Glucose Homeostasis Metabolic Aspects

The blood glucose level of a healthy adult fluctuates between ~70 mg/dl (3.85 mmol/l and ~120 mg/dl (6.6 mmol/ l) postprandially. Beyond a certain blood glucose concentration of between 140 mg/dl and 170 mg/dl (-7.7-9.35 mmol/ l) (depending on the individual), the kidney tubules are no longer capable of reabsorbing the glucose and glucosuria results. Below ~50-70 mg/dl (-2.753.85 mmol/l), the insufficient glucose supply to the CNS causes symptoms of weakness or fatigue. Further lowering may cause seizures, symptoms of shock, and ultimately death.

In the short term, the tightly controlled blood glucose homeostasis is achieved primarily through the effects of insulin and glucagon on the hepatocytes (A). The primary instrument of this homeo-static function is the build-up and breakdown of liver glycogen. Glucose diffuses freely between blood and liver. Postprandially increased glucose levels activate glucokinase in hepatocytes: glucose, now phosphorylated, can no longer exit the cells. This causes a drop in blood glucose—removing the most important stimulant for insulin secretion. In a healthy person, a certain level of insulin, as well as glucagon, is always present. Minor deviations from the blood glucose level control value, however, cause important changes in insu-lin/glucagon ratios. With normal nutrition, about 60 % of the glucose consumed with foods is stored in the liver and later released into the bloodstream through the build-up and subsequent breakdown of glycogen. In the long term, various adaptive mechanisms are used for blood glucose homeostasis, ensuring a minimum use of 4-5 g glucose/h even with carbohydrate-free nutrition (B). Any glucose ingested during the last meal (time 0 hours) is metabolized within a few hours. During this relative high-glucose-supply period, the tissues use glucose exclusively. Subsequent glyco-genolysis in the liver guarantees further stability of glucose levels for the next 12 hours. During this period, however, glucose use by liver, muscles, and fatty tissues is increasingly curtailed. Simultaneously, gluconeogenesis begins in the liver and takes over maintenance of glucose supply after the glycogen storage is exhausted. After 1-2 days without carbohydrate intake, gluconeo-genetic activity decreases. This is a consequence of a metabolic shift in all tissues: increasingly, free fatty acids are used as energy supply, minimizing glucose use. After a few days, even the brain begins to at least partially use ketone bodies for energy (ketosis).

Prolonged survival without carbohydrate intake is, therefore, possible through synthesis of glucose from proteins (gluconeogenesis) and simultaneous reduction of glucose use in the tissues. The proteins used for these metabolic pathways may either come from ingested foods or from body proteins, predominantly muscle. Modern high-protein weight loss diets aim at reducing appetite through induction of ketosis through extreme restriction of carbohydrate intake. Potential side-effects of sustained ketosis are non-specific symptoms like fatigue and disturbances of the gastrointestinal system. Kidney and bile stones as well as loss of bone mass have also been reported. Such extreme ketogenic diets have been used for many years for the treatment of childhood epilepsy, albeit under strict medical supervision.

Metabolic Aspects 67

• A. Glucose Homeostasis—Short-Term

Blood glucose level

Glucosuria -

Blood glucose level control value 100 mg/dl

Insulin

Glycogen synthesis Glycogen breakdown

Glucagon

External disturbance

Blood glucose

Glycogen synthesis Glycogen breakdown

Blood glucose

0 30

0 30

External disturbance

Positive (^J Negative Deviation setoff

. Five Phases of Glucose Homeostasis

Exocrine glandular tissue

B cells (insulin)

- Blood vessel (capillary)

1 1 1

1 1 1

1 1

II

1

Exocrine glandular tissue

B cells (insulin)

- Blood vessel (capillary)

Homeostasis Large Intestine
  • D cells
  • gt; (somatostatin)

A cells (glucagon)

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Supplements For Diabetics

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