Breaking down the microbiology world one bite at a time

I am hungry because my microbiota is hungry?

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Animals, including humans, are composed of many kinds of cells, including their
own cells, but also microbial cells, such as bacteria found in the gut. All gut bacteria are
called gut microbiota, and they play an important role in digestion and nutrient
acquisition. You have probably had an antibiotic treatment, and even after the disease
is gone, you still feel some stomach discomfort when you eat your regular diet. One
reason for this is that antibiotics also kill your microbiota as a side effect, altering
between many other things, food digestion and nutrient absorption.

Your microbiota is all the symbiotic bacteria living in and on your body. In recent
years, many studies have shown that microbiota alteration is associated with several
pathologies, including obesity, however, it is unclear if its alteration is the cause, the
consequence, or both.

Animals’ intestines including mice and humans, have different cell types that
have diverse functions such as nutrient acquisition and regulation of food intake. A
recent study published in Nature Metabolism showed that the depletion of a specialized
cell type, named enteroendocrine cells (EECs) in the colon, produced obese mice.

In the first instance, the authors found that mice without ECCs (EEC ^ΔCol ) were
obese because the food intake was higher compared with wild-type mice [normal mice
without mutations] (red line vs blue line in the figure below). Since EECs play several
endocrine functions that can regulate appetite, it was highly probable that ECCs altered
the production of hormones involved in regulating feeding behavior.

However, they found important changes in the microbiota composition of EEC ^ΔCol
mice. To know if the microbiota alteration was a cause or consequence of obesity, the
EEC ^ΔColmice were treated with antibiotics to remove most of the gut microbiota.
Surprisingly, the EEC ^ΔColdid not gain weight, as happened in the EEC ^ΔColwith microbiota,
suggesting that the microbiota is indeed promoting obesity.

a. Comparison of the weight of wild-type mice (WT) [blue line] and mice without enteroendocrine cells (EEC ΔCol ) [red line]. It’s clear that EEC ΔCol mice increase their weight quickly across their lives (2 months—12 months). b Representative image of WT and EEC ΔCol mice. Source image: (Tan et al., 2024)

Maybe you wonder, how does gut microbiota promote obesity? The gut
microbiota produces many molecules (metabolites) crucial for the correct function of the
body. For example, vitamin K implicated in blood coating is produced by a specific
bacterium of the microbiota. In the current study, the authors found that EEC^ΔCol mice
had higher concentrations of microbiota-derived glutamic acid in stool and blood.

Interestingly, the researchers found that glutamic acid promotes appetite in wild-type
mice, indicating that the microbiota controls the feeding behavior of mice.
In conclusion, this research demonstrated that host cells such as EECs control
the composition of the microbiota. Such alteration in the gut microbiota composition
changes the production of metabolites, including glutamic acid, which controls animal
feeding behavior.

Although our gut microbiota is composed of entirely different organisms, it has a strong relationship with us that greatly impacts many physiological processes, including those implicated in brain functions such as feeding behaviors.

The next time that your intestine makes sounds, and you say to your friend, hey guy let´s go for lunch, my guts are telling me “Feed us now”, think for a moment that probably it is
not a joke.