Home ENGLISH MAGAZINE Microbiota and type 2 diabetes: the fight for health is "intestine"

Microbiota and type 2 diabetes: the fight for health is “intestine”

Very recently, it has been recognized that the bacterial flora of the human gut plays a major role in health and in the appearance of diseases such as obesity, diabetes and cardiovascular diseases. Although many details remain unclear, new technologies have discovered many of the physiological benefits provided by the human microbiota. A healthy microbiota has a role in health, but imbalances can become pathological, increasing inflammation and contributing to metabolic dysfunction. Diet plays a significant role in the formation of the composition and function of the microbiota. Food choices high in fruit, vegetables, whole grains and legumes promote the abundance of healthier bacteria that produce short-chain fatty acids and other health-promoting metabolites.

The composition of the microbiota of the human intestine is highly individualized, with marked variations in the species present. The development of a healthy microbiota is strongly influenced by several factors: the mode of birth at birth, diet and nutrition, genetics, antibiotic use, vaccinations and the environment. Vaginal delivery infants are exposed to species Lactobacillus, Prevotella and Sneathia, while cesarean babies are dominated by bacteria on the skin such as Staphylococcus, Corynebacterium and Propionibacterium. Breastfed infants have larger populations of the genus Bifidobacterium and Ruminococcus, important fundamental species, with lower counts of Escherichia coli, Clostridium difficile, Bacteroides fragilis and Lactobacillus compared to newborns fed with infant formula. In fact, the known pre-biotics galacto-oligosaccharides are a key component in breast milk which increases the proliferation of Bifidobacterium adolescentis and catenulatum.

Bacteria communities become more complex since solid foods are introduced in young children and are complex for the age of 2-3 years as they are adults. The adult microbiota is relatively stable, but may be temporarily altered by dietary variations, diseases and the environment. When organ systems age, the same happens to the microbiota, becoming more susceptible to dysbiosis (imbalance) in older people. Antibiotics are believed to have made permanent changes in the human microbiome, reducing microbial diversity and healthy strains and thus reducing resistance to disease-associated pathogens. Antibiotic exposure during the first post-natal months was associated with a higher weight during adolescence. Similarly, long-term use of antibiotics is associated with weight gain in adults.

Some studies indicate that obese individuals have a higher percentage of Firmicutes and Actinobacteria and a reduced abundance of Bacteroidetes compared to their lean counterparts. The low number of genes, also reported in obese individuals, is associated with weight gain, insulin resistance, dyslipidemia, inflammation and fatty liver (steatosis). While a lower abundance of Prevotella and a greater number of Staphylococcus aureus has been reported in obese women. inflammation related to obesity in children seems to depend on staphylococcus. Dysbiosis related to type 2 diabetes produced similar results, with reductions of Bifidobacterium and Faecalibacterium prausnitzii, two bacteria known to have anti-inflammatory effects. Bacterial genes associated with oxidative stress are more abundant in type 2 diabetes, while butyrate-producing bacteria and those associated with vitamin synthesis have decreased. The abundance of Akkermansia muciniphila is inversely associated with obesity and diabetes and is known to control fat storage, inflammation of adipose tissue and glucose metabolism. Interestingly, metformin (antidiabetic drug) and prebiotics increase the abundance of this bacterium.

It is not completely clear how dysbiosis causes metabolic dysfunctions. It is hypothesized that the alterations in the microbiota interfere with intestinal permeability, allowing the lipopolysaccharide (LPS), a component of the cell walls of Gram-negative bacteria, to enter the host and thus contributing to the inflammation and subsequent resistance to insulin and to type 2 diabetes. Excessive fat intake has been associated with high levels of LPS in the blood and inflammation in humans. Weight gain can also trigger an inflammatory response, causing an increase in pro-inflammatory factors (cytokines) in adipose tissue and also affecting metabolism in liver and muscle tissues. It has also been proposed that the microbiota controls the metabolism of fatty acids, which has not been fully confirmed in humans. Hormones that regulate appetite and insulin sensitivity tend to be lower in people with type 2 diabetes and can be controlled by metabolites produced by the microbiota.

Therefore, if you are diabetic you should always moderate the intake of fats and, even more so, the sugars that are the first to provide energy and nourishment to the intestinal bacterial flora. At present, there are no specific recommendations for the use of probiotics in clinical practice for diabetes, although an increasing number of diabetologists and physicians recognize their potential. Over-the-counter products (supplements, single-stem probiotics, etc.), even if generally recognized as safe, may not contain optimal strains to improve diabetes outcomes. The addition of fermented foods to the diet is harmless and could potentially provide benefits to the health of the intestine. Further investigations will be needed to provide more specific and individualized nutritional recommendations, thus modulating the microbiota to prevent diabetes or improve the results of its drug therapy.

  • edited by Dr. Gianfrancesco Cormaci, specialist in Cinical Biochemistry.

Scientific references

He M, Shi B. Cell Biosci. 2017 Oct 25; 7:54.

Cani PD et al. ​Gut Microbes 2012; 3:279–288.

Tilg H, Moschen AR.Gut 2014; 63:1513–1521.

Shi BY. Chronic Dis Transl Med. 2016; 2(4):204-207.

Caricilli AM, Saad MJ. Nutrients 2013; 5:829–851.

Trasande L et al. Int J Obes (Lond) 2013;37:16–23.

Haro C et al. J Clin Endocrinol Metab 2016; 101:233–242.

Dott. Gianfrancesco Cormaci
- Laurea in Medicina e Chirurgia nel 1998 (MD Degree in 1998) - Specialista in Biochimica Clinica nel 2002 (Clinical Biochemistry residency in 2002) - Dottorato in Neurobiologia nel 2006 (Neurobiology PhD in 2006) - Ha soggiornato negli Stati Uniti, Baltimora (MD) come ricercatore alle dipendenze del National Institute on Drug Abuse (NIDA/NIH) e poi alla Johns Hopkins University, dal 2004 al 2008. - Dal 2009 si occupa di Medicina personalizzata. - Guardia medica presso strutture private dal 2010 - Detentore di un brevetto sulla preparazione di prodotti gluten-free a partire da regolare farina di frumento immunologicamente neutralizzata (owner of a patent concerning the production of bakery gluten-free products, starting from regular wheat flour). - Responsabile del reparto Ricerca e Sviluppo per la società CoFood s.r.l. (leader of the R&D for the partnership CoFood s.r.l.) - Autore di un libro riguardante la salute e l'alimentazione, con approfondimenti su come questa condizioni tutti i sistemi corporei. - Autore di articoli su informazione medica, salute e benessere sui siti web salutesicilia.com e medicomunicare.it