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Page 12 of 17 Sharma et al. Microbiome Res Rep 2024;3:3 https://dx.doi.org/10.20517/mrr.2023.51

Analyzing the commensal interaction between the host and Bifidobacterium, with a particular emphasis on
its impact on the intestinal lining, is crucial for comprehending its role. However, despite their increasing
popularity, there is still a limited understanding of the impacts of probiotics on the indigenous elements of
[96]
the human gut microbiota, as well as on the host organism .

The presence of the infant-type Bifidobacterium plays a major role in modulating the immune system since
infancy, with a possible indication that a reduced ratio of infant-type Bifidobacterium can result in a weaker
immune system, potentially raising the risk of developing autoimmunity in adulthood .
[97]

The production of neurotransmitters is a notable capability of bifidobacteria, as they are able to synthesize
important neurotransmitters such as serotonin, gamma-aminobutyric acid (GABA), and acetylcholine.
These neurotransmitters are essential for the regulation of mood, cognition, and behavior. When
synthesized within the gastrointestinal tract, they can exert a direct influence on the central nervous system.
It is imperative to acknowledge that investigations pertaining to the gut-brain axis are continuously
advancing.

Although there is an increasing body of evidence supporting the impact of bifidobacteria on mental well-
being, further research is required to fully understand the underlying mechanisms. Furthermore, it is
important to note that there can be variations in individual responses to bifidobacteria, and the efficacy of a
particular treatment may differ among individuals .
[98]
There exists an association between reduced quantities of a certain gut microorganism, Bifidobacterium, and
the presence of visceral obesity. Moreover, the association between Bifidobacterium abundance and visceral
fat seems to be influenced by serum uric acid (SUA) levels. Moreover, A negative correlation between SUA
levels and the abundance of Bifidobacterium is observed, suggesting that greater SUA levels were linked to
lower levels of this particular bacterial species. In contrast, there was a positive correlation found between
SUA and visceral fat area, indicating that elevated SUA levels were linked to greater amounts of visceral
[99]
fat .

Reduced levels of bifidobacteria have been observed in persons suffering from many medical disorders, such
as infections, cystic fibrosis, hepatitis B, and both Type I and Type II diabetes mellitus. This trend suggests a
possible role of bifidobacteria in the maintenance of overall physiological health. However, the exact cause-
and-effect relationship between decreased levels of bifidobacteria and the development or advancement of
these listed illnesses has yet to be definitively confirmed and clarified. Additional scientific investigation is
necessary to determine the underlying mechanisms of this apparent correlation .
[50]

Bifidobacteria play a major role in carbohydrate metabolism. Bifidobacteria do not employ the conventional
Embden-Meyerhof-Parnas (EMP) route for the metabolism of hexose carbohydrates. In contrast, the
researchers utilize a technique known as the “bifidshunt”, which specifically targets the enzyme fructose-6-
phosphoketolase. The aforementioned pathway offers a notable benefit in terms of its ability to generate a
greater amount of energy from carbs in comparison to the EMP pathway. In theory, the conversion of 1
mole of glucose yields 2.5 moles of ATP, along with 1.5 moles of acetate and 1 mole of lactate. The relative
proportions of acetate and lactate can exhibit variability, contingent upon the specific carbohydrate
substrate utilized and the developmental stage of the bacterial population. Moreover, the accelerated
utilization of an energy substrate leads to heightened lactate production and diminished acetate production,
[100]
whereas a slower utilization rate promotes elevated acetate production and reduced lactate production .
Thus, reduction in Bifidobacterium can be linked to metabolic dysfunction, thereby leading to metabolic