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and release of glucose by the liver, rate of uptake of glucose by peripheral
tissue, and rate of loss and synthesis by the kidney ( Nordlie, Foster, &
Lange, 1999 ). The apparent blood glucose concentration is therefore depen-
dent upon all these factors ( Fig. 1.1 ) .
In the fasted and postabsorptive states, blood glucose homeostasis is
maintained by the regulation of hepatic and renal glucose production and
the amount of glucose taken up predominantly by noninsulin-dependent
tissue (nervous system, red blood cells, skin, smooth muscles, etc.)
( Cherrington, 1999 ) . In the postprandial state, glucose homeostasis is
maintained by controlling the rate of glucose appearance from the digestive
system and the uptake by noninsulin-dependent tissue, peripheral tissue
(skeletal muscle and adipocytes), kidney, and the liver. In the postprandial
hyperglycemic state, hepatic production ceases and tissues exclusively utilize
glucose derived from food ( Moore, Cherrington, &Wasserman, 2003 ) . The
appearance of glucose in the blood is from either exogenous (digestion of
food and absorption) or endogenous (liver and kidney) sources ( Corssmit,
Romijn, & Sauerwein, 2001; Stumvoll et al., 1995 ). The principle
+
Glucagon/adrenal hormones
Insulin/incretins
-
+
-
Brain and nervous system
Liver
Glycolysis and
gluconeogenesis
Energy
Red blood cells
Plasma glucose
concentration
Kidney
Liver
Gluconeogenesis
4-6 mmol/L
Adipose tissue
Storage
and
energy
Glucose
from food
Skeletal muscle
Disposal and
energy
Digestion and absorption
Kidney
Food intake
Figure 1.1 A graphical representation of glucose homeostasis.
 
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