symptoms of diabetes – excessive thirst, excessive urination and loss of weight. The high blood glucose exceeds the renal threshold of glucose.


You may also like...