LIPID METABOLISM

1. LIPID STRUCTURE AND STORAGE

Triglycerides (also called ‘triacylglycerols’) are energy-storage molecules, consisting of

three fatty acids esterified to a glycerol backbone. Triglycerides can be hydrolysed to produce
fatty acids, which then undergo β-oxidation and produce acetyl-CoA units that enter the citric
acid cycle to produce ATP. The glycerol released when triglycerides are hydrolysed can also
enter the glycolysis pathway to produce ATP, or can undergo gluconeogenesis. Other lipids
include cholesterol (an important component of membranes and lipoproteins), phospholipids
(membrane structural lipids), and various other molecules that can be dissolved in organic
solvents and thus qualify as ‘lipids’.

a) Triglycerides stored in reptiles

 In Adiposa Tissues
Like other vertebrates, reptiles store triglycerides in specialised storage
locations called adipose tissue, which is primarily composed of adipocytes.
Adipose tissue can be diffusely located in the body, for example between muscle
fibres resulting in the ‘marbled ’ appearance of meat (Kwan , 1994 ). Many
reptiles have paired abdominal ‘fat bodies’ (corpora adiposa) that serve at the
primary location for fat storage in adipose tissue. These are often well developed
in snakes and lizards, although there are lepidosaur species that lack abdominal
fat bodies , including tuatara (Sphenodon punctatus ), a number of skinks , and a
few geckos.
Fat storage is the principal function of the tail in some species, and the
importance of this function is likely increased following tail autotomy and
regeneration. Some lizards rely on the fat stores of the tail during hibernation,
starvation, and reproduction. Many turtles do not have discrete abdominal fat
bodies, but instead have many small fat deposits throughout the abdominal
cavity.

 Muscle and Liver

Muscle stores lipid in the form of an intramuscular triglyceride droplet. This is
generally small, and presumably is used only for short-term energy demands to
supplement extramuscular sources of triglycerides. The liver is a major lipid-
processing organ, and also stores some triglyceride. Several studies have found
the reptile liver to carry only about 5% of total body lipids. Fat bodies, by
contrast, may carry the great majority of body lipids (>70%), particularly in
snakes.

b)Seasonal changes in fat stores in reptiles

Like many other vertebrates, most reptiles undergo seasonal variation in the
quantity of stored lipids. One important use of stored lipids is for maintenance
 during a winter dormancy state, during which animals are aphagic; lipid stores are
often deposited prior to dormancy. These lipid stores then decline during winter
dormancy, particularly in the fat bodies. When lipids stored in the fat bodies decline
over a winter dormancy period, it can often be difficult to distinguish between their
use for winter maintenance and their use for reproduction, because many reptiles
deposit lipids into ovarian follicles prior to and/or during winter dormancy/aphagia.
Lipids were not deposited into follicles until after the spring nadir in lipid stores,
demonstrating that stored lipids were used for winter maintenance. Many studies
have suggested that reproduction is the primary function of lipid storage in reptiles.
The lipids of the liver may decline simultaneously with the decline in fat-body
lipids, as is the case in several lizards Often, however, the liver increases in mass
and/or lipid content, at least at the beginning of vitellogenesis.

2. Lipid Transport
Due to their hydrophobic nature, lipids generally need carriers (both intracellular and
extracellular) to aid solubility and transport in aqueous media. Two major routes of transport in
the plasma are: (i) as non-esterified fatty acids (NEFAs; also called ‘free fatty acids’) that are
bound to albumin, a major circulating plasma protein; and (ii) as triglycerides packaged in
lipoproteins. Adipose tissue mobilises fat by exporting NEFAs to the plasma. Triglycerides that
are stored in adipocytes are first hydrolysed, and the fatty acids and glycerol can then be
exported from the cell.
Glycerol is water soluble and needs no blood-borne transport protein; after lipolysis,
glycerol may be transported to the liver for gluconeogenesis. NEFAs bind to circulating albumin,
and are thus made more soluble for transport in the plasma. Albumin-bound NEFAs are then
free to travel to other tissues where the fatty acids can be taken up for oxidation (e.g. muscle)
or modification (e.g. liver). The liver and the intestine export triglyceride contained in
lipoproteins. These lipoprotein particles are secreted by the liver for transport to other tissues
via the blood.

a. Strucure of Lipoprotein
Lipoproteins are aggregates that have a neutral lipid core composed of triglycerides and
cholesterol esters, and have a surface covered with amphipathic molecules such as
phospholipids, cholesterol, and proteins called ‘apolipoproteins’. They are usually
categorised by their density characteristics, i.e. very-low-density lipoproteins (VLDLs),
intermediate-density lipoproteins (IDLs), low-density lipoproteins (LDLs) and high-density
lipoproteins (HDLs). thus, VLDLs are large and heavily laden with triglycerides, while LDLs
are smaller particles carrying less triglyceride. Lipoproteins are also characterised by their
apolipoproteins, which mediate interactions between the lipoprotein particle and
receptors, lipases, and other molecules in the body.
HDLs have cholesterol transport as a principal function, although they are also
important for passing certain apolipoproteins to other types of particles. VLDLs, IDLs, and
 LDLs form a continuum of particles that have the function of transporting triglycerides.
VLDLs are produced by the liver and carry triglycerides to peripheral tissues. As
triglycerides are lost from the VLDLs in the periphery through the action of lipoprotein
lipase (LPL), the particles increase in density, resulting in IDLs; further lipolysis and loss of
triglycerides causes the IDLs to become LDLs, which can then be taken up and degraded by
the liver.
3. Lipid Metabolism During Feeding
Following feeding, macronutrients (fat, carbohydrates, protein) are digested to
monomers and are absorbed by the intestine. After absorption, carbohydrates and amino
acids reach the blood and are transported to the liver via the hepatic portal vein. Dietary
triglycerides are hydrolysed in the intestine by pancreatic lipase to produce NEFAs and
monoacylglycerol, and these components are then absorbed by enterocytes. Fatty acids
and monoacylglycerol are re-esterified inside enterocytes to produce triglycerides.
Triglyceride is then exported from enterocytes by one of several known routes. This loss of
triglycerides turns chylomicrons into chylomicron remnants, which are then taken up and
metabolized by the liver or recycled by enterocytes.
‘enteromicron’ (represent any lipoprotein particle ) (i.e. chylo- or portomicrons or
VLDLs) that exports triglycerides from, and arises in, the intestine. Enteromicrons likely
donate some or most of their triglycerides to peripheral tissues and become enteromicron
remnants, before uptake by the liver. The liver is a central nutrient-processing organ, and
once there, nutrients can have many fates. Excess amino acids can be broken down by the
amino transferase and deamination pathways, resulting in the production of oxaloacetate
or pyruvate. These intermediates can then undergo gluconeogenesis, or be used to
produce acetyl CoA, which can be oxidised or used to synthesise lipids by fatty acid
synthase. Similarly, excess glucose can be exported to other tissues, converted to glycogen
and stored in the liver, or it can be converted to fatty acids via production of acetyl CoA and
fatty acid synthase. Thus, all the major macronutrients can be converted to triglycerides for
storage. Although some triglycerides can be stored in the liver, most are exported to be
stored in adipose tissue.
Triglycerides are transported from the liver via VLDLs. These particles are secreted by
the liver into the blood plasma. The capillaries of target tissues (e.g. muscle or adipose )
have the enzyme LPL attached to the vascular endothelium.These LPLs are able to reach
into the lipoprotein core and interact with triglycerides. There , they hydrolyse triglyceride
such that fatty acids can then be released by the VLDL and taken up by the target tissue . In
adipocytes , fatty acids are re-esteri fied to form triglyceride , but require glycerol -3-
phosphate for this reaction, and therefore cannot use glycerol from the plasma. Instead ,
glycerol-3-phosphate is derived from glycolysis (or other carbon sources via the
glyceroneogenic pathway; and can represent a major pathway by which glucose is
incorporated into lipids.

Plasma metabolites during feeding in reptiles

 Following absorption by enterocytes , non-esterified fatty acids (NEFAs) and glycerol
are re-esterified and exported from the intestine as triglycerides (TRIG).These are
transported in chylomicrons (CM) deposited into the lymph, or possibly as portomicrons
(PM) deposited directly into the hepatic portal vein. Some NEFAs may also remain un-
esterified and pass directly to circulating albumin for transport in blood plasma . Dietary
glucose and amino acids are absorbed directly into the blood, but may undergo lipogenesis
in the liver. The export product of hepatic lipogenesis is triglyceride packaged in very-low-
density lipoprotein (VLDL) particles. Plasma triglycerides – whether packaged in
chylomicrons, portomicrons, or VLDLs – are taken up in peripheral tissues such as adipose
or muscle tissue via the action of lipoprotein lipase (LPL) in the vascular endothelium,
which cleaves triglycerides into NEFAs and glycerol. The NEFAs taken up by peripheral
tissues may be re-esterified to triglyceride forstorage, or can undergo oxidation.The
glycerolreleased can be transported back to the liver(not shown).

LIPID METABOLISM DURING FASTING

During fasting, energetic demand must be supplied by stored nutrients. This might take
the During fasting, energetic demand must be supplied by stored nutrients. This might take the
form of glucose liberated from glycogen stored in liver or muscles. It could instead take the
form of triglycerides, exported from the liver in VLDL, or hydrolysed from intramuscular fat
droplets.
And the Triglycerides (TRIG) can mobilised from adipocyte lipid droplets via enzymatic
hydrolysis to glycerol and non-esterified fatty acids (NEFAs). Both are exported to the blood
plasma, where NEFAs are carried bound to circulating albumin. NEFAs can travel directly to
sites of oxidation (e.g. muscles), or be taken up by the liver. In the liver, NEFAs may be
transformed to ketone bodies, including β-hydroxybutyrate (BUTY), which can be used by some
tissues as a substitute for glucose.Finally, energy can be supplied to tissues from NEFAs that are
mobilised from adipocytes Glycerol can also be taken up by the liver and undergo
gluconeogenesis to maintain glucose levels. The liver also has the potential to export
triglycerides [packaged in very-low-density lipoproteins (VLDLs)] for delivery to energy-
demanding tissues, although it is unclear whether reptiles use this process during fasting.
Nutrient conversions are important during fasting, particularly because some tissues (e.g.
brain) rely heavily on glucose. Although glucose cannot be produced through gluconeogenesis
from fatty acids, fatty acids can be converted to ketone bodies such as β-hydroxybutyrate in the
liver, and these ketone bodies can be used as glucose substitutes by the central nervous system
. Thus, ketone bodies serve to prevent loss of liver glycogen during long-term fasting.

REFERENCE
Price,Edwin R.2016. The Physiology of Lipid Storage and use in Reptil.Denton,United
State of America. Biological Reviews