As we have discussed on numerous occasions, a persistent dramatic change in diet and lifestyle can damage the symbiosis between the microbiota and the human being by producing dysfunctional signaling in peripheral neurons.

Our central nervous system is composed of neurons that coordinate intestinal functions such as gastrointestinal motility, digestion, immunity, feeding behavior and glucose and lipid homeostasis, among others.

The high degree of intercommunication between the intestine and the peripheral nervous system is noteworthy.

THE NEURONS

  • Vagal and spinal neurons innervate digestive touch by monitoring mechanical, chemical, thermal and nociceptive signals related to diet and microbiota.
  • Sympathetic and parasympathetic efferent neurons are secreted according to functions that assist in stress responses (fight or flight) or return to baseline (rest and digestion).
  • Vagal afferent neurons respond to alterations in the intestinal microbiota and modulate intestinal motility.
  • Sensory neurons detect various chemicals or distention caused by the food bolus and coordinate the electrical activity of the neurons and link the activity of the motor networks to allow the "little brain" of the intestine to function autonomously.

The enteric nervous system can function autonomously to digest a meal, but the function of these neurons is modulated by the autonomic nerves according to the internal state.

 

MOLECULAR MECHANISMS MEDIATING MICROBIOTA - SNP COMMUNICATION

Endothelial cells (EECs) represent a very important part of the hormonal pathway of communication between the gut and PNS. They respond to chemical by-products and molecules that are released by intestinal bacteria which, in turn, release neuropeptides that are able to activate sensory neurons to directly target effector tissues and thus control gastric emptying, intestinal motility, insulin release, satiety and hunger.

  • Lipopolysaccharide (LPS) and lipoprotein acid (LTA)

Circulating LPS levels are altered according to diet such that the more weight, the higher the LPS levels increase.

Disruption of signaling in enteric neurons may contribute to impairments in enteric nerve development, intestinal motility, immunity and visceral perception.

  • Serotonin

Intestinal bacteria regulate the production and release of seortonin thanks to bile acids from their metabolism.

Serotonin adjusts motility, intestinal inflammation and visceral pain

  • Bile acids

They are produced by the liver and secreted into the intestine to emulsify dietary fat and cholesterol. Bacteria can modify these acids and convert them into signaling molecules that regulate feeding behavior (reduce food intake preventing diet-induced obesity and regulate glucose homeostasis).

  • GABA

It is a neurotransmitter that can be produced by various Lactobacillus and Bifidobacteria that controls gastric emptying, motility and digestive secretions.

An increase in GABA means an improvement in insulin sensitivity and therefore an improvement in the metabolic syndrome.

  • Short chain fatty acids

Produced by the fermentation of fiber by various genera of bacteria. They regulate intestinal gluconeogenesis, heart rate, energy expenditure and food intake (short-term feeding behavior in adults).

  • Cocaine-amphetamine regulated transcript (CART)

CART is a neuropeptide expressed in the CNS that is modulated as a function of feeding status by the microbiota and regulates glucose homeostasis through direct communication with the pancreas and liver.

 

COMMUNICATION OF THE INTESTINAL MICROBIOTA TO THE SNP AS A THERAPEUTIC TARGET

Sensory and autonomic nerves innervating the GI tract are sensitive to infection, inflammation and local metabolites that can lead to changes in energy and glucose homeostasis, GI motility deficits, SSI, dyspepsia, diabetes or obesity.

Microbiota-targeted treatments for these ailments come in the form of prebiotics, probiotics, postbiotics and fecal microbiota transplantation.