Glucose Space

The glucose space (i.e., the extracellular water volume) is constant in any individual and

Glucose from gut via portal vein

Overflow to urine

Blood glucose concentration

Glucose from gut via portal vein

Overflow to urine

Blood glucose concentration

Glucose

■ Glucose precursors [/j/j Glycogen

Figure 1 Schematic representation of blood glucose concentration and its relationship to the body glucose pool. The central system represents the hypothetical glucose pool, the actual size of which is represented by the horizontal axis (i.e., volume of distribution multiplied by blood (and extracellular fluid) glucose concentration). The postulated homeostatic switch is the cells of the endocrine pancreas, which respond to blood glucose concentration modulated by intestinal hormonal (incretin) and neural factors, which are themselves controlled by messages received from the gut (enteroinsular axis) and the autonomic nervous system. RBC, red blood cells.

Glucose

■ Glucose precursors [/j/j Glycogen

Figure 1 Schematic representation of blood glucose concentration and its relationship to the body glucose pool. The central system represents the hypothetical glucose pool, the actual size of which is represented by the horizontal axis (i.e., volume of distribution multiplied by blood (and extracellular fluid) glucose concentration). The postulated homeostatic switch is the cells of the endocrine pancreas, which respond to blood glucose concentration modulated by intestinal hormonal (incretin) and neural factors, which are themselves controlled by messages received from the gut (enteroinsular axis) and the autonomic nervous system. RBC, red blood cells.

consequently the amount of glucose in the body (the glucose pool) is directly proportional to its concentration in the blood. This is controlled through a series of complicated control mechanisms, the most important of which involve individual pancreatic islets of Langerhans. These function semiautono-mously and release either insulin or glucagon according to need.

When pool size increases above a threshold, corresponding to a concentration in blood of approximately 10mmoll_1, glucose filtered at the glomeruli exceeds tubular capacity to reabsorb it and consequently spills over into the urine, producing glyco-suria. Temporary increases in glucose pool size (hyperglycemia) are not immediately harmful but in the long term give rise to the so-called complications of diabetes. Decreases in glucose pool size (hypoglycemia), on the other hand, are immediately harmful and potentially so dangerous that many defence mechanisms have evolved to prevent or overcome them.

Blood Glucose

The brain, which can remove glucose from the extra-cellular fluid (ECF) in the absence of insulin, is the only important drain on the glucose pool in the fasting subject when plasma insulin levels are minimal. It consumes glucose at the rate of approximately 78 mg per gram of tissue per day. This amounts to approximately 110 g per day in an adult man or 75 g per day in a 1-year-old child. Estimates of glucose turnover suggest that approximately 9 g of glucose enters and leaves the glucose pool every hour in the average overnight fasting healthy subject.

The concentrations of glucose in venous and arterial blood are similar in the fasting subject because peripheral tissues, such as muscle, skin, and connective tissue, do not extract significant amounts of glucose from the blood in these circumstances. In the recently fed subject, however, glucose uptake by peripheral tissues increases markedly under the influence of insulin released in response to the ingestion of a meal. This can produce a difference in arterial and venous blood glucose concentrations of 2 mmol l-1 or more. This fact, known for more than 80 years, is still often forgotten or ignored by both experimentalists and clinicians. It not only has implications with regard to our understanding of the physiology of glucose homeostasis but also sometimes has unfortunate consequences for patients who may, if only venous blood is sampled, be misdiagnosed as suffering from hypoglycemia (i.e., blood glucose <3.0mmoll-1).

It is, after all, arterial and not venous blood glucose that is homeostatically controlled and relevant to brain physiology, but because venous blood is more easily obtained, it is often used in studies of glucose homeostasis and clinical practice. Arteria-lized venous blood, collected from heat-distended veins on the back of the hands, is the best substitute for arterial blood in studies of glucose homeostasis. Finger-prick or earlobe capillary blood can also be used, although it is difficult to obtain in more than small amounts.

Blood glucose concentrations are generally 3.5-6.0moll-1 in healthy fasting adult subjects and seldom rise above 11 mmol l-1 in arterial or 10 mmol l-1 in venous blood, even after a large carbohydrate-rich meal. Glucose and other simple sugars given in solution produce more rapid and greater increases in blood glucose than equal or larger amounts of glucose-yielding carbohydrate taken as part of a solid mixed meal. Conversely, prolonged starvation for as long as several weeks rarely causes the blood glucose concentration to fall below 3 mmol l-1, except in children and adults with metabolic defects associated with impaired gluconeogenesis.

The remarkable ability of the body to regulate the size of the glucose pool under such widely diverse conditions depends mainly on two organs, the liver and the pancreas, although during prolonged starvation the kidneys become important generators of new glucose molecules.

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