Anaerobic
and aerobic oxidation of glucose. Alternative ways of monosaccharide metabolism.
Carbohydrates
have the general molecular formula CH2O, and thus were once thought
to represent "hydrated carbon". However, the arrangement of atoms in
carbohydrates has little to do with water molecules.
Starch
and cellulose are two common carbohydrates. Both are macromolecules with molecular weights in the hundreds of thousands.
Both are polymers (hence "polysaccharides"); that is,
each is built from repeating units, monomers, much as a chain is built from its links.
The
monomers of both starch and cellulose are the same: units of the sugar glucose.
Three common sugars share the same molecular formula:
C6H12O6. Because of their six carbon atoms,
each is a hexose.
They are:
·
glucose,
"blood sugar", the immediate source of energy for cellular respiration
·
galactose, a
sugar in milk (and yogurt), and
·
fructose, a sugar found in honey.
Although
all three share the same molecular formula (C6H12O6),
the arrangement of atoms differs in each case. Substances such as these three,
which have identical molecular formulas but different structural formulas, are
known as structural isomers.
Glucose, galactose, and fructose are "single" sugars or monosaccharides.
Two monosaccharides can be linked together to form a "double" sugar
or disaccharide.
Three common disaccharides:
·
sucrose —
common table sugar = glucose + fructose
·
lactose —
major sugar in milk = glucose + galactose
·
maltose —
product of starch digestion = glucose + glucose
Although the process of linking the two monomers is rather complex, the
end result in each case is the loss of a hydrogen atom (H) from one of the monosaccharides
and a hydroxyl group (OH) from the other. The resulting linkage between the
sugars is called a glycosidic bond. The molecular formula of each of
these disaccharides is
C12H22O11
= 2 C6H12O6 − H2O
All
sugars are very soluble in water because of their many hydroxyl groups. Although not as concentrated a fuel as fats, sugars are the most
important source of energy for many cells.
Carbohydrates provide the bulk of the calories (4 kcal/gram) in most diets, and starches provide
the bulk of that. Starches are polysaccharides.
Starches are polymers of glucose. Two types are found:
·
amylose consists of linear, unbranched chains of several
hundred glucose residues (units). The glucose residues are linked by a
glycosidic bond between their #1 and #4 carbon atoms.
·
amylopectin differs from amylose in being highly branched. At
approximately every thirtieth residue along the chain, a short side chain is
attached by a glycosidic bond to the #6 carbon atom (the carbon above the
ring). The total number of glucose residues in a molecule of amylopectin is
several thousand.
Starches
are insoluble in water and thus can serve as storage depots of glucose. Plants
convert excess glucose into starch for storage. The image shows starch grains
(lightly stained with iodine) in the cells of the white potato. Rice, wheat,
and corn are also major sources of starch in the human diet.
Before starches can enter (or leave) cells, they must be digested.
The hydrolysis of starch is done by amylases. With the aid of an amylase
(such as pancreatic amylase), water molecules enter at the 1 -> 4 linkages,
breaking the chain and eventually producing a mixture of glucose and maltose.
A different amylase is needed to break the 1 -> 6 bonds of amylopectin.
Animals
store excess glucose by polymerizing it to form glycogen. The structure
of glycogen is similar to that of amylopectin, although the branches in
glycogen tend to be shorter and more frequent.
Glycogen
is broken back down into glucose when energy is needed (a process called
glycogenolysis).
In glycogenolysis,
·
phosphate groups — not water — break the 1 -> 4 linkages
·
the phosphate group must then be removed so that glucose can leave the
cell.
The
liver and skeletal muscle are major depots of
glycogen.
There
is some evidence that intense exercise and a high-carbohydrate diet
("carbo-loading") can increase the reserves of glycogen in the
muscles and thus may help marathoners work their muscles somewhat longer and
harder than otherwise. But for most of us, carbo loading leads to increased
deposits of fat.
Cellulose
is probably the single most abundant organic molecule in the biosphere. It is
the major structural material of which plants are made. Wood is largely
cellulose while cotton and paper are almost pure cellulose.
Like starch, cellulose is a polysaccharide with glucose as its monomer. However,
cellulose differs profoundly from starch in its properties.
·
Because of the orientation of the glycosidic bonds linking the glucose residues,
the rings of glucose are arranged in a flip-flop manner. This produces a long,
straight, rigid molecule.
·
There are no side chains in cellulose as there are in starch. The
absence of side chains allows these linear molecules to lie close together.
·
Because of the many -OH groups, as well as the oxygen atom in the ring,
there are many opportunities for hydrogen bonds to form between adjacent chains.
The
result is a series of stiff, elongated fibrils — the perfect material for
building the cell walls of plants.
This
electron micrograph (courtesy of R. D. Preston) shows the cellulose fibrils in
the cell wall of a green alga. These long, rigid fibrils are a clear reflection of
the nature of the cellulose molecules of which they are composed.
Carbohydrates
and Metabolism Chart - Carb Chart
Digestion of Dietary Carbohydrates
Dietary
carbohydrate from which humans gain energy enter the body in complex forms,
such as disaccharides and the polymers starch
(amylose and amylopectin) and glycogen.
The polymer cellulose is also consumed
but not digested. The first step in the metabolism of digestible carbohydrate
is the conversion of the higher polymers to simpler, soluble forms that can be
transported across the intestinal wall and delivered to the tissues. The
breakdown of polymeric sugars begins in the mouth. Saliva has a slightly acidic
pH of 6.8 and contains lingual amylase that begins the digestion of
carbohydrates. The action of lingual amylase is limited to the area of the
mouth and the esophagus; it is virtually inactivated by the much stronger acid
pH of the stomach. Once the food has arrived in the stomach, acid hydrolysis
contributes to its degradation; specific gastric proteases and lipases aid this
process for proteins and fats, respectively. The mixture of gastric secretions,
saliva, and food, known collectively as chyme, moves to the small
intestine.
The main
polymeric-carbohydrate digesting enzyme of the small intestine is -amylase.
This enzyme is secreted by the pancreas and has the same activity as salivary
amylase, producing disaccharides and trisaccharides. The latter are converted
to monosaccharides by intestinal saccharidases, including maltases that
hydrolyze di- and trisaccharides, and the more specific disaccharidases,
sucrase, lactase, and trehalase. The net result is the almost complete
conversion of digestible carbohydrate to its constituent monosaccharides. The
resultant glucose and other simple carbohydrates are transported across the
intestinal wall to the hepatic portal vein and then to liver parenchymal cells
and other tissues. There they are converted to fatty acids, amino acids, and
glycogen, or else oxidized by the various catabolic pathways of cells.
Oxidation of
glucose is known as glycolysis.Glucose
is oxidized to either lactate or pyruvate. Under aerobic conditions, the
dominant product in most tissues is pyruvate
and the pathway is known as aerobic
glycolysis. When oxygen is depleted, as for instance during prolonged
vigorous exercise, the dominant glycolytic product in many tissues is lactate and the process is known as anaerobic glycolysis.
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The Energy Derived from Glucose Oxidation
Aerobic glycolysis of glucose to pyruvate, requires two equivalents of
ATP to activate the process, with the subsequent production of four equivalents
of ATP and two equivalents of NADH. Thus, conversion of one mole of glucose to
two moles of pyruvate is accompanied by the net production of two moles each of
ATP and NADH.
Glucose
+ 2 ADP + 2 NAD+ + 2 Pi -----> 2 Pyruvate + 2 ATP + 2
NADH + 2 H+
The NADH generated during glycolysis is used to fuel mitochondrial ATP
synthesis via oxidative phosphorylation,
producing either two or three equivalents of ATP depending upon whether the glycerol phosphate shuttle
or the malate-aspartate shuttle
is used to transport the electrons from cytoplasmic NADH into the mitochondria.
The net yield from the oxidation of 1 mole of glucose to 2 moles of pyruvate
is, therefore, either 6 or 8 moles of ATP. Complete oxidation of the 2 moles of
pyruvate, through the TCA cycle, yeilds
an additional 30 moles of ATP; the total yield, therefore being either 36 or 38
moles of ATP from the complete oxidation of 1 mole of glucose to CO2
and H2O.
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The Individual Reactions of Glycolysis
The pathway of glycolysis can be seen as consisting of 2 separate
phases. The first is the chemical priming phase requiring energy in the form of
ATP, and the second is considered the energy-yielding phase. In the first
phase, 2 equivalents of ATP are used to convert glucose to fructose
1,6-bisphosphate (F1,6BP). In the second phase F1,6BP is degraded to pyruvate,
with the production of 4 equivalents of ATP and 2 equivalents of NADH.
Pathway of glycolysis from glucose to pyruvate. Substrates and products
are in blue, enzymes are in green. The two high energy intermediates whose
oxidations are coupled to ATP synthesis are shown in red
(1,3-bisphosphoglycerate and phosphoenolpyruvate).
The Hexokinase Reaction:
The ATP-dependent phosphorylation of glucose to form glucose 6-phosphate
(G6P)is the first reaction of glycolysis, and is catalyzed by tissue-specific
isoenzymes known as hexokinases. The phosphorylation accomplishes two goals:
First, the hexokinase reaction converts nonionic glucose into an anion that is
trapped in the cell, since cells lack transport systems for phosphorylated
sugars. Second, the otherwise biologically inert glucose becomes activated into
a labile form capable of being further metabolized.
Four mammalian isozymes of hexokinase are known (Types I - IV), with the
Type IV isozyme often referred to as glucokinase. Glucokinase is the form of
the enzyme found in hepatocytes. The high Km of glucokinase for
glucose means that this enzyme is saturated only at very high concentrations of
substrate.
Comparison of the activities of hexokinase and glucokinase. The Km
for hexokinase is significantly lower (0.1mM) than that of glucokinase (10mM).
This difference ensures that non-hepatic tissues (which contain hexokinase)
rapidly and efficiently trap blood glucose within their cells by converting it
to glucose-6-phosphate. One major function of the liver is to deliver glucose
to the blood and this in ensured by having a glucose phosphorylating enzyme
(glucokinase) whose Km for glucose is sufficiently higher that the
normal circulating concentration of glucose (5mM).
This feature of hepatic glucokinase allows the liver to buffer blood glucose. After meals,
when postprandial blood glucose levels are high, liver glucokinase is significantly
active, which causes the liver preferentially to trap and to store circulating
glucose. When blood glucose falls to very low levels, tissues such as liver and
kidney, which contain glucokinases but are not highly dependent on glucose, do
not continue to use the meager glucose supplies that remain available. At the
same time, tissues such as the brain, which are critically dependent on
glucose, continue to scavenge blood glucose using their low Km
hexokinases, and as a consequence their viability is protected. Under various
conditions of glucose deficiency, such as long periods between meals, the liver
is stimulated to supply the blood with glucose through the pathway of gluconeogenesis.
The levels of glucose produced during gluconeogenesis are insufficient to
activate glucokinase, allowing the glucose to pass out of hepatocytes and into
the blood.
The regulation of hexokinase and glucokinase activities is also
different. Hexokinases I, II, and III are allosterically inhibited by product
(G6P) accumulation, whereas glucokinases are not. The latter further insures
liver accumulation of glucose stores during times of glucose excess, while
favoring peripheral glucose utilization when glucose is required to supply
energy to peripheral tissues.
Phosphohexose Isomerase:
The second
reaction of glycolysis is an isomerization, in which G6P is converted to
fructose 6-phosphate (F6P). The enzyme catalyzing this reaction is phosphohexose
isomerase (also known as phosphoglucose isomerase). The reaction is freely
reversible at normal cellular concentrations of the two hexose phosphates and
thus catalyzes this interconversion during glycolytic carbon flow and during
gluconeogenesis.
6-Phosphofructo-1-Kinase
(Phosphofructokinase-1, PFK-1):
The next
reaction of glycolysis involves the utilization of a second ATP to convert F6P
to fructose 1,6-bisphosphate (F1,6BP). This reaction is catalyzed by
6-phosphofructo-1-kinase, better known as phosphofructokinase-1 or PFK-1.
This reaction is not readily reversible because of its large positive free
energy (G0'
= +5.4 kcal/mol) in the reverse direction. Nevertheless, fructose units readily
flow in the reverse (gluconeogenic) direction because of the ubiquitous
presence of the hydrolytic enzyme, fructose-1,6-bisphosphatase (F-1,6-BPase).
The presence
of these two enzymes in the same cell compartment provides an example of a
metabolic futile cycle, which if unregulated would rapidly deplete cell energy
stores. However, the activity of these two enzymes is so highly regulated that
PFK-1 is considered to be the rate-limiting
enzyme of glycolysis and F-1,6-BPase is considered to be the rate-limiting enzyme in
gluconeogenesis.
Aldolase:
Aldolase
catalyses the hydrolysis of F1,6BP into two 3-carbon products: dihydroxyacetone
phosphate (DHAP) and glyceraldehyde 3-phosphate (G3P). The aldolase reaction
proceeds readily in the reverse direction, being utilized for both glycolysis
and gluconeogenesis.
Triose Phosphate
Isomerase:
\
The two products of the
aldolase reaction equilibrate readily in a reaction catalyzed by triose
phosphate isomerase. Succeeding reactions of glycolysis utilize G3P as a
substrate; thus, the aldolase reaction is pulled in the glycolytic direction by
mass action principals.
Glyceraldehyde-3-Phosphate
Dehydrogenase:
The second
phase of glucose catabolism features the energy-yielding glycolytic reactions
that produce ATP and NADH. In the first of these reactions, glyceraldehyde-3-P
dehydrogenase (G3PDH) catalyzes the NAD+-dependent oxidation of G3P
to 1,3-bisphosphoglycerate (1,3BPG) and NADH. The G3PDH reaction is reversible,
and the same enzyme catalyzes the reverse reaction during gluconeogenesis.
Phosphoglycerate Kinase:
The
high-energy phosphate of 1,3-BPG is used to form ATP and 3-phosphoglycerate
(3PG) by the enzyme phosphoglycerate kinase. Note that this is the only
reaction of glycolysis or gluconeogenesis that involves ATP and yet is
reversible under normal cell conditions. Associated with the phosphoglycerate
kinase pathway is an important reaction of erythrocytes, the formation of
2,3-bisphosphoglycerate, 2,3BPG (see Figure below) by the enzyme
bisphosphoglycerate mutase. 2,3BPG is an important regulator of hemoglobin's
affinity for oxygen. Note that 2,3-bisphosphoglycerate phosphatase degrades
2,3BPG to 3-phosphoglycerate, a normal intermediate of glycolysis. The 2,3BPG
shunt thus operates with the expenditure of 1 equivalent of ATP per triose
passed through the shunt. The process is not reversible under physiological
conditions.
The pathway
for 2,3-bisphosphoglycerate (2,3-BPG)
synthesis within erythrocytes. Synthesis of 2,3-BPG represents a major reaction
pathway for the consumption of glucose in erythrocytes. The synthesis of
2,3-BPG in erythrocytes is critical for controlling hemoglobin affinity for
oxygen. Note that when glucose is oxidized by this pathway the erythrocyte
loses the ability to gain 2 moles of ATP from glycolytic oxidation of 1,3-BPG
to 3-phosphoglycerate via the phosphoglycerate kinase reaction.
Phosphoglycerate Mutase
and Enolase:
The
remaining reactions of glycolysis are aimed at converting the relatively low
energy phosphoacyl-ester of 3PG to a high-energy form and harvesting the
phosphate as ATP. The 3PG is first converted to 2PG by phosphoglycerate mutase
and the 2PG conversion to phosphoenoylpyruvate (PEP) is catalyzed by enolase
Pyruvate Kinase:
The final reaction of aerobic glycolysis is catalyzed by the highly
regulated enzyme pyruvate kinase (PK). In this strongly exergonic reaction, the
high-energy phosphate of PEP is conserved as ATP. The loss of phosphate by PEP
leads to the production of pyruvate in an unstable enol form, which
spontaneously tautomerizes to the more stable, keto form of pyruvate. This
reaction contributes a large proportion of the free energy of hydrolysis of
PEP.
Anaerobic Glycolysis
Under aerobic conditions, pyruvate in most cells is further metabolized
via the TCA cycle. Under
anaerobic conditions and in erythrocytes under aerobic conditions, pyruvate is
converted to lactate by the enzyme lactate dehydrogenase (LDH), and the lactate
is transported out of the cell into the circulation. The conversion of pyruvate
to lactate, under anaerobic conditions, provides the cell with a mechanism for
the oxidation of NADH (produced during the G3PDH reaction) to NAD+;
which occurs during the LDH catalyzed reaction. This reduction is required
since NAD+ is a necessary substrate for G3PDH, without which
glycolysis will cease. Normally, during aerobic glycolysis the electrons of
cytoplasmic NADH are transferred to mitochondrial carriers of the oxidative phosphorylation
pathway generating a continuous pool of cytoplasmic NAD+.
Aerobic glycolysis generates substantially more ATP per mole of glucose
oxidized than does anaerobic glycolysis. The utility of anaerobic glycolysis,
to a muscle cell when it needs large amounts of energy, stems from the fact
that the rate of ATP production from glycolysis is approximately 100X faster
than from oxidative phosphorylation. During exertion muscle cells do not need
to energize anabolic reaction pathways. The requirement is to generate the
maximum amount of ATP, for muscle contraction, in the shortest time frame. This
is why muscle cells derive almost all of the ATP consumed during exertion from
anaerobic glycolysis.
The reactions catalyzed by hexokinase, PFK-1 and PK all proceed with a
relatively large free energy decrease. These nonequilibrium reactions of glycolysis
would be ideal candidates for regulation of the flux through glycolysis.
Indeed, in vitro studies have shown all three enzymes to be
allosterically controlled.
Regulation of hexokinase, however, is not the major control point in
glycolysis. This is due to the fact that large amounts of G6P are derived from
the breakdown of glycogen (the predominant mechanism of carbohydrate entry into
glycolysis in skeletal muscle) and, therefore, the hexokinase reaction is not
necessary. Regulation of PK is important for reversing glycolysis when ATP is
high in order to activate gluconeogenesis. As such this enzyme catalyzed
reaction is not a major control point in glycolysis. The rate limiting step in
glycolysis is the reaction catalyzed by PFK-1.
PFK-1 is a tetrameric enzyme that exist in two conformational states
termed R and T that are in equilibrium. ATP is both a substrate and an
allosteric inhibitor of PFK-1. Each subunit has two ATP binding sites, a
substrate site and an inhibitor site. The substrate site binds ATP equally well
when the tetramer is in either conformation. The inhibitor site binds ATP
essentially only when the enzyme is in the T state. F6P is the other substrate
for PFK-1 and it also binds preferentially to the R state enzyme. At high concentrations
of ATP, the inhibitor site becomes occupied and shifting the equilibrium of
PFK-1 comformation to that of the T state decreasing PFK-1's ability to bind
F6P. The inhibition of PFK-1 by ATP is overcome by AMP which binds to the R
state of the enzyme and, therefore, stabilizes the conformation of the enzyme
capable of binding F6P. The most important allosteric regulator of both
glycolysis and gluconeogenesis is fructose
2,6-bisphosphate, F2,6BP, which is not an intermediate in glycolysis or
in gluconeogenesis.
Regulation of glycolysis and gluconeogenesis by fructose 2,6-bisphosphate (F2,6BP).
The major sites for regulation of glycolysis and gluconeogenesis are the
phosphofructokinase-1 (PFK-1) and fructose-1,6-bisphosphatase (F-1,6-BPase)
catalyzed reactions. PFK-2 is the kinase activity and F-2,6-BPase is the
phosphatase activity of the bi-functional regulatory enzyme,
phosphofructokinase-2/fructose-2,6-bisphosphatase. PKA is cAMP-dependent
protein kinase which phosphorylates PFK-2/F-2,6-BPase turning on the
phosphatase activity. (+ve) and (-ve) refer to positive and negative
activities, respectively.
The synthesis of F2,6BP is catalyzed by the bifunctional enzyme
phosphofructokinase-2/fructose-2,6-bisphosphatase (PFK-2/F-2,6-BPase). In the
nonphosphorylated form the enzyme is known as PFK-2 and serves to catalyze the
synthesis of F2,6BP by phosphorylating fructose 6-phosphate. The result is that
the activity of PFK-1 is greatly stimulated and the activity of F-1,6-BPase is greatly
inhibited.
Under conditions where PFK-2 is active, fructose flow through the
PFK-1/F-1,6-BPase reactions takes place in the glycolytic direction, with a net
production of F1,6BP. When the bifunctional enzyme is phosphorylated it no
longer exhibits kinase activity, but a new active site hydrolyzes F2,6BP to F6P
and inorganic phosphate. The metabolic result of the phosphorylation of the
bifunctional enzyme is that allosteric stimulation of PFK-1 ceases, allosteric
inhibition of F-1,6-BPase is eliminated, and net flow of fructose through these
two enzymes is gluconeogenic, producing F6P and eventually glucose.
The interconversion of the bifunctional enzyme is catalyzed by
cAMP-dependent protein kinase (PKA), which in turn is regulated by circulating
peptide hormones. When blood glucose levels drop, pancreatic insulin production
falls, glucagon secretion is stimulated, and circulating glucagon is highly
increased. Hormones such as glucagon bind to plasma membrane receptors on liver
cells, activating membrane-localized adenylate cyclase leading to an increase
in the conversion of ATP to cAMP (see diagram below). cAMP binds to the
regulatory subunits of PKA, leading to release and activation of the catalytic
subunits. PKA phosphorylates numerous enzymes, including the bifunctional
PFK-2/F-2,6-BPase. Under these conditions the liver stops consuming glucose and
becomes metabolically gluconeogenic, producing glucose to reestablish
normoglycemia.
Representative pathway for the activation of cAMP-dependent protein kinase (PKA). In this example
glucagon binds to its' cell-surface receptor, thereby activating the receptor.
Activation of the receptor is coupled to the activation of a receptor-coupled
G-protein (GTP-binding and hydrolyzing protein) composed of 3 subunits. Upon
activation the alpha subunit dissociates and binds to and activates adenylate
cyclase. Adenylate cylcase then converts ATP to cyclic-AMP (cAMP). The cAMP
thus produced then binds to the regulatory subunits of PKA leading to
dissociation of the associated catalytic subunits. The catalytic subunits are
inactive until dissociated from the regulatory subunits. Once released the
catalytic subunits of PKA phosphorylate numerous substrate using ATP as the
phosphate donor.
Regulation
of glycolysis also occurs at the step catalyzed by pyruvate kinase, (PK). The
liver enzyme has been most studied in vitro. This enzyme is inhibited by
ATP and acetyl-CoA and is activated by F1,6BP. The inhibition of PK by ATP is
similar to the effect of ATP on PFK-1. The binding of ATP to the inhibitor site
reduces its affinity for PEP. The liver enzyme is also controlled at the level
of synthesis. Increased carbohydrate ingestion induces the synthesis of PK
resulting in elevated cellular levels of the enzyme.
A number of PK
isozymes have been described. The liver isozyme (L-type), characteristic of a
gluconeogenic tissue, is regulated via phosphorylation by PKA, whereas the
M-type isozyme found in brain, muscle, and other glucose requiring tissue is
unaffected by PKA. As a consequence of these differences, blood glucose levels
and associated hormones can regulate the balance of liver gluconeogenesis and
glycolysis while muscle metabolism remains unaffected.
In
erythrocytes, the fetal PK isozyme has much greater activity than the adult
isozyme; as a result, fetal erythrocytes have comparatively low concentrations
of glycolytic intermediates. Because of the low steady-state concentration of
fetal 1,3BPG, the 2,3BPG shunt (see diagram above) is greatly reduced in fetal
cells and little 2,3BPG is formed. Since 2,3BPG is a negative effector of
hemoglobin affinity for oxygen, fetal erythrocytes have a higher oxygen
affinity than maternal erythrocytes. Therefore, transfer of oxygen from
maternal hemoglobin to fetal hemoglobin is favored, assuring the fetal oxygen
supply. In the newborn, an erythrocyte isozyme of the M-type with comparatively
low PK activity displaces the fetal type, resulting in an accumulation of
glycolytic intermediates. The increased 1,3BPG levels activate the 2,3BPG
shunt, producing 2,3BPG needed to regulate oxygen binding to hemoglobin.
Genetic
diseases of adult erythrocyte PK are known in which the kinase is virtually
inactive. The erythrocytes of affected individuals have a greatly reduced
capacity to make ATP and thus do not have sufficient ATP to perform activities
such as ion pumping and maintaining osmotic balance. These erythrocytes have a
short half-life, lyse readily, and are responsible for some cases of hereditary hemolytic anemia.
The liver PK
isozyme is regulated by phosphorylation, allosteric effectors, and modulation
of gene expression. The major allosteric effectors are F1,6BP, which stimulates
PK activity by decreasing its Km(app) for PEP, and for the negative
effector, ATP. Expression of the liver PK gene is strongly influenced by the
quantity of carbohydrate in the diet, with high-carbohydrate diets inducing up
to 10-fold increases in PK concentration as compared to low carbohydrate diets.
Liver PK is phosphorylated and inhibited by PKA, and thus it is under hormonal
control similar to that described earlier for PFK-2.
Muscle PK
(M-type) is not regulated by the same mechanisms as the liver enzyme.
Extracellular conditions that lead to the phosphorylation and inhibition of
liver PK, such as low blood glucose and high levels of circulating glucagon, do
not inhibit the muscle enzyme. The result of this differential regulation is
that hormones such as glucagon and epinephrine favor liver gluconeogenesis by
inhibiting liver glycolysis, while at the same time, muscle glycolysis can
proceed in accord with needs directed by intracellular conditions.
Pyruvate is
the branch point molecule of glycolysis. The ultimate fate of pyruvate depends on
the oxidation state of the cell. In the reaction catalyzed by G3PDH a molecule
of NAD+ is reduced to NADH. In order to maintain the re-dox state of
the cell, this NADH must be re-oxidized to NAD+. During aerobic
glycolysis this occurs in the mitochondrial electron transport chain generating
ATP. Thus, during aerobic glycolysis ATP is generated from oxidation of glucose
directly at the PGK and PK reactions as well as indirectly by re-oxidation of
NADH in the oxidative phosphorylation
pathway. Additional NADH molecules are generated during the complete aerobic
oxidation of pyruvate in the TCA cycle.
Pyruvate enters the TCA cycle in the form of acetyl-CoA which is the product of the pyruvate dehydrogenase
reaction. The fate of pyruvate during anaerobic glycolysis is reduction to
lactate.
During
anaerobic glycolysis, that period of time when glycolysis is proceeding at a
high rate (or in anaerobic organisms), the oxidation of NADH occurs through the
reduction of an organic substrate. Erythrocytes and skeletal muscle (under
conditions of exertion) derive all of their ATP needs through anaerobic
glycolysis. The large quantity of NADH produced is oxidized by reducing
pyruvate to lactate. This reaction is carried out by lactate dehydrogenase,
(LDH). The lactate produced during anaerobic glycolysis diffuses from the
tissues and is transproted to highly aerobic tissues such as cardiac muscle and
liver. The lactate is then oxidized to pyruvate in these cells by LDH and the
pyruvate is further oxidized in the TCA cycle. If the energy level in these
cells is high the carbons of pyruvate will be diverted back to glucose via the
gluconeogenesis pathway.
Mammalian
cells contain two distinct types of LDH subunits, termed M and H. Combinations
of these different subunits generates LDH isozymes with different
characteristics. The H type subunit predominates in aerobic tissues such as
heart muscle (as the H4 tetramer) while the M subunit predominates in anaerobic
tissues such as skeletal muscle as the M4 tetramer). H4 LDH has a low Km
for pyruvate and also is inhibited by high levels of pyruvate. The M4 LDH enzyme
has a high Km for pyruvate and is not inhibited by pyruvate. This
suggsts that the H-type LDH is utilized for oxidizing lactate to pyruvate and
the M-type the reverse.
Ethanol Metabolism
Animal cells
(primarily hepatocytes) contain the cytosolic enzyme alcohol dehydrogenase
(ADH) which oxidizes ethanol to acetaldehyde. Acetaldehyde then enters the
mitochondria where it is oxidized to acetate by acetaldehyde dehydrogenase
(AcDH).
Acetaldehyde
forms adducts with proteins, nucleic acids and other compounds, the results of
which are the toxic side effects (the hangover)
that are associated with alcohol consumption. The ADH and AcDH catalyzed
reactions also leads to the reduction of NAD+ to NADH. The metabolic
effects of ethanol intoxication stem from the actions of ADH and AcDH and the
resultant cellular imbalance in the NADH/NAD+. The NADH produced in
the cytosol by ADH must be reduced back to NAD+ via either the malate-aspartate shuttle
or the glycerol-phosphate shuttle.
Thus, the ability of an individual to metabolize ethanol is dependent upon the
capacity of hepatocytes to carry out eother of these 2 shuttles, which in turn
is affected by the rate of the TCA cycle in the
mitochondria whose rate of function is being impacted by the NADH produced by
the AcDH reaction. The reduction in NAD+ impairs the flux of glucose
through glycolysis at the glyceraldehyde-3-phosphate dehydrogenase reaction,
thereby limiting energy production. Additionally, there is an increased rate of
hepatic lactate production due to the effect of increased NADH on direction of
the hepatic lactate dehydrogenase (LDH) reaction. This reverseral of the LDH
reaction in hepatocytes diverts pyruvate from gluconeogenesis leading to a
reduction in the capacity of the liver to deliver glucose to the blood.
In addition
to the negative effects of the altered NADH/NAD+ ratio on hepatic
gluconeogenesis, fatty acid oxidation is also reduced as this process requires
NAD+ as a cofactor. In fact the opposite is true, fatty acid
synthesis is increased and there is an increase in triacylglyceride production
by the liver. In the mitocondria, the production of acetate from acetaldehyde
leads to increased levels of acetyl-CoA. Since the increased generation of NADH
also reduces the activity of the TCA cycle, the acetyl-CoA is diverted to fatty
acid synthesis. The reduction in cytosolic NAD+ leads to reduced
activity of glycerol-3-phosphate dehydrogenase (in the glcerol 3-phosphate to
DHAP direction) resulting in increased levels of glycerol 3-phosphate which is
the backbone for the synthesis of the triacylglycerides. Both of these two
events lead to fatty acid deposition in the liver leading to fatty liver syndrome.
Regulation of Blood Glucose Levels
If for no other reason, it is because of the demands of the brain for
oxidizable glucose that the human body exquisitely regulates the level of
glucose circulating in the blood. This level is maintained in the range of 5mM.
Nearly all carbohydrates ingested in the diet are converted to glucose
following transport to the liver. Catabolism of dietary or cellular proteins
generates carbon atoms that can be utilized for glucose synthesis via gluconeogenesis.
Additionally, other tissues besides the liver that incompletely oxidize glucose
(predominantly skeletal muscle and erythrocytes) provide lactate that can be
converted to glucose via gluconeogenesis.
Maintenance of blood glucose homeostasis is of paramount importance to
the survival of the human organism. The predominant tissue responding to
signals that indicate reduced or elevated blood glucose levels is the liver.
Indeed, one of the most important functions of the liver is to produce glucose
for the circulation. Both elevated and reduced levels of blood glucose trigger
hormonal responses to initiate pathways designed to restore glucose
homeostasis. Low blood glucose triggers release of glucagon from pancreatic -cells. High
blood glucose triggers release of insulin
from pancreatic -cells.
Additional signals, ACTH and growth
hormone, released from the pituitary act to increase blood glucose by
inhibiting uptake by extrahepatic tissues. Glucocorticoids also act to increase blood glucose levels by
inhibiting glucose uptake. Cortisol,
the major glucocorticoid released from the adrenal cortex, is secreted in
response to the increase in circulating ACTH. The adrenal medullary hormone, epinephrine, stimulates production of
glucose by activating glycogenolysis in response to stressful stimuli.
Glucagon binding to its' receptors on the surface of liver cells
triggers an increase in cAMP production leading to an increased rate of glycogenolysis by
activating glycogen phosphorylase via the PKA-mediated cascade. This is the
same response hepatocytes have to epinephrine release. The resultant increased
levels of G6P in hepatocytes is hydrolyzed to free glucose, by
glucose-6-phosphatase, which then diffuses to the blood. The glucose enters
extrahepatic cells where it is re-phosphorylated by hexokinase. Since muscle
and brain cells lack glucose-6-phosphatase, the glucose-6-phosphate product of
hexokinase is retained and oxidized by these tissues.
In opposition to the cellular responses to glucagon (and epinephrine on
hepatocytes), insulin stimulates extrahepatic uptake of glucose from the blood
and inhibits glycogenolysis in extrahepatic cells and conversely stimulates
glycogen synthesis. As the glucose enters hepatocytes it binds to and inhibits
glycogen phosphorylase activity. The binding of free glucose stimulates the
de-phosphorylation of phosphorylase thereby, inactivating it. Why is it that
the glucose that enters hepatocytes is not immediately phosphorylated and
oxidized? Liver cells contain an isoform of hexokinase called glucokinase.
Glucokinase has a much lower affinity for glucose than does hexokinase.
Therefore, it is not fully active at the physiological ranges of blood glucose.
Additionally, glucokinase is not inhibited by its product G6P, whereas,
hexokinase is inhibited by G6P.
One major response of non-hepatic tissues to insulin is the recruitment,
to the cell surface, of glucose transporter complexes. Glucose transporters
comprise a family of five members, GLUT-1
to GLUT-5. GLUT-1 is ubiquitously distributed in various tissues. GLUT-2
is found primarily in intestine, kidney and liver. GLUT-3 is also found in the
intestine and GLUT-
Hepatocytes, unlike most other cells, are freely permeable to glucose
and are, therefore, essentially unaffected by the action of insulin at the
level of increased glucose uptake. When blood glucose levels are low the liver
does not compete with other tissues for glucose since the extrahepatic uptake
of glucose is stimulated in response to insulin. Conversely, when blood glucose
levels are high extrahepatic needs are satisfied and the liver takes up glucose
for conversion into glycogen for
future needs. Under conditions of high blood glucose, liver glucose levels will
be high and the activity of glucokinase will be elevated. The G6P produced by
glucokinase is rapidly converted to G1P by phosphoglucomutase, where it can
then be incorporated into glycogen.
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Digestion &
Absorption of Proteins & Carbohydrates
Digestion and Absorption
of Proteins
General Information:
1.
Humans must ingest proteins, carbohydrates and lipids to maintain tissue and
organ functions.
2.
Most of these nutrients consist of large polymers that must be broken down
before they can be made available to the intestinal cells for transport.
3.
Dietary proteins are cleaved by hydrolases with specificity for the peptide
bond (peptidases).
4.
Endopeptidases (aka Proteases): attack internal protein bonds
liberating large peptide fragments.
Exopeptidases: cleave off one amino acid at a time from
the....
NH3+, aminopeptidases or COO-
terminus, carboxypeptidase.
5.
Endo- and Exopeptidases work in concert
The Big Picture:
Protein Digestion and Absorption
Gastric (Stomach) Digestion:
1.
Gastric HCl is responsible for the low pH <2 of gastric juice.
2.
Gastric acid kills microorganisms and denatures dietary proteins
preparing them for hydrolysis by proteases.
3.
Gastric juices contain the acid stable proteases of the pepsin family,
which produce large peptide fragments and some free amino acids.
4.
Protein digestion at this stage is partial, as the amino acids enter the
duodenum, they trigger the release of cholectystokinin-pancreozymin (CCK-PZ)
into the bloodstream.
This
release initiates the secretion of protease zymogens from the pancreas
and releases of enteropeptidase in the gut.
Pancreatic Proteases:
1.
The pancreatic juice is rich in the proenzymes of endopeptidase and carboxypeptidases.
2.
Enteropeptidase activates pancreatic trypsinogen to trypsin.
3.
Trypsin autocatalytically activates more trypsinogen and other
proenzymes, liberating chymotrypsin, elastase and the carboxypeptidases
A and B.
Secretion and Activation of Pancreatic Proteases:
Digestion at the Brush Border (surface of intestinal epithelial cells):
1.
Since pancreatic juice does not contain appreciable aminopeptidase activity,
final digestion of di- and small peptides depends on brush border enzymes.
2.
The surface of intestinal epithelial cells is rich in endopeptidases and
aminopeptidases.
3.
The end products of cell surface digestion are free amino acids and di-
and tripeptides.
Absorption:
1.
Following digestion, amino acids and small peptides are co-absorbed
w/ sodium via group specific amino acid or peptide transport
systems.
2.
These processes are carrier mediated, discriminating between natural, L
amino acids and D-amino acids, require energy (from the Na+
gradient, Na-K ATPase) and physiologic temperatures.
At least five brush border transport systems exist:
1.
neutral amino acids (uncharged aliphatic and aromatic)
2.
basic amino acids (
3.
acidic amino acids (Asp, Glu)
4.
imino acids (Pro), Hydroxyproline)
5.
di- and tripeptides
Clinical Correlates:
1.
Hartnup Disease:
Genetic
defect in the neutral amino acid transporter.
Symptoms:
dermatitis due to tryptophan malabsorption ("niacin" flush)
Consequences:
not serious di- and tripeptide absorption supply minimal amounts of dietarily
essential neutral amino acids.
2.
Cystinuria:
Precursor
to kidney stones
Symptoms:
painful kidney stone formation due to malabsoprtion of cystine (two disulfide
linked cysteines)
3.
Sprue:
Destruction
and flattening of the intestinal villi resulting in generalized malabsorption.
Causes:
bacterial infection or gluten (contained in certain grains such as wheat and
barley) sensitivity.
Digestion and Absorption of Carbohydrates
General Information:
1.
Carbohydrates provide a major component of the daily caloric requirement, ~40%.
2.Distinguish
between mono-, di- and polysaccharides.
Monosaccharides- do not need hydrolysis prior to absorption.
Disaccharides-
require brush border enzymes.
Polysaccharides- require brush border enzymes, as well as, pancreatic
amylase and salivary amylase for digestion.
Starch:
Hydrolyzed
by -amylase into
Maltotriose, -Limit Dextrin, Maltose,
Glucose
-1,4-glucosidic linkages
(non-branching, amylose) and branched chains -1,6 linkages (branch
points, amylopectin)
-amylase:
Present
in saliva and pancreatic juice.
Specific
for internal -1,4-glucosidic bonds.
Brush Border
Carbohydrate Digestion:
Final hydrolysis of di-
and oligosaccharides to monosaccharides is carried out by -glucosidases on the
surface of the small intestine.
Monosaccharides are
absorbed by carrier mediated transport.
At least two types are
known:
1. Na+monosaccharide
transporter
2. Na+ independent,
diffusion type monosaccharide transport system
Undigested Carbohydrates:
1. Di-, oligo- and
polysaccharides that are not hydrolyzed by -amylase and/or brush
border enzymes cannot be absorbed.
2. These carbohydrates
reach the lower tract of the intestine which contains bacteria.
3. The bacteria utilize
many of the remaining carbohydrate, metabolizing them and producing by-
products such as: hydrogen gas, methane and carbon dioxide.
Carbohydrates
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Carbohydrates are one of three macronutrients
that provide the body with energy (protein and fats being the
other two). The chemical compounds in carbohydrates are found in both simple
and complex forms, and in order for the body to use carbohydrates for energy,
food must undergo digestion, absorption, and glycolysis. It is
recommended that 55 to 60 percent of caloric intake come from carbohydrates.
Chemical Structure
Carbohydrates are a main source of
energy for the body and are made of carbon, hydrogen, and oxygen.
Chlorophyll in plants absorbs light energy from the sun. This energy is used in
the process of photosynthesis, which allows green plants to take in carbon
dioxide and release oxygen and allows for the production of carbohydrates. This
process converts the sun's light energy into a form of chemical energy useful
to humans. Plants transform carbon dioxide (CO2) from the air, water
(H2O) from the ground, and energy from the sun into oxygen (O2)
and carbohydrates (C6H12O6) (6 CO2 +
6 H2O + energy = C6H12O6 + 6 O2).
Most carbohydrates have a ratio of 1:2:1 of carbon, hydrogen, and oxygen,
respectively.
Humans and other animals obtain
carbohydrates by eating foods that contain them. In order to use the energy
contained in the carbohydrates, humans must metabolize, or break down,
the structure of the molecule in a process that is opposite that of
photosynthesis. It starts with the carbohydrate and oxygen and produces carbon
dioxide, water, and energy. The body utilizes the energy and water and rids
itself of the carbon dioxide.
Simple
Carbohydrates
Simple carbohydrates, or simple
sugars, are composed of monosaccharide or disaccharide units.
Common monosaccharides (carbohydrates composed of single sugar units) include glucose,
fructose, and galactose. Glucose is the most common type of sugar and the
primary form of sugar that is stored in the body for energy. It sometimes is
referred to as blood sugar or dextrose and is of particular importance to
individuals who have diabetes or hypoglycemia. Fructose, the
primary sugar found in fruits, also is found in honey and high-fructose corn
syrup (in soft drinks) and is a major source of sugar in the diet of
Americans. Galactose is less likely than glucose or fructose to be found in
nature. Instead, it often combines with glucose to form the disaccharide
lactose, often referred to as milk sugar. Both fructose and galactose are
metabolized to glucose for use by the body.
Oligosaccharides are carbohydrates made of two to
ten monosaccharides. Those composed of two sugars are specifically referred to
as disaccharides, or double sugars. They contain two monosaccharides bound by
either an alpha bond or a beta bond. Alpha bonds are digestible by the human
body, whereas beta bonds are more difficult for the body to break down.
There are three particularly
important disaccharides: sucrose, maltose, and lactose. Sucrose is
formed when glucose and fructose are held together by an alpha bond. It is
found in sugar cane or sugar beets and is refined to make granulated table
sugar. Varying the degree of purification alters the
SUGAR COMPARISON
|
Sugar
|
Carbohydrate
|
Monosaccharide or disaccharide
|
Additional information
|
|
Beet sugar (cane sugar) |
Sucrose |
Disaccharide (fructose and
glucose) |
Similar
to white and powdered sugar, but varied degree of purification |
|
Brown sugar |
Sucrose |
Disaccharide (fructose and
glucose) |
Similar
to white and powdered sugar, but varied degree of purification |
|
Corn syrup |
Glucose |
Monosaccharide |
|
|
Fruit sugar |
Fructose |
Monosaccharide |
Very sweet |
|
High-fructose corn syrup |
Fructose |
Monosaccharide |
Very
sweet and inexpensive |
|
Honey |
Fructose and glucose |
Monosaccharides |
|
|
Malt sugar |
Maltose |
Disaccharide (glucose and glucose)
|
Formed
by the hydrolysis of starch, but sweeter than starch |
|
Maple syrup |
Sucrose |
Disaccharide (fructose and
glucose) |
|
|
Milk sugar |
Lactose |
Disaccharide (glucose and galactose)
|
Made
in mammary glands of most lactating animals |
|
Powdered sugar |
Sucrose |
Disaccharide (fructose and
glucose) |
Similar
to white and brown sugar, but varied degree of purification |
|
White sugar |
Sucrose |
Disaccharide (fructose and
glucose) |
Similar
to brown and powdered sugar, but varied degree of purification |
|
SOURCE:
Mahan and Escott-Stump, 2000; Northwestern University; Sizer and Whitney,
1997; and Wardlaw and Kessel, 2002. |
|||
final product, but white, brown, and
powdered sugars all are forms of sucrose. Maltose, or malt sugar, is composed
of two glucose units linked by an alpha bond. It is produced from the chemical
decomposition of starch, which occurs during the germination of seeds and the
production of alcohol. Lactose is a combination of glucose and galactose.
Because it contains a beta bond, it is hard for some individuals to digest in
large quantities. Effective digestion requires sufficient amounts of the enzyme
lactase.
Complex Carbohydrates
Complex
carbohydrates, or polysaccharides, are composed of simple sugar units in
long chains called polymers. Three polysaccharides are of particular importance
in human nutrition: starch, glycogen, and dietary fiber.
Starch and
glycogen are digestible forms of complex carbohydrates made of strands of
glucose units linked by alpha bonds. Starch, often contained in seeds, is the
form in which plants store energy, and there are two types: amylose and
amylopectin. Starch represents the main type of digestible complex
carbohydrate. Humans use an enzyme to break down the bonds linking glucose
units, thereby releasing the sugar to be absorbed into the bloodstream. At that
point, the body can distribute glucose to areas that need energy, or it can
store the glucose in the form of glycogen.
Glycogen is
the polysaccharide used to store energy in animals, including humans. Like
starch, glycogen is made up of chains of glucose linked by alpha bonds; but
glycogen chains are more highly branched than starch. It is this highly
branched structure that allows the bonds to be more quickly broken down by
enzymes in the body. The primary storage sites for glycogen in the human body
are the liver and the muscles.
Another type
of complex carbohydrate is dietary fiber. In general, dietary fiber is
considered to be polysaccharides that have not been digested at the point of
entry into the large intestine. Fiber contains sugars linked by bonds that
cannot be broken down by human enzymes, and are therefore
![Pastas and whole-grain breads contain complex carbohydrates, which are long strands of glucose molecules. Nutritionists recommend that 55–60 percent of calories come from carbohydrates, and especially complex carbohydrates. [Photograph by James Noble. Corbis. Reproduced by permission.]](Anaerobic%20and%20aerobic%20oxidation%20of%20glucose.%20Alternative%20ways%20of%20monosaccharide%20metabolism..files/image032.jpg)
Pastas and whole-grain breads contain complex carbohydrates, which are
long strands of glucose molecules. Nutritionists recommend that 55–60 percent
of calories come from carbohydrates, and especially complex carbohydrates.
[Photograph by James Noble. Corbis. Reproduced by permission.]
labeled as indigestible. Because of this, most fibers do not provide
energy for the body. Fiber is derived from plant sources and contains
polysaccharides such as cellulose, hemicellulose, pectin, gums,
mucilages, and lignins.
The
indigestible fibers cellulose, hemicellulose, and lignin make up the structural
part of plants and are classified as insoluble fiber because they
usually do not dissolve in water. Cellulose is a nonstarch carbohydrate polymer
made of a straight chain of glucose molecules linked by beta bonds and
can be found in whole-wheat flour, bran, and vegetables. Hemicellulose is a
nonstarch carbohydrate polymer made of glucose, galactose, xylose, and other
monosaccharides; it can be found in bran and whole grains. Lignin, a
noncarbohydrate polymer containing alcohols and acids, is a woody fiber found
in wheat bran and the seeds of fruits and vegetables.
In contrast,
pectins, mucilages, and gums are classified as soluble fibers because they
dissolve or swell in water. They are not broken down by human enzymes, but
instead can be metabolized (or fermented) by bacteria present in the
large intestine. Pectin is a fiber made of galacturonic acid and other
monosaccharides. Because it absorbs water and forms a gel, it is often used in
jams and jellies. Sources of pectin include citrus fruits, apples,
strawberries, and carrots. Mucilages and gums are similar in structure.
Mucilages are dietary fibers that contain galactose, manose, and other
monosaccharides; and gums are dietary fibers that contain galactose, glucuronic
acid, and other monosaccharides. Sources of gums include oats, legumes,
guar, and barley.
Digestion
and Absorption
Carbohydrates must be digested and
absorbed in order to transform them into energy that can be used by the body.
Food preparation often aids in the digestion process. When starches are heated,
they swell and become easier for the body to break down. In the mouth, the
enzyme amylase, which is contained in saliva, mixes with food products and
breaks some starches into smaller units. However, once the carbohydrates reach
the acidic environment of the stomach, the amylase is inactivated. After the
carbohydrates have passed through the stomach and into the small intestine, key
digestive enzymes are secreted from the pancreas and the small intestine where
most digestion and absorption occurs. Pancreatic amylase breaks starch into
disaccharides and small polysaccharides, and enzymes from the cells of the
small-intestinal wall break any remaining disaccharides into their
monosaccharide components. Dietary fiber is not digested by the small
intestine; instead, it passes to the colon unchanged.
Sugars such as galactose, glucose,
and fructose that are found naturally in foods or are produced by the breakdown
of polysaccharides enter into absorptive intestinal cells. After absorption,
they are transported to the liver where galactose and fructose are converted to
glucose and released into the bloodstream. The glucose may be sent directly to
organs that need energy, it may be transformed into glycogen (in a process
called glycogenesis) for storage in the liver or muscles, or it may be
converted to and stored as fat.
Glycolysis
The molecular bonds in food products
do not yield high amounts of energy when broken down. Therefore, the energy
contained in food is released within cells and stored in the form of adenosine
triphosphate (ATP), a high-energy compound created by cellular
energy-production systems. Carbohydrates are metabolized and used to produce
ATP molecules through a process called glycolysis.
Glycolysis breaks down glucose or
glycogen into pyruvic acid through enzymatic reactions within the cytoplasm
of the cells. The process results in the formation of three molecules of ATP
(two, if the starting product was glucose). Without the presence of oxygen,
pyruvic acid is changed to lactic acid, and the energy-production
process ends. However, in the presence of oxygen, larger amounts of ATP can be
produced. In that situation, pyruvic acid is transformed into a chemical
compound called acetyle coenzyme A, a compound that begins a complex
series of reactions in the Krebs Cycle and the electron transport
system. The end result is a net gain of up to thirty-nine molecules of ATP from
one molecule of glycogen (thirty-eight molecules of ATP if glucose was used).
Thus, through certain systems, glucose can be used very efficiently in the
production of energy for the body.
Recommended
Intake
At times, carbohydrates have been
incorrectly labeled as "fattening." Evidence actually supports the
consumption of more, rather than less, starchy foods. Carbohydrates have four calories
per gram, while dietary fats contribute nine per gram, so diets high in complex
carbohydrates are likely to provide fewer calories than diets high in fat.
Recommendations are for 55 to 60 percent of total calories to come from
carbohydrates (approximately 275 to
Low-Carb
Diets
Low-carbohydrate diets, such as the
Atkins and
—Paula Kepos
It is important to consume a minimum
amount of carbohydrates to prevent ketosis, a condition resulting from
the breakdown of fat for energy in the absence of carbohydrates. In this
situation, products of fat breakdown, called ketone bodies, build up in the
blood and alter normal pH balance. This can be particularly harmful to a
fetus. To avoid ketosis, daily carbohydrate intake should include a minimum of
50 to
Exchange
System
The exchange system is composed of
lists that describe carbohydrate, fat, and protein content, as well as caloric
content, for designated portions of specific foods. This system takes into
account the presence of more than one type of nutrient in any given food.
Exchange lists are especially useful for individuals who require careful diet
planning, such as those who monitor intake of calories or certain nutrients. It
is particularly useful for diabetics, for whom carbohydrate intake must be
carefully controlled, and was originally developed for planning diabetic diets.
Diabetes,
Carbohydrate-Modified Diets, and Carbohydrate Counting
Diabetes is a condition that alters
the way the body handles carbohydrates. In terms of diet modifications,
diabetics can control blood sugar levels by appropriately managing the
carbohydrates, proteins, and fats in their meals. The amount of carbohydrates,
not necessarily the source, is the primary issue. Blood glucose levels after a
meal can be related to the process of food preparation, the amount of food
eaten, fat intake, sugar absorption, and the combination of foods in the meal
or snack.
One method of monitoring
carbohydrate levels—carbohydrate counting—assigns a certain number of
carbohydrate grams or exchanges to specific foods. Calculations are used to
determine insulin need, resulting in better control of blood glucose
levels with a larger variety of foods. Overall, diabetic diets can include
moderate amounts of sugar, as long as they are carefully monitored.
Glycolysis
(detailed)
Nomenclature of carbohydrates - the naming of carbohydrates - much more
information than most of us need
1. Glucose - a monosaccharide - what you measure in your blood.
The chemical formula for glucose is C6H12O6.
2. Sucrose - a disaccharide - table sugar. Is made of one molecule of
glucose and one fructose.
3. Starch - amylose and amylopectin - a polysaccharide - potatoes.
Amylose is a straight chain of glucose molecules linked together.
Amylopectin is a branched chain of glucose molecules.
4. Glycolysis is the breakdown of glucose to release its energy in the
form of ATP.
Carbohydrate
metabolism - a slide presentation from the
more chemistry than most people will want.
From The
Biology Home Page produced by Jerry
Johnson from Frederick, Okl.