Page 269 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

!
surface of TGs and VLDL activates LPL. The in- the upper part of the small intestine (! B,
sulin secreted after a meal induces LPL (! D), bottom). Mucosal cells contain an enzyme that
which promotes the rapid degradation of reab- re-esterifies part of the absorbed CHO: ACAT
sorbed dietary TGs. LPL is also activated by he- (acyl-CoA-cholesterol acyltransferase) so that
parin (from endothelial tissue, mast cells, etc.), both cholesterol and CHO-esters can be inte-
which helps to eliminate the chylomicrons in grated in chylomicrons (! A). CHO and CHO-
cloudy plasma; it therefore is called a clearance esters in the chylomicron remnants (see above)
factor. Albumin-complexed FFAs in plasma are are transported to the liver, where lysosomal
mainly transported to the following target acid lipases again break the CHO-esters down
sites (! D): into CHO. This CHO and that taken up from
! Cardiac muscle, skeletal muscle, kidneys and other sources (LDL, HDL) leave the liver (! B):
other organs, where they are oxidized to CO 2 1. by excretion into the bile (! p. 248), 2. by
Nutrition and Digestion or use them to synthesize TG. When energy re- VLDL, the hepatic lipoprotein for export of
and H 2O in the mitochondria (! oxidation) and
conversion into bile salts which also enter the
bile (! p. 249 B), and 3. by incorporation into
used as a source of energy.
! Fat cells (! D), which either store the FFAs
lipids to other tissues. Under the influence of
quirements increase or intake decreases, the
LPL (see above), the VLDL yield IDL and later
LDL (! B, left). The LDL transport CHO and
FFAs are cleaved from triacylglycerol in the fat
CHO-esters to cells with LDL receptors (he-
cells (lipolysis) and transported to the area
where they are needed (! D). Lipolysis is
ceptor density on the cell surface is adjusted
stimulated by epinephrine, glucagon and corti-
according to the prevailing CHO requirement.
10 sol and inhibited by insulin (! p. 282ff.). patic and extrahepatic cells; ! B, top). The re-
Like hepatic cells (see above) extrahepatic cells
! The liver, where the FFAs are oxidized or
used to synthesize TG. take up the LDL by receptor-mediated endocy-
tosis, and lysosomal acid lipases reduce CHO-
Cholesterol (CHO) esters to CHO (! B, top right). The cells can
Cholesterol esters (CHO-esters), like TGs, are then insert the CHO in their cell membranes or
apolar lipids. In the watery milieu of the body, use it for steroid synthesis. A cholesterol excess
they can only be transported when incor- leads to (a) inhibition of CHO synthesis in the
porated in lipoproteins (or bound to proteins) cells (3-HMG-CoA-reductase) and (b) activa-
and can be used for metabolism only after they tion of ACAT, an enzyme that esterifies and
have been converted to CHO, which is more stores CHO in the form of its ester (see above).
polar (! B). CHO-esters serve as stores and in Hyperlipoproteinemia. An excess of lipids in the
some cases the transported form of CHO. CHO- blood can be reflected by elevation of triacylglycerol
esters are present in all lipoproteins, but are levels and/or CHO levels (! 200–220 mg/dL serum;
most abundant (42%) in LDL (! A). affects about one in five adults in Western countries).
Cholesterol is an important constituent of In the most severe form, familial hypercholesterole-
cell membranes (! p. 14). Moreover, it is a pre- mia, a genetic defect causes elevated plasma CHO
cursor for bile salts (! B and p. 248), vitamin D concentrations from birth on, which can result in
(! p. 292), and steroid hormones (! p. 294ff.). myocardial infarction in juvenile age. The disease is
Each day ca. 0.6 g of CHO is lost in the feces (re- caused by genetic defects of the high-affinity LDL re-
ceptors. The serum CHO level rises since the cells
duced to coprosterol) and sloughed off skin. take up smaller quantities of cholesterol-rich LDLs.
The bile salt loss amounts to about 0.5 g/day. Extrahepatic tissues synthesize larger quantities of
These losses (minus the dietary CHO intake) CHO because 3-HMG-CoA-reductase fails to inhibit
must be compensated for by continuous re- CHO synthesis due to the decreased absorption of
synthesis of CHO in the intestinal tract and LDLs. As a result, more LDLs bind to the low-affinity
liver (! B). CHO supplied by the diet is ab- scavenger receptors that mediate the storage of CHO
sorbed in part as such and in part in esterified in macrophages, cutaneous tissues, and blood ves-
sels. Hypercholesterolemia therefore increases the
form (! B, lower right). Before it is reabsorbed, risk of arteriosclerosis and coronary disease.
CHO-esters are split by unspecific pancreatic
256 carboxylesterase to CHO, which is absorbed in
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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