Microbiome Relation to obesity

 

Can you explain your first impression of this image?

Yeah, there are 2 persons one is obese and the other one is thin or let me say of normal weight.

okay, After your explanation let's discuss the topic together...

Obesity is one of the most serious multifactorial diseases(occurs due to more than one factor which is classified into exogenous factors like unhealthy lifestyle, inadequate physical exercise, fast food, etc...)

and endogenous factors like genes, improper metabolic processes, and Gut microbiome...

The microbiome has relation to obesity also?????!!!!!

Recent studies illustrating that the microbiome has a strong relation to the occurrence of obesity...

The gut microbiome has control over our metabolic processes and obesity is one of the metabolic diseases. That's why recent studies have demonstrated that microbiome disturbance can lead to obesity.

To prove microbiome relation to obesity. Let's discuss this experiment:

 We have a group of germ-free mice

and 2 groups of obese and lean mice 

We colonize half of the germ-free mice with microbiota from lean mice. we call them group1.

and the other half of the germ-free mice are colonized with microbiota from obese mice. We call them group2.

Results:

Group 2 mice extracted more calories from food, and their body contents of fat become increased in a greater form than the Group1.

The percentage of difference that group2 is 47% greater than the group1 which is 27% only.Regarding the increase in body fat content.

These results illustrate that the microbiome affects caloric extraction and body fat content.

Consequently, We can relate microbiome disturbance to obesity.

Let's discuss simply the normal microbiome role in Carbohydrate metabolism(CHO):

Polysaccharides and complex CHO can't be digested through our digestive system. Here, the microbiome role comes.

The microbiome can metabolize them into Short-chain fatty acid (SCFA)like Butyrate, Propionate, and Acetate.

Butyrate:

• The primary energy source for colonocytes by promoting proliferation and maturation of colonocytes.
• Responsible for mucin production in the colon.

Acetate and Propionate:

 Can cross the intestine toward the liver and work on 2 metabolic processes which are lipogenesis(fat formation) and gluconeogenesis(carbohydrates formation).

Short-chain fatty acids(SCFs) are responsible for the release of the hormone of hunger which is (ghrelin) (orexigenic hormone)before the meal.

Followed by the release of GLP-1 (glucagon-like peptide1) and peptide YY(anorexigenic peptide) after the meal in the bloodstream.

Can you determine the function of GLP-1 and peptide YY????!!!

yes, GLP-1 and peptide YY are responsible for the Stimulation of insulin hormone release from the pancreas.

More increase in Short-chain fatty acids (SCFs) results in:

• Increase levels of GLP-1 and peptide YY.

• Decrease levels of ghrelin(hormone of hunger).

Consequently, there is an increase in satiety and decrease food intake.

Is Appetite decreased by this mechanism only??????!!!!

My dear reader Let me illustrate the situation, increase in SCFs can reduce appetite by:

• increase leptin hormone expression in adipocytes leading to reducing food intake and increasing energy expenditure.

For more illustration of the relation between microbiome and obesity. Let's discuss this experiment together:

We have :

•  Group A of germ-free mice (raised in a sterile environment) their gut is free from any microorganisms.

•  Group B of conventionally reared mice.

Then we feed Group A fatty diet more than Group B.

The result is :

• Group B mice have a 40% increase in body fat content. Although group B consume fatty food less than group A.

This result illustrates that microbiome has a relation to obesity.

Confirmatory step:

• Extract gut microbiota from conventional mice 
• Transplant this gut microbiota into germ-free mice(GroupA).

Result:

• There is a 60% increase in body fat content in germ-free mice (GroupA) within 2 weeks without any increase in food consumption or obvious difference in energy expenditure.

Consequently, those studies are suggestive to microbiome relation to obesity.

NOTE:

Microbiome not only works on caloric release but also affect host genes which are (FIAF) (Fasting Induced Adipocytic Factor)...

What FIAF do????????

FIAF is a lipoprotein lipase inhibitor.

Let's discuss how it works:

Firstly, Lipoprotein lipase is responsible for hydrolysis (destruction of Very low-density lipoprotein) which is circulating in the bloodstream into Triglyceride ( Fatty compound). So instead of fatty acid oxidation and energy production. lipoprotein lipase store fats in our tissues.

After that can you determine the role of FIAF???

 FIAF can inhibit lipoprotein lipase. So, it can reduce our body fat contents(adiposity).

From our discussion about microbiome functions. We can conclude that microbiome not only responsible for caloric release through short chains of fatty acids (SCFs) and energy expenditure through genetic modification of (FIAF).

Just microbiome relates to obesity through those mechanisms???!!

There is another so important mechanism which is microbiome diversity.

Recent studies illustrate that obese mice have :

• ↑ level of firmicutes phylum.
• ↓ level of Bacteroides phylum.

And the vice versa with the germ-free mice.

Let's prove our talk by this experiment:

• We have a group of mice we depend on their nutrition on a low-fat and sugar diet).
• Then we change their diet style to western diet(high-fat and sugar content).

• Let's observe what will happen with those mice.

Results:

• After one day to 2 weeks, there is a change in their contents of the gut microbiota and their gene expression.

Changes like what?????????

Those group of mice develop more adiposity.

For an accurate illustration of the change in their contents of gut microbiota. We note that those mice have :

• ↑ in firmicutes phylum.
• ↓ in Bacteroidetes phylum.

We discussed multiple studies on mice, Let's discuss this one on humans:

• Group1: African children depend on fibres mainly on their diet.
• Group2: European children depend on fat mainly on their diet.

We analysed their gut microbiota and we have found that:

• Group1 have more Bacteroidetes than group2.
• Group2 have more Firmicutes than group1.

The Bacteroidetes phylum is associated with a healthy diet rich in fibre.

The Firmicutes phylum is associated with an unhealthy diet rich in fats.

If this question comes in your mind now, you are an excellent reader.

What'S the question??????

If I depend on the fatty diet, is there any chance to change my microbiota to the healthy Bacteroidetes???

Don't worry gut microbiota are changeable. If you changed your diet style to a diet rich in fibres and low in sugars and fats, your microbiota would start to be changed within a day.

The more healthy diet you take, the more change in your gut microbiota.

But why more Firmicutes are associated with obesity regarding recent studies.

Firmicutes are responsible for fatty acid absorption and lipid droplets information.

Simply, I mean the more Firmicutes in our gut, the more fat absorption and higher chances of obesity.

But, Bacteriodetes are responsible for energy release from dietary fibres that's why Bacteriodetes are more abundant in healthy persons.

Consequently, We want to conclude regarding all previous evidence that microbiome has a strong relation to one of the most common health problems like obesity.

our health starts by having healthy microbiome.

If you are interested in gaining more knowledge about microbiome relation to body weight, Stay tuned for our next article to explore microbiome relation to insulin resistance.

References

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5082693/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4841968/

https://www.frontiersin.org/articles/10.3389/fphys.2019.00428/full

https://microbewiki.kenyon.edu/index.php/Firmicutes_and_Obesity

https://rdcu.be/b62qj

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