20. ANALYTE NORMAL VALUE
Total plasma lipids 400-600mg/dl
Total cholesterol 140-200mg/dl
HDL cholesterol 40–60 mg/dL
LDL cholesterol 80-130mg/dl
Triglycerides 50-150mg/dl
28. • PGA Keto group at C9; double bond C10 and 11
• PGB Keto group at C9; double bond C8 and 12
• PGD OH group at C9; keto group at C11
• PGE Keto group at C9; OH group at C11
• PGF OH groups at C9 and C11 (Fig.14.2)
• PGG Two oxygen atoms, interconnected to each
• other, and bonded at C9 and C11;
• hydroperoxide group at C15
• PGH Same ring as PGG; but C15 has OH group
• PGI Double ring. Oxygen attached to C6 and
• C9, to form another 5-membered ring.
• Hence called prostacyclin.
Lipids need to be transported in plasma to tissues and organs to perform their metabolic functions.
Given the hydrophobic nature of the neutral fats (TG and cholesterol esters), lipid transport via plasma would not be possible without some form of hydrophillic adaptation.
The lipids are transported by a series of micelles called lipoproteins, which consist of an outer monolayer of protein (apolipoprotein) and polar lipids (phospholipid and unesterified cholesterol).
The inner core consists of the hydrophobic lipids which is the cholesteryl esters & TAG.
Lipoproteins function both to keep their component lipids soluble as they transport them in the plasma, and also to provide an efficient mechanism for transporting their lipid contents and to (and from) the tissues.
NB. In humans the transport system is less perfect than in other animals, that is why they experience a gradual deposition of lipid especially cholesterol in tissues (atherosclerosis).
Almost all mammalian cells except red blood cells produce
prostaglandins and their related compounds, the
prostacyclins, thromboxanes, leukotrienes and lipoxins,
known collectively as eicosanoids since they are all C20 compounds;
Greek: eikosi, twenty). The eicosanoids, like endocrine
hormones, have profound physiological effects at
extremely low concentrations. For example, they mediate
the following: (1) the inflammatory response, notably as it
involves the joints (rheumatoid arthritis), skin (psoriasis),
and eyes; (2) the production of pain and fever; (3) the regulation
of blood pressure; (4) the induction of blood clotting;
(5) the control of several reproductive functions such
as the induction of labor; and (6) the regulation of the
sleep/wake cycle. The enzymes that synthesize these compounds
and the receptors to which they bind are therefore
the targets of intensive pharmacological research. The eicosanoids are also hormonelike in that they bind to
G-protein-coupled receptors (Section 19-2B), and many of
their effects are intracellularly mediated by cAMP. Unlike
endocrine hormones, however, they are not transported in
the bloodstream to their sites of action. Rather, these
chemically and biologically unstable substances (some decompose
within minutes or less in vitro) are local mediators
(paracrine hormones; Section 19-1); that is, they act in
the same environment in which they are synthesized.
Prostaglandins are all derivatives of the hypothetical C20 fatty acid prostanoic acid in which carbon atoms 8 to 12 form a cyclopentane ring (Fig. 25-66a). Prostaglandins A through I differ in the substituents on the cyclopentane ring (Fig. 25-66b):PGAs are ,-unsaturated ketones,PGEs are-hydroxy ketones, PGFs are 1,3-diols, etc. In PGF, the C9 OH group is on the same side of the ring as R1; it is on the
opposite side in PGF.The numerical subscript in the namerefers to the number of double bonds contained on the side chains of the cyclopentane ring (Fig. 25-66c).
In humans, the most prevalent prostaglandin precursor is
arachidonic acid (5,8,11,14-eicosatetraenoic acid), a C20
polyunsaturated fatty acid that has four nonconjugated double
bonds.The double bond at C14 is six carbon atoms from
the terminal carbon atom (the carbon atom), making
arachidonic acid an –6 fatty acid. As Sune Bergström and
Bengt Samuelsson demonstrated, arachidonic acid is synthesizedsynthesized
from the essential fatty acid linoleic acid (also an
–6 fatty acid). This occurs via its desaturation with a 6-
desaturase to yield -linolenic acid (GLA), followed by
elongation and a second desaturation, this time with a 5-
desaturase (Fig. 25-67; Section 25-4E). Prostaglandins with
the subscript 1 (the “series-1” prostaglandins) are synthesized
from dihomo--linolenic acid (DGLA; 8,11,14-
eicosatrienoic acid), whereas “series-2” prostaglandins are
synthesized from arachidonic acid. -Linolenic acid
(ALA), another essential fatty acid since the 15-desaturase
required for its synthesis occurs only in plants, is a precursor
of 5,8,11,14,17-eicosapentaenoic acid (EPA) and the
“series-3” prostaglandins. Since arachidonate is the primary
prostaglandin precursor in humans, we shall mostly refer to
the series-2 prostaglandins in our examples. Note, however,
that when dietary linoleic acid and -linolenic acid are
equally available, the relative activities of the 5- and 6-
desaturases are important in determining the relative
amounts of these prostaglandin precursors.
Hvon Euler thought that these compounds originated in the
prostate gland (hence their name) but they were later
shown to be synthesized in the seminal vesicles.
