section 22.6
Lipid Homeostasis
and export are stimulated by insulin and glucose and in-
hibited by catecholamines. Mammary gland lipoprotein
lipase activity is elevated maximally at parturition when
lipid is needed for milk formation. Cardiac lipoprotein li-
pase is elevated during starvation. The lipoproteins trans-
port triacylglycerol and cholesterol (Chapter 20).
Production of Triacylglycerol from Carbohydrate
Processes involved in triacylglycerol storage are presented
in Figure 22-18. When dietary carbohydrate exceeds re-
quirements, it is converted into triacylglycerol within
adipocytes or hepatocytes. The liver daily synthesizes
40-100 g of triacylglycerols, partly from glucose and
partly from free fatty acids present in excess of its energy
needs. Their transport to adipocytes occurs via VLDLs,
whose synthesis, secretion, and fate are analogous to those
of chylomicrons.
Release of Lipid from Adipose Tissue Stores
During fasting or exercise and at times of stress, lipid
is used as a source of energy. Hormone-sensitive lipase
catalyzes the sequential hydrolysis of triacylglycerol to
T A B L E 2 2 -3
Hormonal Regulation o f Adipocyte Lipolysis
Growth hormone
Prostaglandin E ,
yield ultimately 3 mol of fatty acids and 1 mol of glycerol.
Hormone-sensitive lipase is regulated by phosphorylation
by cAMP-dependent protein kinase. Listed in Table 22-3
are hormones that affect lipase. Epinephrine, glucagon,
and the other rapid stimulators release free fatty acids
within minutes. The actions of growth hormone and of
glucocorticoids require hours, but their sites of action are
unknown. Insulin and prostaglandin Ei suppress lipolysis
by depressing cAMP levels.
The major activities of adipocytes are summarized in
Figure 22-19. Glucagon, an indicator of the need for
F I G U R E 2 2 - 1 9
Regulation of adipocyte triacylglycerol synthesis and degradation. FA, Fatty acid; PDE, phosphodiesterase.
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