500

chapter

22

Metabolic Homeostasis

F I G U R E 2 2 -1 1

Disposition of high glucose intake. FA, Fatty acid; TG, triacylglycerol; VLDL, very-low-density lipoprotein; LDL,

low-density lipoprotein.

of glucose, initially derived from hepatic glycogenolysis

but with an ever-increasing contribution from gluconeo-

genesis.

Utilization of Hepatic Glycogen

The signal for glycogen breakdown is glucagon secreted

in

response

to

hypoglycemia.

Glucagon

stimulates

hepatic glycogenolysis by the adenylate cyclase cascade

(Figure 22-13). The hepatic plasma membrane is markedly

sensitive to glucagon, which stimulates adenylate cyclase

with formation of cAMP, activation of phosphorylase

kinase and phosphorylase, and degradation of glycogen

to glucose-

1

-phosphate, then to glucose-

6

-phosphate, and

finally to blood glucose. In hypoglycemia, insulin levels

are low, and no hepatic glycogen synthesis occurs. Thus,

F I G U R E 2 2 - 1 2

Typical glucose tolerance response for a normal individual and one with

mild glucose intolerance. The shaded area shows the range for plasma

glucose levels in normal fasting individuals. At the peak value, the level for

a glucose-intolerant individual often is not significantly different from that

of a normal individual; thus, intolerance is best detected at the later time

points when glucose values remain higher.