Page 53 - MI-2-4

Microbes & Immunity Management of obesity

In the context of precision nutrition, fecal energy loss the host and to identify the biological, physiological, and
varies among individuals (ranging from 2% to 16%) due to sociodemographic factors that contribute to interindividual
methodological and biological differences. 26,27 variability. 32

7.1. Digestible energy uptake 7.2.1. Energy regulation
Research suggests that the gut microbiota in obese Multiple bacterial taxa have been associated with energy
individuals enhances energy extraction from food absorption or obesity. However, the mechanisms
33
compared to non-obese controls. This occurs through underlying these associations in humans remain unclear,
increased secretion of nutrient transporters and due to the reliance on relative abundance metrics of
fermentation of enzymes. Specifically, an elevation in microbial composition and the lack of investigation into
Clostridium ramosum (from the Firmicutes phylum) has community-wide functional interactions. A. muciniphila
been associated with upregulated expression of GLUT2 is a widely studied species inversely correlated with
(a glucose transporter) and CD36 (a fatty acid translocase), obesity in various model systems. A distinctive feature
34
thereby improving energy absorption. In addition, a of A. muciniphilla’s action is that a surface protein
higher Firmicutes/Bacteroidetes ratio in obese individuals (a postbiotic) mediates several of its metabolic effects.
correlates with increased digestion of polysaccharides, Its protective mechanisms against obesity involve
leading to greater production of monosaccharides and enhanced energy expenditure and increased fecal energy
35
SCFAs, such as acetate and butyrate. SCFAs contribute loss. B. thetaiotaomicron has shown decreased relative
significantly to the body’s energy supply – providing abundance in individuals with obesity. Treatment of mice
around 5 – 15% of total caloric intake and fulfilling 60 – with live B. thetaiotaomicron, but not heat-killed variants,
70% of the energy requirements of colonic epithelial cells. has been shown to reduce fat accumulation and increase
Furthermore, interspecies hydrogen (H ) transfer between lean mass. Methanobrevibacter smithii, the predominant
36
2
bacteria and archaea enhances energy uptake in obesity. methanogen in the gastrointestinal tract, is thought to
29
The coexistence of H -utilizing methanogenic archaea contribute to energy extraction by interacting with SCFA-
2
37
alongside H -producing bacteria facilitates the breakdown producing bacteria. Activation of the Takeda G protein-
2
of polysaccharides into SCFAs by relieving thermodynamic coupled receptor 5 in brown adipose tissue enhances
constraints during fermentation processes. mitochondrial biogenesis and thermogenesis by increasing
thyroid hormone activation. Similarly, activation of
7.2. Energy expenditure FXR in the intestine stimulates fibroblast growth factor
The absorption of food energy in the small intestine 15/19 secretion, which alters bile acid composition and
determines the fraction that can reach the colon. The promotes fat burning. However, gut dysbiosis associated
energy that arrives in the colon then becomes available with obesity reduces beneficial bile acid levels, impairing
to the gut microbiota for fermentation. The ultimate fate these energy-expending processes. 7
of the energy extracted by gut microorganisms remains
unclear, yet it is a crucial component of overall energy 7.3. SCFAs and metabolic impact
balance. 26,27 A compelling set of hypotheses has emerged Fecal and circulatory metabolites can indicate
regarding the quantitative exchange of energy between host–diet–microbiome interactions that influence energy
38
humans and gut microbes. It has been established that the balance. It is improbable that metabolites derived from
negative energy balance achieved through the alteration microbes significantly influence energy absorption
of the gut microbiota through a high-fiber, whole-food directly, as the energy content lost in feces is anticipated
diet is partially due to the diversion of energy from to be minimal. Nonetheless, there may be indirect
39
microbial activity in the colon toward microbial biomass involvement in energy balance associated with signaling
proliferation rather than host energy reserves. This is processes or due to these metabolites serving as indicators
26
likely a significant quantitative factor in energy balance, as of fermentation. The signaling roles of SCFAs are well-
mathematical modeling and previous studies 30,31 indicate documented in pre-clinical models and are thought to
that 25 – 50% of fecal energy originates from microbial influence adipose tissue through enhanced expression and
biomass. The correlation observed between microbial signaling from G-protein-coupled receptors 41 and 43.
40
biomass and changes in energy absorption on a high-fiber, SCFAs may also induce a transition from lipogenesis to
whole-food diet suggests that microbial growth serves as fat oxidation through peroxisome proliferator-activated
40
a mechanism to modify energy balance through precision receptor gamma-mediated signaling. Nonetheless,
nutrition. Further research is needed to quantify the there is debate as to whether individuals with obesity
26
bidirectional energy transfer between microorganisms and generate a greater or lesser quantity of SCFAs, rendering

Volume 2 Issue 4 (2025) 45 doi: 10.36922/MI025160036