Biological Chemistry - Berezov T. T., Korovkin B. F. 1998

Lipid Metabolism
Regulation of Lipid Metabolism

Lipid METABOLISM is regulated by the Central Nervous system. The Cerebral Cortex exerts a trophic influence on adipose tissue either through lower centers of the central nervous system—specifically the sympathetic and parasympathetic systems—or via Endocrine glands. Currently, A number of biochemical mechanisms underlying the Action of Hormones on lipid metabolism have been established.

It is well known that prolonged negative emotional stress, accompanied by an increased release of catecholamines into the bloodstream, can cause marked weight loss. It is worth recalling that Adipose tissue is richly innervated by sympathetic nerve fibers; excitation of these fibers leads to the release of norepinephrine directly into the adipose tissue. Adrenaline and noradrenaline accelerate The rate of lipolysis in adipose tissue, which enhances the mobilization of Fatty acids from fat depots and increases the level of non-esterified fatty acids in Blood Plasma. As noted previously, tissue lipases (triglyceride lipase) exist in two interconvertible forms: one is phosphorylated and catalytically active, while the other is dephosphorylated and inactive. Adrenaline stimulates cAMP synthesis via adenylate cyclase. In turn, cAMP activates the corresponding protein kinase, which promotes the phosphorylation of lipase, i.e., The formation of its active form. It should be noted that The Effect of Glucagon on the lipolytic system is similar to that of catecholamines.

There is no doubt that secretions from the anterior pituitary, particularly Growth Hormone (somatotropic hormone), influence lipid metabolism. Hypofunction of the gland leads to fat accumulation in the body, resulting in pituitary obesity. Conversely, increased production of growth hormone stimulates lipolysis, and plasma fatty acid levels rise. It has been proven that growth hormone-stimulated lipolysis is blocked by mRNA synthesis inhibitors. Furthermore, the effect of growth hormone on lipolysis is known to feature a lag phase of about 1 hour, whereas adrenaline stimulates lipolysis almost instantly. In other words, it can be concluded that the primary action of these Two Types of hormones on lipolysis occurs via different pathways: adrenaline stimulates adenylate cyclase activity, whereas growth hormone induces the synthesis of this enzyme. The exact mechanism by which growth hormone selectively increases adenylate cyclase synthesis remains unknown.

Insulin exerts an effect on lipolysis and fatty acid mobilization that is opposite to that of adrenaline and glucagon. It has recently been demonstrated that insulin stimulates phosphodiesterase activity in adipose tissue. Phosphodiesterase plays a crucial role in maintaining a constant level of cAMP in Tissues; therefore, an increase in insulin levels should enhance phosphodiesterase activity, which in turn leads to a decrease in intracellular cAMP concentration and, consequently, to a reduction in the Formation of the active form of lipase.

Undoubtedly, Other Hormones, particularly thyroxine and Sex Hormones, also affect lipid metabolism. For example, it is known that the removal of Gonads (castration) causes excessive fat accumulation in animals. However, available data do not yet provide a sufficient basis to speak with certainty about the specific mechanism of their action on lipid metabolism. Table 11.2 summarizes data on The Influence of various factors on the mobilization of fatty acids from fat depots.

Class="center">Table 11.2. The influence of certain factors on the mobilization of fatty acids from adipose tissue (after A.N. Klimov et al., 1978)