Glucose tissue stores

Glycogen A glucose polymer stored in animal tissue and also known as animal starch. 

After a meal, glucose concentrations in the portal venous blood can easily reach 20 mM. Much of this excess will be removed by the liver. Stimulation of insulin release results in the uptake of glucose by the peripheral tissues (muscle and adipose tissue). Surplus glucose is stored locally in tissues as glycogen, but mostly it is converted into fats. 

The glucose from the intestine that is not metabolized by the liver travels in the blood to peripheral tissues (most other tissues), where it can be oxidized for energy. Glucose is the one fuel that can be used by all tissues. Many tissues store small amounts of glucose as glycogen. Muscle has relatively large glycogen stores. 

An intriguing discovery was that euglycemic and improved glucose tolerance, along with plasma, cardiac, and adipose tissue abnormalities were maintained for a long period (up to 30 weeks) after vanadyl treatment was withdrawn. This maybe attributed partly to an accumulation of vanadium in various tissue stores or to the preservation or improvement of pancreatic )S-cell insulin content in vanadium treated rats, leading to an indefinite period of near-normal glucose homeostasis in the fed state in these animals (unpublished observations). 

In adipose tissue as in liver, glucose is taken up from the plasma and used as a substrate for the synthesis of fatty acids and triglycerides. Muscle takes up plasma glucose and stores it as glycogen, while the brain uses glucose as its major energy source. 

The first hormonal signal found to comply with the characteristics of both a satiety and an adiposity signal was insulin [1]. Insulin levels reflect substrate (carbohydrate) intake and stores, as they rise with blood glucose levels and fall with starvation. In addition, they may reflect the size of adipose stores, because a fatter person secretes more insulin than a lean individual in response to a given increase of blood glucose. This increased insulin secretion in obesity can be explained by the reduced insulin sensitivity of liver, muscle, and adipose tissue. Insulin is known to enter the brain, and direct administration of insulin to the brain reduces food intake. The adipostatic role of insulin is supported by the observation that mutant mice lacking the neuronal insulin receptor (NDRKO mice) develop obesity. 

Insulin appears to activate a process that helps glucose molecules enter the cells of striated muscle and adipose tissue Figure 49-1 depicts normal glucose metabolism. Insulin also stimulates die synthesis of glycogen by die liver. In addition, insulin promotes protein syntiiesis and helps the body store fat by preventing its breakdown for energy. 

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