Page 98 - Small Animal Clinical Nutrition 5th Edition

98 Small Animal Clinical Nutrition

Dogs, but not cats, are able to elongate and desaturate linoleic
VetBooks.ir Box 5-10. Lipoprotein Lipase. acid to form arachidonic acid (MacDonald et al, 1984b, 1984c;
McLean and Monger, 1989). Thus, linoleic acid is usually list-
Lipoprotein lipase is an enzyme that hydrolyzes triglycerides
ed as an EFA for dogs, whereas, both linoleic acid and arachi-
into nonesterified fatty acids (NEFA) and glycerol. Lipoprotein
lipase is located within the cell and is under hormonal control, donic acid are EFAs for cats. The omega-6 fatty acid family is
specifically insulin. In its inactive state, lipoprotein lipase lies required for growth, reproduction and precursors of eicosanoid
underneath the cell membranes that surround blood vessels. It and prostaglandin synthesis.
is attached to the inner surface of the cell via a rope-like pro- Members of the omega-3 family include α-linolenic
tein connection. Under the influence of insulin, this connection (18:3n-3), eicosapentaenoic (20:5n-3) (EPA) and docosa-
is loosened and the lipoprotein lipase is allowed to “float” to the hexaenoic (22:6n-3) acids (DHA). The omega-3 fatty acid
cell surface where it can hydrolyze triglycerides in lipoproteins. family, especially 22:6n-3, is required for brain and retinal
Apo-CII is required as a coenzyme for lipoprotein lipase. The function (Neuringer et al, 1984; Arbuckle and Innis, 1992).
resulting NEFA diffuse into the cell for metabolism and glycerol Both fatty acid families contribute to cell membrane fluidity
is transported back to the liver for metabolism. Some lines of
domestic cats have a genetic defect that results in absence of and skin health. Processing EFA in pet foods may affect their
lipoprotein lipase activity. biologic activity (Box 5-8). Table 5-19 summarizes the fami-
lies, common names and biologic uses of several fatty acids
found in nature.

Lipid Metabolism
Box 5-11. Good and Bad Cholesterol. GI Handling of Dietary Lipid
Lipids in foods include triglycerides, phospholipids, choles-
High-density lipoprotein (HDL) is the smallest of the lipoprotein
molecules and is synthesized primarily in the liver and to a less- terol, cholesteryl esters and fat-soluble vitamins. Long-chain
er degree in enterocytes. HDL is involved in reverse cholesterol NEFA make up a very small percentage of dietary lipids and
transport. HDL transfers free cholesterol from cell membranes will not be discussed here. Dogs and cats digest dietary lipids
to the HDL molecule as cholesterol esters via an enzyme efficiently, with apparent lipid digestibility normally ranging
lecithin: cholesterol acyl transferase.The cholesterol esters may between 80 and 95%. Increased levels of saturated and trans
be transferred to very low-density lipoproteins (VLDL) by cho- fatty acids reduce lipid digestibility (Box 5-8).
lesterol ester transfer protein to eventually form low-density Fats and oils must undergo digestion via enzymatic and phys-
lipoprotein (LDL), which provides cholesterol to peripheral cells. ical processes before they can be absorbed from the lumen of the
Alternatively, the cholesterol esters may be delivered to the liver gut. The following steps are involved in lipid digestion, absorp-
in HDL for excretion as bile salts. Because HDL is capable of tion and initial metabolism (Figure 5-19) (Brody, 1994a):
transporting cholesterol from the periphery to the liver for dis-
posal, it is said to contain “good cholesterol.” LDL, on the other • Gastric lipase in the stomach and duodenum degrades
hand, is said to contain “bad cholesterol” because it transports triglycerides of intact lipid micelles.
cholesterol to the periphery where excess may result in arterial • Bile salts emulsify lipid micelles to form mixed micelles and
plaque and cardiovascular disease. coactivate pancreatic lipase.
• Pancreatic lipase and colipase hydrolyze triglycerides in
mixed micelles.
• Gastric and pancreatic lipase activity results in 2-monoacyl-
omega-9 family. The omega-3 and omega-6 fatty acid families glyceride + two NEFA.
are EFA because they cannot be synthesized de novo in mam- • NEFA and 2-monacylglyceride are absorbed into entero-
mals; lack of EFA in foods results in suboptimal physiologic cytes.
activity (MacDonald et al, 1984a). Mammals are capable of de • Triglycerides are reformed in enterocytes from long-chain
novo synthesis of saturated fatty acids and fatty acids of the NEFA and 2-monoacylglyceride.
omega-9 series up to 18 carbons (McGarry, 1986). • Apolipoproteins + triglycerides + cholesterol form chylomi-
Subsequently, mammals may elongate and desaturate de novo crons in enterocytes and enter lymphatics.
or dietary fatty acids of all classes via enzymes specific for cer- • Chylomicrons in lymphatics enter the general circulation
tain carbons in the hydrocarbon chain (Figure 5-19). However, via the thoracic duct.
mammals cannot desaturate fatty acids between the n-1 carbon • Chylomicrons are partially metabolized and remnants
and the n-3, n-6 or n-9 double bond. Because of the specifici- attach to liver receptors.
ty of these enzyme systems, unsaturated fatty acids cannot be Triglyceride-containing medium-chain fatty acids undergo
converted between families (e.g., omega-6 or omega-9 to similar processing until they enter the enterocyte at which point
omega-3). Also, because of limitations and specificity in metab- they are not re-esterified, but transported via albumin directly
olism, monounsaturated and saturated fatty acids cannot be to the liver for metabolism (Box-5-9).
converted to EFA (e.g., omega-9 or stearate to omega-6). Short-chain fatty acids (particularly butyrate) resulting from
Members of the omega-6 family include linoleic acid (18:2n- fiber fermentation in the large intestine are an important source
6), γ-linolenic acid (18:3n-6) and arachidonic acid (20:4n-6). of fuel for colonocytes. Excess short-chain fatty acids enter the