I.
BACKGROUND
A complex community of microorganisms inhabits the mammalian gastrointestinal
tract from mouth to anus, but the colon is, by far, the main site of this
microbial colonization. As a consequence, progress in biology, physiology, and
nutrition has considerably broadened our view of the function and the
pathophysiological roles of the intestine, especially the large bowel. This
organ is no longer viewed solely as a storage vessel that produces feces and
eventually absorbs water and a few other simple molecules of both nutritive and
endogenous origin. Indeed, recent researchs has convincingly shown that the
large bowel and its microbiota form a strong symbiotic association and interact
with each other to play major roles not only in colonic function but also in
whole body physiology including endocrine activities, immunity, and even brain
function.
Bifidobacteria and Lactobacillus live
in great concentrations at the lower region of the small intestine and
predominantly in the large intestine. These beneficial bacteria take a role as
guards against harmful microbes living in the large intestine, keeping them
from invading the small intestine. The small intestine functions to digest and
absorb the majority of nutrients. When the body's immunity declines the risk of
infection increases, it is essential to keep the immune capacity high for
preventing or decreasing infection. Bifidobacteria and Lactobacillus have
recently been shown to increase gut and overall immunity.
There are several aspects of an
individual's health and diet that can adversely affect the gut microflora. High
levels of fat in the diet can negatively affect the level of Bifidobacteria in
the gut, as these beneficial bacteria are sensitive to increased levels of
faecal bile acids, which are directly related to the amount of fat in the diet.
Fatty diets may increase the amounts of bile acids in the faeces, and
consequently increase their inhibitory effect to Bifidobacteria. The nature of
the diet may also indirectly influence the gut conditions, which affect the
activity of Bifidobacteria. Disorders of gastric function or intestinal
motility may disturb the normal microbial balance.
Numerous studies have shown that an
imbalance of friendly to unfriendly gut bacteria (too few friendly bacteria)
can cause or aggravate various health conditions. Moreover, supplements aimed
at increasing the number of friendly bacteria have been shown to help combat
many types of diarrhea, irritable bowel syndrome, eczema, ulcerative colitis;
reduce the incidence of canker sores and vaginal yeast infections; and exert
positive effects on the immune system. Friendly gut bacteria consist of Lactobacillus
acidophilus, L. bulgaricus,L. reuteri, L. plantarum, L. casei, B. bifidus, S.
salivarius, S. thermophilus and the yeast Saccharomyces boulardi.
II. OBJECTIVES
The main objective of this paper is
to showcase :
1.
Brief
introduction of prebiotics
2.
Health
benefits of prebiotics
3.
Prebiotics
in food applications
III.
INTRODUCTION
The term “prebiotic”
was coined in 1995 by Gibson and Roberfroid,although prebiotics were recognized
as early as the 1950s when György and coworkers described “bifidus factor”, a
bifidogenic substance that selectively promoted the growth of bifidobacteria
(called Lactobacillus bifidus at that time). Human milk and colostrums were
found to contain large amounts of “bifidus factor”. In the 1970s and ’80s,
Japanese investigators pioneered the use of digestion-resistant saccharides to
favorably modify the intestinal microbiota using fructooligosaccharides,
galactooligosaccharides, and lactulose The 1980s and ’90s saw a marked increase
in the use of probiotics to favorably modify the intestinal microbiota and a concomitant
growth in interest in using prebiotics to achieve the same goal. In contrast to
the probiotic strategy for microflora modification by providing living
microorganisms, the prebiotic strategy seeks to stimulate the growth and/or
enhance the metabolic activity of the healthful bacteria already colonizing the
intestines. Prebiotics offer the ability to enhance the healthful strains in a
person’s unique community of bacteria including beneficial strains not
available as probiotics, such as Eubacterium species.
In 1995, Gibson and Roberfroid defined a prebiotic as a
“nondigestible food ingredient that beneficially affects the host by
selectively stimulating the growth and/or activity of one or a limited number
of bacteria in the colon, and thus improves host health.” This definition only
considers microbial changes in the human colonic ecosystem.Later, it was
considered timely to extrapolate this into other areas that may benefit from a
selective targeting of particular microorganisms and to propose a refined
definition of a prebiotic as (Gibson et al.2004): “a selectively fermented
ingredient that allows specific changes, both in the composition and/or
activity in the gastrointestinal microflora that confers benefits”
By definition, a prebiotic classifies
as a specific colonic nutrient. Most potential prebiotics are carbohydrates,
but the definition does not exclude non-carbohydrates to be used as a
prebiotic. Accordingly, the key characteristics that serve as criteria for
classification of a compound as prebiotics are resistance to digestive
processes in the upper part of the gastro intestinal tract and selective
fermentation by one or a limited number of the microorganisms in the intestinal
microbiota, especially the colonic microbiota, thus giving these a
proliferation advantage and consequently modifying the microbiota composition.
In order for a food ingredient to be
classified as a prebiotic , it must :
1) be neither hydrolyzed nor absorbed in the
upper part of the gastrointestinal tract.
2) be a selective substrate for one or a
limited number of beneficial bacteria commensal to the colon which are
stimulated to grow and/or are metabolically activated.
3) consequently, be able to alter the
colonie flora in favor of a healthier composition.
4) induce luminal or systemic effects
that are beneficial to the host health.
Prebiotics can be classified as a
type of digestion-resistant carbohydrate or dietary fiber. Like all fibers,
prebiotics resist breakdown by human digestive secretions and arrive relatively
unchanged in the lower regions of the intestinal tract where they can be
utilized as an energy source by the resident microflora. What distinguishes
prebiotics from other fibers is that prebiotics by definition selectively
stimulate the growth of only beneficial microfloral organisms such as
lactobacilli and bifidobacteria. A number of important dietary fibers like
cellulose and pectin fail to meet this definition. Prebiotic properties have
been ascribed to many types of carbohydrates, but they have been best
documented for digestion-resistant oligosaccharides (DGOs).
DGOs include
- inulin-type fructans
- galactooligosaccharides
-lactulose
-isomaltooligosaccharides
-xylooligosaccharides
-soy-oligosaccharides
-gentiooligosaccharide
-nigeroligosaccharides (Stephen
Olmstead, MD, David Wolfson)
Most prebiotics and prebiotic
candidates identified today are nondigestible oligosaccharides. They are
obtained either by extraction from plants (e.g.,chicory inulin), possibly
followed by an enzymatic hydrolysis (e.g., oligofructose from inulin) or by
synthesis (by trans-glycosylation reactions) from mono- or disaccharides such
as sucrose (fructooligosaccharides) or lactose (trans-galactosylated
oligosaccharides or galactooligosaccharides) .
IV.COMMONLY
USED PREBIOTICS
Inulin-type Fructans:
The prebiotic effects of inulin-type
fructans are well-established. Inulin-type fructans are linear DGOs composed of
fructose moieties linked by β(2à1) bonds. Inulin is arbitrarily
defined as a mixture of oligosaccharides with chain lengths of 2-60 fructose
molecules, with or without an initial glucose. Inulin-type fructans are storage
carbohydrates commonly found in wheat, onions,asparagus, bananas, garlic,
artichokes, and leeks. Inulin-type fructans have their greatest effect on
intestinal Bifidobacterium populations
Galactooligosaccharides:
Galactooligosaccharides are
digestion-resistant oligosaccharides naturally found in both human and cow’s milk.
They can also be derived from specific microbial fermentation of lactose or
synthesized using the enzyme β-galactosidase and lactose syrup. Galactooligosaccharides
selectively augment Bifidobacterium and Lactobacillus numbers
within the human intestinal microbiota. Prebiotic applications of
galactooligosaccharides are of great interest because of their natural
occurrence in human milk. Administration of galactooligosaccharides to
formula-fed infants has been shown to engender an intestinal flora similar to
that of breast-fed infants
Lactulose:
Lactulose is synthetic
galacto-fructose made by the isomerization of lactose. Although technically a
disaccharide, lactulose is generally grouped together with the DGOs. Lactulose
is not usually present in nature although very small amounts may be found in
heat-treated milk products as a result of non-catalyzed isomerization.. The β(1à4) bond in lactulose cannot be split
by human intestinal enzymes and is preferentially metabolized by colonic lactic
acid bacteria with lactate and short-chain fatty acids as major end products
with with significant increases in Bifidobacterium and Lactobacillus numbers
and reductions in Clostridium perfringens, Bacteroides, Enterobacteriaceae,
and Streptococcus populations
Fig: Different prebiotics |
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