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Gut bacteria in the cecum and large intestine produce SCFAs mainly from nondigestible carbohydrates that pass the small intestine unaffected

plant cell-wall polysaccharides, oligosaccharides, and resistant starches

inulin shifted the relative production of SCFAs from acetate to propionate and butyrate

age of approximately 3–4 years, when it becomes mature

SCFAs affect lipid, glucose, and cholesterol metabolism

colonocytes, the first host cells that take up SCFAs and which depend largely on butyrate for their energy supply

the microbiota educate the immune system and increase the tolerance to microbial immunodeterminants

the microbiota act as a metabolic organ that can break down otherwise indigestible food components, degrade potentially toxic food compounds like oxalate, and synthesize certain vitamins and amino acids

a large part of the SCFAs is used as a source of energy

The general idea is that colonocytes prefer butyrate to acetate and propionate, and oxidize it to ketone bodies and CO2

Exogenous acetate formed by colonic bacterial fermentation enters the blood compartment and is mixed with endogenous acetate released by tissues and organs (103, 104). Up to 70% of the acetate is taken up by the liver (105), where it is not only used as an energy source, but is also used as a substrate for the synthesis of cholesterol and long-chain fatty acids and as a cosubstrate for glutamine and glutamate synthesis

SCFAs regulate the balance between fatty acid synthesis, fatty acid oxidation, and lipolysis in the body.

Fatty acid oxidation is activated by SCFAs, while de novo synthesis and lipolysis are inhibited

obese animals in this study showed a 50% reduction in relative abundance of the Bacteroidetes (i.e., acetate and propionate producers), whereas the Firmicutes (i.e., butyrate producers) were proportionally increased compared with the lean counterparts.

increase in total fecal SCFA concentrations in obese humans.

In humans the distinct relation between the Firmicutes:Bacteroidetes ratio and obesity is less clear.

weight loss in obese individuals results in an increase in the abundance of Bacteroidetes

there is conflicting evidence on the composition of the obese microbiota phenotype with regards to Bacteroidetes and Firmicutes ratios

Bifidobacteria spp. from the phyla Actinobacteria, has been shown to be depleted in both obese mice and human subjects

While it is not yet clear which specific microbes are inducing or preventing obesity, evidence suggests that the microbiota is a factor.

targeted manipulation of the microbiota results in divergent metabolic outcomes depending on the composition of the diet

The microbiota has been linked to insulin resistance or type 2 diabetes (T2D) via metabolic syndrome and indeed the microbiota of individuals with T2D is also characterized by an increased Bacteroidetes/Firmicutes ratio, as well as an increase in Bacillus and Lactobacillus spp

It was also observed that the ratio of Bacteriodes-Prevotella to C. coccoides-E. rectale positively correlated with glucose levels but did not correlate with body mass index [80]. This suggests that the microbiota may influence T2D in conjunction with or independently of obesity

In humans, high-fat Western-style diets fed to individuals over one month can induce a 71% increase in plasma levels of endotoxins, suggesting that endotoxemia may develop in individuals with GI barrier dyfunction connected to dysbiosis

LPS increases macrophage infiltration essential for systemic inflammation preceding insulin resistance, LPS alone does not impair glucose metabolism

early treatment of dysbiosis may slow down or prevent the epidemic of metabolic diseases and hence the corresponding lethal cardiovascular consequences

increased Firmicutes and decreased Bacteroidetes, which is the microbial profile found in lean phenotypes, along with an increase in Bifidobacteria spp. and Lactobacillus spp

mouse and rat models of T1D have been shown to have microbiota marked by decreased diversity and decreased Lactobacillus spp., as well as a decrease in the Firmicutes/Bacteroidetes ratio

microbial antigens through the innate immune system are involved in T1D progression

The microbiota appears to be essential in maintaining the Th17/Treg cell balance in intestinal tissues, mesenteric and pancreatic lymph nodes, and in developing insulitis, although progression to overt diabetes has not been shown to be controlled by the microbiota

There is evidence that dietary and microbial antigens independently influence T1D

Lactobacillus johnsonii N6.2 protects BB-rats from T1D by mediating intestinal barrier function and inflammation [101,102] and a combination probiotic VSL#3 has been shown to attenuate insulitis and diabetes in NOD mice

breast fed infants have higher levels of Bifidobacteria spp. while formula fed infants have higher levels of Bacteroides spp., as well as increased Clostridium coccoides and Lactobacillus spp

the composition of the gut microbiota strongly correlates with diet

In mice fed a diet high in fat, there are many key gut population changes, such as the absence of gut barrier-protecting Bifidobacteria spp

diet has a dominating role in shaping gut microbiota and changing key populations may transform healthy gut microbiota into a disease-inducing entity

“Western” diet, which is high in sugar and fat, causes dysbiosis which affects both host GI tract metabolism and immune homeostasis