The key peripheral tissues whose metabolic activities affect glucose homeostasis are the liver, muscle, adipose tissue, and kidney. These tissues play different roles in blood-glucose regulation in the fed and resting postabsorptive states, as well as during extended periods of fasting (1). Depending on the nutrient and the nutritional status, nutrients are processed primarily to provide the body's energy needs and to replenish or augment body stores of glycogen and fat. In the fed state, excess amino acids not utilized for proteins synthesis are preferentially catabolized over glucose and fat for energy, because there are no significant storage sites for amino acids and proteins, while an accumulation of nitrogen products results in toxicity in the body. During fasting, the adipose tissue, muscle, liver, and kidneys work in different capacities to supply, convert, or conserve metabolic fuel for the body (1). In the resting, postabsorptive state, blood-glucose homeostasis is achieved by balanced contributions from glycogenolysis by the liver and lipolysis by the adipose tissue. If fasting is continued, proteolysis in the muscle ensues to supply glycogenic amino acids for gluconeogenesis in the liver and kidneys (1, 2). In periods of starvation, defined as three or more days of fasting, the body strives to conserve protein and to obtain greater supplies of its energy needs from alternative metabolic fuels, primarily fatty acids and ketone bodies. Under these circumstances, the ability of the kidneys to preserve ketone bodies prevents the loss of this valuable energy source, and the delicate interplay among these key tissues in the regulation of energy needs permits survival for extended periods of caloric deprivation (1).
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