Transcript Nutrient Interaction

NUTRIENT INTERACTION
Nutrient
A chemical compound (such as protein, fat, carbohydrate, vitamins,
or minerals) that make up foods. These compounds are used by the
body to function and grow.
Nutrient can be classified as
Macronutrients
There are three macronutrients defined as being the classes of
chemical compounds humans consume in the largest quantities and
which provide bulk energy .These are organic nutrients like PROTEIN,
FAT and CARBOHYDRATES.
Micronutrients
These are inorganic nutrients such as minerals and vitamins which are
required by body in very small quantities.
Nutrient Interaction
It can be defined as the physical chemical interaction between
nutrients, or between nutrients and other components of the diet or
other compounds, including desirable or undesirable results.
Carbohydrate –carbohydrate
interaction
Carbohydrates are important nutrient which provide energy to our
body .It is an organic compound made up by carbon ,hydrogen and
oxygen.
1. Inter- relation between Fructose and Sucrose
When fructose is ingested as a part of the dissaccharide sucrose
,absorption capacity is much higher because fructose exists in a 1 : 1
ratio with glucose.
In addition ,serum galactose levels following galactose ingestion are
reduced when accompanied by glucose.
2. Inter –relation between Carbohydrate – Fiber
FIBER is a type of polysaccharides which found in plants and it gives
structure to plants.
There is a 2 type of fibers like soluble and insoluble fiber.
Soluble fiber such as pectin etc mixes with water to form gummy
substances that coats the insides of the intestinal tract
During digestion, wave-like currents caused by contractions of the
intestinal muscles bring nutrients to the surface of the intestinal wall
for absorption. After soluble fiber dissolves in water, however, it
traps nutrients inside its gummy gel and slows down considerably
while moving through the digestive tract. Inside the gel, nutrients are
shielded from digestive enzymes and less likely to reach the wall of
the intestines.
Dietary sugars like carbohydrates and starch are among the
nutrients trapped inside this gel. Consequently, sugar is absorbed
into the bloodstream more slowly, blunting the sharp spike in blood
glucose typically experienced by diabetic patients after a meal. Fewer
spikes in blood glucose lead to greater sensitivity to the action of
insulin. Avoiding high peaks and low valleys in blood glucose places
less stress on the pancreas and is important not only to diabetics but
also to those who want to prevent the development of type 2 diabetes
Glycemic Index
The glycemic index is a measure of the effects of carbohydrates in food
on blood sugar levels. It estimates how much each gram of available
carbohydrate (total carbohydrate minus fiber) in a food raises a person's
blood glucose level following consumption of the food, relative to
consumption of glucose.
Plasma glucose level rise 5-45 min after any meal that contains sugars or
digestible starch and return to fasting levels 2-hours later.White bread has a
glycemic index of 100 and other foods have a lower glycemic index.
Foods with a high glycemic index, such as processed starches and the
sugar in soft drinks, break down into glucose and enter the bloodstream
relatively quickly.
Unrefined, complex carbohydrates, on the other hand, have a low
glycemic index and digest more slowly. Diabetic patients should consume
food with a low glycemic index because rapid increases in blood glucose
exacerbate overproduction of insulin by the pancreas and insulin
resistance.
The glycemic index depends on:
1.Composition and size of starch particles
Smaller the particle size more is the glycemic effect .Raw
foods with large particles therefore have a lower effect on
glycemic index.
2.Their digestibility
Presence of amylopectin that gets rapidly digested also has a
greater glycemic effect whereas the amount of amylose
which is digested slowly has low gycemic index.
3.Cooking methods employed
Foods cooked by boiling and long cooking process makes it
easy to digest and reduces the particle size thus increasing
the glycemic index.
Carbohydrate –Protein Inter-relations
1.
Carbohydrate and Hormones
 Glucagon, a hormone secreted by the pancreas, raises blood
glucose levels. Its effect is opposite that of insulin, which lowers
blood glucose levels.
The pancreas releases glucagon when blood sugar (glucose) levels
fall too low. Glucagon causes the liver to convert stored glycogen
into glucose, which is released into the bloodstream and also
from non CHO substances like amino acids etc.
High blood glucose levels stimulate the release of insulin. Insulin
allows glucose to be taken up and used by insulin-dependent
tissues.
Thus, glucagon and insulin are part of a feedback system that
keeps blood glucose levels at a stable level.
So, Glucagon is responsible for gluconeogenesis and glycogenolysis.

Cortisol
It is a hormone produced by adrenal gland .
Its function is to increase blood sugar through gluconeogenesis ; suppress
the immune system; and aid in fat, protein and carbohydrate
metabolism so , it is an overall catabolic hormone ,which decreases lean
body mass and muscle mass and may increase energy expenditure.
Cortisol withdrawal increase insulin sensitivity interms of increased glucose
oxidation and decrease glucose production . This may include
hypoglycemia in adrenocortical failure.
2.Protein sparing action
During fasting or starvation or insufficient carbohydrates and fats for
fuel ,body stores of glycogen are exhausted.Body adapts to use of
muscle protein to meet most of the need of glucose production
,mainly needed for brain , RBCs etc, and this is done by
gluconeogenesis .
But to use protein instead of carbohydrates to give energy is not a wise
contribution as the urinary nitrogen excretion increases during
starvation.
If carbohydreates are sufficient, then protein can be spared of tissue
building process.
3.Glucose and Alanine
 Alanine plays a key role in glucose–alanine cycle between tissues
and liver. In muscle and other tissues that degrade amino acids for
fuel, amino groups are collected in the form of glutamate by
transamination. Glutamate can then transfer its amino group
through the action of alanine aminotransferase to pyruvate forming
alanine and α-ketoglutarate. The alanine formed is passed into the
blood and transported to the liver.
 A reverse of the alanine aminotransferase reaction takes place in
liver. Pyruvate regenerated forms glucose through gluconeogenesis,
which returns to muscle through the circulation system. Glutamate
in the liver enters mitochondria and degrades into ammonium ion
through the action of glutamate dehydrogenase, which in turn
participate in the urea cycle to form urea.
 The glucose–alanine cycle enables pyruvate and glutamate to be
removed from the muscle and find their way to the liver. Glucose is
regenerated from pyruvate and then returned to muscle: the
energetic burden of gluconeogenesis is thus imposed on the liver
instead of the muscle. All available ATP in muscle is devoted to
muscle contraction
4.Fiber and Trypsin
Fiber i.e. cellulose has also been shown to reduce the actvitiy of
human pancreatic trypsin in protein digestion.This is shown as
slightly increased faecal loses of nitrogen on increased fiber diet
. In addition amylase and lipase activity is also depressed.
5. Maillard reaction
When a reducing sugar is heated with protein , a maillard reaction
occurs that reduces the availability of some amino acids , like
lysine. The monosaccharide in intestinal lumen may influence
rate of uptake of certain amino acids ,fructose seeming to
accelerate this reaction e.g.
During milk processing or heat treatment ,milk sugar lactose react
with free side chains of lysine residues to render it unavailable .
Under sever heating conditions,in presence of sugar ,food protein
becomes resistant to digestion so that availability of amino acid
is reduced.
6.Enzymes and carbohydrate hydrolysis
When enzymes concerned with hydrolysis of carbohydrate are missing or
inadequate, common symptom is osmotic diarrhea .This condition may
arise because of congenital absence of appropriate enzyme required for
digestion of lactose ,sucrose or maltose. Inadequancies of these enzyme
may also be secondary to gut mucosal damage due to such condition as
celiac disoder or protein deficiency.
7. Glucose and tryptophan
Amino acid uptake across the blood brain barrrier is influenced indirectly by
serum glucose in that the insulin concentration is directly related to
movement of tryptophan into brain.
The disorders fructose malabsorption and lactose intolerance cause improper
absorption of tryptophan in the intestine, reduced levels of tryptophan in
the blood and depression.
8.Glucosamine and Collagen
Glucosamine (an amino monosaccharide found in chitin ,glycoproteins and
glycosaminoglycans such as hyaluronic acid and heparin sulfate) provides
the primary substrate for both collagen and proteoglycan synthesis.
9.Genetic errors
Genetic errors may also occur in conversion of fructose and
galactose .Absence of enzyme fructokinase in liver prevents
fructose breakdown and is excreted in urine i.e. fructosuria.
Diminished activity of fructose -1-phosphate aldose in liver
results in hypoglycemia and hypophosphatemia with
associated vomiting.
Clinical forms of glactosemia occur as inborn errors of
metabolism and result of enzyme deficincies
.Deficient enzyme is galactokinase in which galactose is not
phosphorylated.This may lead to cataract in otherwise
normal subject .Also glucose-6-phosphate dehdrogenase
deficiency result in inability to maintain glutathione in
reduced form during exposure to drugs such as
sulfonamides or some antimalarials ,leading to haemolysis
or anemia.
Carbohydrate – Fat Inter-relation
1.Conversion into fat
Glucose is a six-carbon sugar molecule and body first converts this molecule into
two three-carbon pyruvate molecules through the process of glycolysis and then
into acetyl CoA
. When body requires immediate energy, acetyl CoA enters the Citric Acid Cycle
creating energy molecules in the form of ATP. But when glucose intake exceeds
then acetyl CoA begins the process of fatty acid synthesis becoming
triglycerides that are stored in the fat tissues of body. These triglycerides are
stored energy molecules which can be broken down later to give energy when
need , for example, get up off the couch and go for a bike ride.
 Regulation of Fatty Acid Synthesis
Fatty acid synthesis is influenced by foods which we eat and hormones we release.
When blood glucose levels are high, such as after eating a sugary meal, body
releases insulin. Insulin stimulates the formation of Fatty Acid Synthase, an
enzyme that increases fat storage.
 On the other hand, polyunsaturated fatty acids decrease the formation
of the Fatty Acid Synthase enzyme, implying that eating foods
containing polyunsaturated fats may not lead to as much increased fat
storage as eating sugary foods. In addition, when fat cells increase their
fat storage, a molecule called leptin is produced. Leptin leads to
decreased food intake, increased energy expenditure, as well as
inhibition of fatty acid synthesis.
2.Prevent ketosis
The primary function of CHO is to provide energy .However during low
CHO intake ,fats are mobilized to meet the energy requirement of
body . This result in increased plasma free fatty acids and ketone
bodies .Hence, sufficient amount of CHO spares fats from being
broken down.
3.Chitin and Cholesterol
Chitin (a polysaccharide found in the exoskeleton of some invertebrates
e.g. Insects ,crustaceans0 and chitosan, have hypocholestrolemic
effect . The strong positive charge on chitosan binds negatively
charged lipids blocking their absorption.
4.Fiber and Lipid
Serum lipid concentration can be modified by insoluble fibers
such as cellulose ,lignin,chitin and more soluble fibers because
 Fibers bind faecal bile acid and increases excretion of bile acidderived cholesterol.
 Fiber prevents dietary fat and cholesterol absorption by binding
bile acids or fats and lipids.
 Fermentable oligosaccharides and dietary fiber are converted
by intestinal bacteria to short chain fatty acids, which lower
blood lipids by mechanisms that are currently unclear.
So Fiber decreases the absorption of dietary cholesterol from
the intestine.
Further ,fiber binds with bile salts and reduces their
enterohepatic circulation.This cause increased degradation of
cholesterol to bile salts and its disposal from the body.
Carbohydrate-Mineral interrelations
Carbohydrate and Zinc
Highe fiber diet is associated with zinc deficiency .Zinc
absorption may be enhanced by glucose and lactose intake.
Carbohydrate and Calcium
It is seen that lactose improves the absorption of
calcium from the gut . Even in adults with lactose
intolerance ,lactose probably improves Ca
absorption. Sugars and organic acids produced by
microbial fermentation of sugars in the gut
increases the solubility of calcium salts and
increases their absorption .
Fiber may decrease calcium absorption ,this process
occurs if calcium intake is more than 30gm per day.
3. Carbohydrate and Iron
Wheat bran includes low serum iron levels as they
contains phytate which inhibits iron absorption . In
this regard iron absorption from unpolished rice is
significantly worse then from polished rice.
4.Phosphorus and Carbohydrates
Phosphorus plays an essential part in carbohydrate metabolism
in phoshoryalation of glycogen.Phosphorus is an essential
constituent of coenzyme I and co- carboxylase enzyme system
in the oxidation of carbohydrate , fat and protein.
.5.Copper and Fiber
Dietary fiber do not inhibits copper absorption.
6.Chromium and Carbohydrates
The high sugar diet enhanced urinary chromium losses
7.Magnesium and carbohydrates
Magnesium deficiency has been linked to insulin resistance and
metabolic syndrome because magnisium is required for CHO
metabolism.
Increased intakes of dietary fiber have been reported to decrease
magnesium utilization in humans presumably by decreasing
absorption.
Vitamin- Carbohydrates inter-relations
1. Vitamin –C and Carbohydrate
Vitamin – C has been found to affect the regulating CHO
metabolism either at the level of rate of absorption of CHO
from intestine ,or of glycogen level alteration of liver and
other tissues . It has been found that in scorbutic animals
,there is a diminution of glutathione levels with
simultaneously depression in insulin secretion. This is due
to the reason as there is an increase in dehydro ascorbic
level in tissues which may combine with sulfydral groups of
glutathione making it unavailable for the protective role in
beta cells of pancreas and causes diminished insulin
secretion.
There is a severe depression in hexokinase activity and in the
turnover rate of phosphorylated intermediates of CHO
metabolism in scorbutic conditions.
A depression in phosphoglucomutase and
phosphohexoseisomerase activity with stimulation in glucose
-6-phosphate dehydrogenase activity were noted.The
depression in glycogen synthesis in scurvy was mostly due to
the limiting availability of uridine triphosphate and the
diminished activities of hexokinase and
phosphoglucomutase under vitamin-C deprivation . In
scorbutic conditions, there is also a depression in the TCA
cycle and electron transport chain whee V-C act as electron
acceptor and its function is highly specific.
2.Biotin and Carbohydrate
Replacing glucose in the diet with other
carbohydrates of low molecular weight like
sorbitol and fructose elevates the severity of biotin
deficiency.Since glucose utilization is impaired ,it
is likely that provision of other CHO, improves the
energy supply.
LIPID-LIPID INTER-RELATIONSHIPS
Lipids may be regarded as organic substances relatively insoluble in
water ,soluble in organic solvents (alcohol,ether etc ) ,actually or
potentially related to fatty acids and utilized by the living cells.
Lipids are the concentrated form of energy.
Lipid lipid interaction is that in which TRANS FATTY acids inhibit the
desaturation and elongation of linoleic acid and alpha –linolenic
acid to form long chain essential fatty acids .
Trans fatty acid -----Linoleic acid --------- alpha – linolenic acid--Essential fatty acid
Trans fatty acids
The food industry incorporates fats and oils into margarines ,
biscuits,cake,chocolates and other manufactures products.Food
manufactures use fats and oils that have been
 altered by the process of hydrogenation,i.e. adding hydrogen
atoms to the double bonds in monounsaturated fatty acids
and polyunsaturated fatty acids in order to increase the
degree of saturation of fatty acids in the oils.
Hydrogenation changes the configuration of some
monounsaturated fatty acids and polyunsaturated fatty acids.
Cis fatty acids have two hydrogen atoms attached to the
carbon on the same side of the double bond and molecule
bends at the double bond.In trans fatty acids , the hydrogen
atoms are placed on the opposite sides of the double bond
and the molecule stays straight at the double bond.
Trans fatty acids behave biologically as saturated fats rather
than like cis unsaturated fatty acids .The bulk of trans fatty
acids in hydrogenated fats are monounsaturated fatty acid –
Eladic acid which is trans equivalent to oleic acid.
Most of the dietary intake of fatty acids is derived from margarine ,
dalda and other foods manufactures from hydrogenated fats.
Saturated and short chain fatty acids
Stearic acid is a saturated fatty acid with no double bond .
It lowers the HDL but does not raise serum cholesterol reducing
both total and saturated fat.
Short chain fatty acids are organic anoins predominantly acetate ,
butyrate and propionate. In the caecum , these exist in the
production of 70%, 20% and 10% respectively.
Short chain fatty acids are produced by the colonic bacteria from
unabsorbed carbohygrates. They are utilized as a source of energy
by large intestine and stimulate its mucosal growth . The fatty
acids hydrolyzed from short chain fatty acids are transported to
the liver as free acids via the portal vein. They enter the
mitochondria of the liver cells and are oxidised rapidly.
Short chain fatty acids
intestine
Carbohydrates
Large
Protein- Lipids inter- relationships
1. Starvation Conditions
If gluconeogenesis were to contiue at accelerated rate during
early starvation ,skeletal muscles would soon be exhausted.
An adaptation in lipid metabolism occurs in long term
starvation so that ketone bodies (acetoacetate, beta
hydroxybutyrate) are formed. Ketone bodies cross blood
barrier to provide energy to brain and thereby spare body
protein from degradation .Production and utilization of
these ketone bodies result in reduction in protein
degradation and oxidation of amino acids . These
adaptations help conserve both energy and amino acids and
is reflected in output of nitrogen in urine , which is
decreased from 12gms in early starvation to 3gms nitrogen
per day by several weeks of starvation .
 When body fats stores are exhausted , body protein is again
mobilized for energy by means of an increase in muscle
protein degradation .This final increase in degradation of
body protein cannot be sustained for long if feeding does not
occur and death ensues.
2.Methionine and choline
The most abundant phospholipids in eukaryotic cells are
phosphatidylcholine and phosphatidylethanolamine. Both
can be synthesized from phosphatidylserine or through
alternative pathways that start with free choline or
ethanolamine respectively. 3 methyl groups of choline are
derived from amino acid methionine.
Choline
Phosphoatidycholine/ phosphatidyethanolamine
3. Glucagon and Lipid
Glucagon promotes fatty acid oxidation resulting in energy production and
ketone body synthesis .
Fatty acid
___oxidation_______
ATP + ketone
bodies
Fat – Mineral inter-relation
1. Fats and Calcium
An individual suffering from fat malabsorption shows decreased
calcium absorption due to the formation of fatty acid soaps
which are not absorbed and are excreted in faeces as ca soaps.
Fat intake has a negative impact on ca balance only during
steaorrhoea. Ca forms insoluble soaps with fatty acids in the
gut.
2.Lipids and Phosphorus
Phosphorus is bound with lipids to form phospholipids,like
lecithin and cephlain, which are present in every cell
membrane in the body
These are the integral part of cell structure and also act as an
intermediate in fat transport and absorption.
3.Iron and Fats
Poor fat digestion leads to steaorrhoea which also leads to a
decrease in iron absorption.
4.Fats and Sodium
Bacterial action on CHO and fibers in large bowel generates
short chain fatty acids: acetate, propionate and butyrate.
These are widely absorbed and stimulates sodium
absorption.
Fat – Vitamin inter-relation
1.Vitamin -c and Cholesterol
a) Ascorbic acid participates in hydroxylation of certain steroid
hormones synthesis in adrenal tissues.V- C con. decreases in
periods of stress when adrenal cortical hormone activity is high .
V-C
when Adernal cortical hormone
During periods of emotional , psychological stress , urinary
excretion of V – C inreacses.
b) The rate limiting step of bile acid synthesis in liver involves the
Cholesterol
7- alpha-hydroxylase
The activity of this pathway is reduced in V – C deficient animals
and is associated with elevated plasma cholesterol con. This leads
to hypercholesterolemia.
3. Vitamin –A and Fat
Retinoids and Cartenoids are incorporated into micelles along
with other lipids for passive absorption into mucosal cells of
small intestines . These then are incorporated
chylomicrons for transport
lymph and eventually
blood stream which then finally pass to liver and tissues .
The absorption of alpha ,beta, gamma ,carotene (provitamin A )
requires fat.
In the absence of fat in diet , they are not absorbed .
Rancid fats destroy the vitamin A and beta carotene present in
the diet.
2.V- D and Cholesterol
2 sterols one in lipids of animals i.e. 7-dehydrocholesterol
and one in plants i.e ergosterol- serve as precursor of V- D
And 7-dehydrocholesterol under UV rays
cholecalciferol(vitamin-D3).
Ergosterol
Ergocalciferol(Vitamin D2)
Then these D2 and D3 require further metabolism to yield
metabolically active form of 1,25 dehydroxy vitamin D or
cacitriol.
Dietary vitamin D is incorporated into other lipids into micells
and absorbed with lipids in intestine. Inside absorptive cells,
vitamin is incorporated into chylomicrons , enters lymphatic
system and subsequently enters plasma,where it delivered to
cells.
4. Vitamin E and Fat
Tocopherols act as antioxidant i.e. they can prevent the
oxidation of various other oxidized substances such as fats
and vitamin –A.
It is located in the lipid portion of cell membranes it protects
unsaturated phospholipids of the membrane from
oxidative degradation from highly reactive oxygen species
and other free radicals .Vitamin E perform this function
through its ability to reduce such radicls into harmless
metabolites by donating a hydrogen to them . This process
is called free radicals scavenging
As a membrane free radicals scavenger, V – E is an important
component of the cellular antioxidant defence system which
involves other enzymes such as SOD(superoxide
dismutases), glutathione peroxidases(GPxs), GR (
glutathione reductase, catalase and also non enzyme
factors many of which depends on other essential nutrients.
For eg – GSHxs, and TR depend on on slenium status etc .
So, the antioxidant function of vitamin E can be affected by the
levels of many other nutrients.
Fatty acids with 2 or more double bonds i.e. polyunsaturated
fatty acids are abundant in cell membrane and have important
infulence on membrane fluidity and function . However , their
double bonds make them susceptible to oxidation by free
radicals .
Fortunately , most V – E in body is found in cell membrane
where it functions to protect polyunsaturated fatty acids
from free radical attack .V- E stabilizes free radicals and
prevent it from reacting with adjacent polyunsaturated
fatty acids.
Also plasma lipoproteins, like cell membrane , contain an
abundance of lipid including proportions of
polyunsaturated fatty acids .
They also contain fat soluble V- E which plays an essential
role in protecting lipoproteins from oxidative damage.
This is particularly important in low density lipoproteins
(LDL) because lipid peroxides can oxidize apolipoprotein B
resulting in formation of oxidatively modified LDL.
apolipoprotein B
LDL
This oxidized LDL accumulates in walls of arteries at
greater rate than normal LDL which is non oxidised , thus
accelerating development of artherosclerotic plaques.
 Morover, V – E is absorbed in manner similar to most
other dietary lipids and requires fat digestion to be
functioning normally.
 The presence of fat in small intestine enhances V – E
absorption because the products of triglyceride
breakdown into gut promote the formation of mixed
micells , the vehicle from which V – E is absorbed into
the mucosal cell lining of the small intestine.
 Lack of the bile acids or fat digestive enzymes damage
to gastrointestinal wall or inability to synthesize
chylomicrons which will decrease V – E
absorption .
 Disease in which V – E absorption is reduced includes
pancreatic diseases and sometime other genetic
inability to make chylomicrons.
5. Vitamin K and
Fat
Like other fat soluble vitamin absorption of V - K is also depends
upon on minimum amount of dietary fat and on bile salts and
pancreatic juices . The absorbed V – K is incorporated to
chylomicrons in lymph and taken to liver , where are incorporated
VLDL and subsequently delivered to to peripheral tissues by LDL.
V- K
Chylomicrons(lymph --- liver )
VLDL
Tissues (LDL)
6. Fat and Choline
Choline is a methyl rich essential component of animal tissues ,
where it is a structural unit of lecithin (i.e. phosphatidylcholine or
phospholipids containing choline which is a part of bile where it
emulsifies fats and is a part of lipoprotein also) and
neurotransmitter acetylcholine. Thus choline is widely distributed
in fats , existing predominantly in form of lecithin in eggs , liver,
soyabeans , beef , milk and peanuts. Choline has several functions:
1.
2.
3.
4.
5.
As phosphatidycholine, it is a structural element of
membrane.
A precursor to spingolipids ( lipids esters attached to
spingosine base rather than glycerol and present in
nervous system of animals and membrane of plants and
lower eukaryotes such as yeast)
A promoter to lipid transport
As acetylcholine , it is a neurotransmitter.
It functions as emulsifier in bile , thues helping with
absorption of fat i.e. lipotropic factor and prevents
accumulation of fat in liver i.e. it prevents fatty liver.