Page 267 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003
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Lipid Distribution and Storage   High-density lipoproteins (HDL) exchange
                                       certain apoproteins with chylomicrons and
       Lipids in the blood are transported in lipo-  VLDL and absorb superfluous CHO from the
       proteins, LPs (! A), which are molecular  extrahepatic cells and blood (! B). With their
       aggregates (microemulsions) with a core of  ApoAI, they activate the plasma enzyme LCAT
       very hydrophobic lipids such as triacylglycerols  (lecithin–cholesterol acyltransferase), which
       (TG) and cholesterol esters (CHO-esters) sur-  is responsible for the partial esterification of
       rounded by a layer of amphipathic lipids  CHO. HDL also deliver cholesterol and CHO-
       (phospholipids, cholesterol). LPs also contain  esters to the liver and steroid hormone-pro-
       several types of proteins, called apolipo-  ducing glands with HDL receptors (ovaries,
       proteins. LPs are differentiated according to  testes, adrenal cortex).
       their size, density, lipid composition, site of  Triacylglycerol (TG)
    Nutrition and Digestion  elements of LPs (e.g. ApoAII and ApoB48), lig-  acids (FFA) and 2-monoacylglycerol (MG) in the
       synthesis, and their apolipoprotein content.
       Apolipoproteins (Apo) function as structural
                                       Dietary TGs are broken down into free fatty
                                       gastrointestinal tract (! C and p. 252). Since
       ands (ApoB100, ApoE, etc.) for LP receptors on
       the membranes of LP target cells, and as
                                       short-chain FFAs are water-soluble, they can
       enzyme activators (e.g. ApoAI and ApoCII).
                                       be absorbed and transported to the liver via
         Chylomicrons transport lipids (mainly tri-
                                       the portal vein. Long-chain FFAs and 2-mono-
       acylglycerol, TG) from the gut to the periphery
                                       re-synthesized to TG in the mucosa cells (! C).
       ! D), where their ApoCII activates endothelial
                                       (The FFAs needed for TG synthesis are carried
    10  (via intestinal lymph and systemic circulation;  acylglycerols are not soluble in water. They are
       lipoprotein lipase (LPL), which cleaves FFA
                                       by FFA-binding proteins from the cell mem-
       from TG. The FFA are mainly absorbed by myo-  brane to their site of synthesis, i.e., the smooth
       cytes and fat cells (! D). With the aid of ApoE,  endoplasmic reticulum.) Since TGs are not
       the chylomicron remnants deliver the rest of  soluble in water, they are subsequently loaded
       their TG, cholesterol and cholesterol ester load  onto chylomicrons, which are exocytosed into
       to the hepatocytes by receptor-mediated en-  the extracellular fluid, then passed on to the
       docytosis (! B, D).             intestinal lymph (thereby by-passing the
         Cholesterol (CHO) and the TG imported  liver), from which they finally reach the
       from the gut and newly synthesized in the liver  greater circulation (! C, D). (Plasma becomes
       are exported inside VLDL (very low density  cloudy for about 20–30 minutes after a fatty
       lipoproteins) from the liver to the periphery,  meal due to its chylomicron content). The liver
       where they by means of their ApoCII also acti-  also synthesizes TGs, thereby taking the re-
       vate LPL, resulting in the release of FFA (! D).  quired FFAs from the plasma or synthesizing
       This results in the loss of ApoCII and exposure  them from glucose. Hepatic TGs are loaded
       of ApoE. VLDL remnants or IDL (intermediate-  onto VLDL (see above) and subsequently
       density lipoproteins) remain. Ca. 50% of the IDL  secreted into the plasma (! D). Since the ex-
       returns to the liver (mainly bound by its ApoE  port capacity of this mechanism is limited, an
       on LDL receptors; see below) and is re-  excess of FFA or glucose (! D) can result in the
       processed and exported from the liver as VLDL  accumulation of TGs in the liver (fatty liver).
       (! B).                           Free fatty acids (FFAs) are high-energy sub-
         The other 50% of the IDL is converted to LDL  strates used for energy metabolism (! p. 228).
       (low density lipoprotein) after coming in con-  Fatty acids circulating in the blood are mainly
       tact with hepatic lipase (resulting in loss of  transported in the form of TG (in lipoproteins)
       ApoE and exposure of ApoB100). Two-thirds of  whereas plasma FFA are complexed with al-
       the LDLs deliver their CHO and CHO-esters to  bumin. Fatty acids are removed from TGs of
       the liver, the other third transfers its CHO to  chylomicrons and VLDL by lipoprotein lipase
       extrahepatic tissue (! B). Binding of ApoB100  (LPL) localized on the luminal surface of the
       to LDL receptors is essential for both processes  capillary endothelium of many organs (mainly
  254  (see below).                    in fat tissue and muscles) (! D). ApoCII on the
                                                                   !
       Despopoulos, Color Atlas of Physiology © 2003 Thieme
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