More and more insulin forces more storage but also causes hypertension, heart disease, stroke, cancer and type 2 diabetes.

Type 2 diabetes takes a long time to develop and complete recovery also takes a while. Obesity stores enough energy to last for at least 2 months.

Even reversal of diabetes is not complete recovery. Clearing sugar from blood is only part of the process. Insulin resistance lasts until fat consumed and not used is quickly stored.

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Fat Tissue Regulates Sensitivity To Insulin And Insulin Resistance

Insulin promotes transport of sugar, fat and protein into skeletal muscle. It promotes formation of fat from sugar in the liver. It also promotes clearance of sugar and fat into subcutaneous fat tissue (SFT).

First, sugar and then fat are cleared from blood into skeletal muscle and SFT. As sugar increases during a meal, insulin is secreted and enhances what started by basic cell transport. As long as muscle, liver and fat have storage space, sugar and fat are cleared quickly. Protein is cleared more slowly into organs all over the body. Sugar and a special form of fat are taken up by the brain and nerves.

Subcutaneous fat is special. It’s a little different in everybody. Sugar is combined into fat and cells store fat in globules. Insulin stimulates cells to make globules and when cells get full, it stimulates creation of new cells.

Here’s what’s special! It’s how soon SFT cells get full and how quickly and for how long new cells keep appearing. In particular, some people are able to keep forming new fat cells and some people simply fill the cells they’ve got and that’s it.

When SFT cells are full they simply will not take in more fat. As long as new cells keep forming, the SFT keeps getting bigger. Forming new cells requires expression of genes that start new cell formation. The new cells keep taking in fat and adding to the size of SFT.

When gene expression fails, level of insulin in blood and tissue increases more and more. SFT cells are forced still bigger but most of the sugar and fat in blood gets forced into skeletal muscle as well as liver and other organs in the abdomen.

Type 2 diabetes occurs when gene expression fails. When SFT cells are so big they can’t accept more sugar and sugar combined with fat. Levels of sugar and fat increase in the blood and insulin levels keep rising higher and higher. Failure of gene expression to create new cells causes existing cells in SFT to keep getting bigger as glucose and insulin levels keep rising.

Samples of SFT from 42 obese individuals with type 2 diabetes in the Look AHEAD study were compared with samples from 25 obese individuals who did not have diabetes. The metabolic response to sugar and insulin were tested in all subjects.

Insulin sensitivity was measured by slowly infusing insulin and sugar intravenously for 3 hours. The same amount of insulin was infused in all subjects. The amount of sugar infused was adjusted in each subject to keep concentration in blood at low normal levels.

Sugar infused into all subjects was cleared from their blood into skeletal muscle, liver and fat. Subjects with high sensitivity to insulin were able to clear large amounts of sugar from their blood. Those with high resistance to insulin could not clear as much sugar as those with high insulin sensitivity.

As shown in the Figure, obese subjects with diabetes had larger size of their fat cells than obese subjects without diabetes. Also, the subjects with diabetes could not clear as much sugar from their blood.

Subcutaneous fat tissue regulates insulin resistance. The ability of SFT to store excess fat determines how quickly sugar and fat are cleared from the blood and how much insulin is secreted by the pancreas.

The ability to differentiate precursor cells into fat storage cells is under genetic control. Impaired ability to create new fat cells is what causes type 2 diabetes. As long as intake of sugar, fat and protein matches metabolic and physical work requirements the surges in blood levels with meals and snacks are accommodated. When excess nutrients can be stored in SFT, levels of sugar, fat and insulin in blood remain low.

When SFT cells become full and new cells do not form, high levels of insulin persist between meals and overnight. Eventually, the result is elevations of sugar and fat that are forced into abnormal storage sites in skeletal muscle and intraabdominal fat depots.

Exercise Enhances Fat Storage Capacity

Reduction in mass of SFT with exercise is the most obvious effect. Decreased fat content of cells simply makes it possible to clear more sugar and fat from circulating blood. Exercise training increases capacity for fat storage and delays onset of insulin resistance.

Increased insulin sensitivity of SFT also occurs with exercise training. SFT in type 2 diabetes always has less than half the insulin sensitivity of SFT in subjects without diabetes. Exercise training increases insulin sensitivity of SFT even without decreasing cell volume.

New cell formation in SFT also is enhanced by exercise. Studies of gene expression indicate that exercise training enhances the potential for new cell formation in SFT.

Epigenetic alterations are an enormous benefit from both endurance and strength exercise training. The epigenetic alterations can be transferred by inheritance. The result is to restore potential for SFT storage capacity as an inherited family physical and medical characteristic. The benefit is inherited at conception, amplified during pregnancy and continued after birth to early adult life.

Resting Heart Rate Increased By Insulin Resistance

Insulin resistance is the best predictor of type 2 diabetes. It can be measured before elevations of blood sugar become evident. Insulin resistance also is a predictor of high blood pressure and abnormal cholesterol metabolism. Usually insulin resistance is calculated from levels of insulin and sugar in fasting blood samples.

Insulin resistance also causes abnormalities in nervous system control of heart rate and blood pressure. These abnormalities can be detected even before blood sugar tolerance decreases. Imbalance in control of heart rate even precedes insulin resistance.

High levels of resting heart rate frequently indicate insulin resistance. Normal values for resting heart rate are 60 to 90 beats per minute. The most reliable values of resting heart rate are measured upon awakening first thing in the morning.

Low normal values below 65 beats per minute frequently can be used to determine success in preventing or correcting insulin resistance.

Summary

Insulin promotes transport of sugar, fat and protein into skeletal muscle. It promotes formation of fat from sugar in the liver. It also promotes clearance of sugar and fat into subcutaneous fat tissue (SFT).

When SFT cells are full they simply will not take in more fat. As long as new cells keep forming, the SFT keeps getting bigger. Forming new cells requires expression of genes that start new cell formation.

Type 2 diabetes occurs when gene expression fails. When all SFT cells are full, they can’t accept more sugar and sugar combined with fat.

Subcutaneous fat tissue regulates insulin resistance. The ability of SFT to store excess fat determines how quickly sugar and fat are cleared from the blood and how much insulin is secreted by the pancreas.

Exercise enhances fat storage capacity. Reduction in mass of SFT, increased insulin sensitivity of SFT and new cell formation in SFT all enhance fat storage capacity

Epigenetic alterations are an enormous benefit from both endurance and strength training.

Low normal values of resting heart rate can be used to determine success in preventing or correcting insulin resistance.

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