Adipose Tissuetriacylglycerol

Fatty acids are stored in the body as triacylglycerols (triglyceride) in fat cells which make up the adipose tissue. Fat is also stored in muscle tissue in the form of triglyceride, present in small intramuscular fat droplets. After a meal, fat is absorbed and circulates in the blood as triglycerides in the form of circulating lipid particles (HDL, VLDL, LDL, chylomicrons) or as free fatty acids bound to albumin, called non-esterified fatty acids (NEFA). As with glycogen, the synthesis of fat or its degradation depend on the concentration of the 'building blocks', in this case fatty acids. This concentration is determined mainly by uptake of free fatty acids in and from triacylglycerols and their rate of utilization for energy metabolism.

Thus, when energy production is low, the supply of fatty acids after a meal will lead to an increase in the fatty acid concentration within the cell. This will stimulate esterification and the amount of triacylglycerol within the fat cell will increase. Such a process is mediated by a large number of

Meals-.. .-Body metabolism

Triacylglycerols Glycerol + Fatty acids

Triacylglycerols Glycerol + Fatty acids

Figure 52

interactions, in which hormonal and nervous influences play a major role. In the case of increased energy requirement, fatty acids will be used in energy production. This will result in a decrease in the fatty acid concentration, which will stimulate the breakdown of triacylglycerols into glycerol and free fatty acids to compensate for this.


The process of binding fatty acids (esterification) in the form of triglyceride and their release from it is called the triglyceride/fatty acid cycle. The activity of this cycle is determined by the metabolic need for fatty acids for energy production and by the supply of fatty acids from external sources. The glycerol necessary for esterification is derived from glycolysis.


Free fatty acids are metabolized by aerobic metabolism within the citric acid cycle.

For this chain of metabolic steps, fatty acids are converted to fatty acyl CoA. This can enter the Krebs cycle where it is converted to acetyl coenzyme A. When fat oxidation is high there is increased production of acetyl CoA, which is converted into citrate—the first citric acid cycle intermediate. Acetyl CoA is known to inhibit the conversion of pyruvate to acetyl CoA. Additionally, citrate will inhibit glycolysis. Thus, increased

Figure 53

fatty acid oxidation inhibits both the rate of glycolysis and the first conversion step of pyruvate in the citric acid cycle. As a result, total carbohydrate oxidation will be reduced.

Conversely, increased carbohydrate metabolism, e.g. after intake of oral CHO, inhibits lipolysis, reduces the availability of fatty acids and thus their oxidation. In exercise metabolism these processes of carbohydrate and fat utilization are tightly coupled and controlled by nervous and hormonal mechanisms. They may be influenced by exogenous supply of either carbohydrate or fat, or by substances which stimulate the metabolism of either substrate.

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