Figure 23.4 shows how blood glucose levels are maintained in the body under varying dietary conditions.

Blood glucose increases shortly after a carbohydrate-containing meal, which stimulates the secretion of insulin and suppresses the secretion of glucagon, in order to remove glucose from the blood. These effects promote the uptake of glucose into the liver, stimulate glycogen synthesis, and suppress glycogen breakdown. Activation of acetyl-CoA carboxylase in the liver stimulates fatty acid synthesis, with subsequent transport to adipose tissue as triacylglycerols in very low-density lipoproteins. There, increased levels of glycolytic intermediates and fatty acids stimulate triacylglycerol synthesis. Finally, increased glucose uptake into muscle increases levels of substrates for glycogen synthesis in that tissue as well.

Several hours later, when dietary glucose is not available, the above events are reversed in order to elevate blood glucose levels. Insulin secretion slows, and glucagon secretion increases. This promotes glycogen breakdown in liver via the cAMP-dependent cascade mechanisms that activate glycogen phosphorylase and inactivate glycogen synthase. Triacylglycerol breakdown in adipocytes is activated as well, via the action of hormone-sensitive lipase, generating fatty acids for use as fuel by liver and muscle. At the same time, the decrease in insulin levels reduces glucose use by muscle, liver, and adipose tissue. Consequently, nearly all the glucose produced in the liver is exported to the blood and is available for use by the brain.