Hormonal Regulation of Fuel Metabolism:- Insulin Counters High Blood Glucose
Insulin stimulates glucose uptake by muscle and adipose tissue (Table 23–3), where the glucose is converted to glucose 6-phosphate. In the liver, insulin also activates glycogen synthase and inactivates glycogen phosphory lase, so that much of the glucose 6-phosphate is channeled into glycogen. Insulin also stimulates the storage of excess fuel as fat (Fig. 1). In the liver, insulin activates both the oxidation of glucose 6-phosphate to pyruvate via glycolysis and the oxidation of pyruvate to acetyl-CoA. If not oxidized further for energy production, this acetyl CoA is used for fatty acid synthesis in the liver, and the fatty acids are exported as the TAGs of plasma lipoproteins (VLDLs) to the adipose tissue. Insulin stimulates TAG synthesis in adipocytes, from fatty acids released from the VLDL triacylglycerols. These fatty acids are ultimately derived from the excess glucose taken up from the blood by the liver. In summary, the effect of insulin is to favor the conversion of excess blood glucose to two storage forms: glycogen (in the liver and muscle) and triacylglycerols (in adipose tissue) (Table 23–3).
FIGURE 1 The well-fed state: the lipogenic liver. Immediately after a calorie-rich meal, glucose, fatty acids, and amino acids enter the liver. Insulin released in response to the high blood glucose concentration stimulates glucose uptake by the tissues. Some glucose is exported to the brain for its energetic needs, and some to fat and muscle tissue. In the liver, excess glucose is oxidized to acetyl-CoA, which is used to synthesize fatty acids for export as triacylglycerols in VLDLs to fat and muscle tissue. The NADPH necessary for lipid synthesis is obtained by oxidation of glucose in the pentose phosphate pathway. Excess amino acids are converted to pyruvate and acetyl CoA, which are also used for lipid synthesis. Dietary fats move via the lymphatic system, as chylomicrons, from the intestine to muscle and fat tissues.
