Organizm każdego człowieka składa się z tysięcy genów, miliardów neuronów i trylionów bakterii. Liczba danych łączących mikrobiotę jelit i prawidłowy rozwój oraz funkcjonowanie centralnego układu nerwowego stale wzrasta. Podnosi się także poziom wiedzy na temat związku pomiędzy florą bakteryjną jelit a zaburzeniami psychicznymi. Zjawisko to zostało nazwane ,,osią jelito-mózg". Dotychczas najsilniejsze dowody na rolę, jaką pełnią mikroby w osi jelito-mózg, pochodzą z badań na zwierzętach. Oś jelito-mózg jest systemem dwukierunkowej komunikacji, który nie tylko zapewnia homeostazę układu pokarmowego, lecz także może mieć wpływ na motywację oraz inne wyższe funkcje mózgu, w tym funkcje poznawcze. Flora bakteryjna jelit może mieć ponadto związek z otyłością oraz chorobami zapalnymi układu pokarmowego, w których ryzyko wystąpienia zaburzeń psychicznych wzrasta. Wyniki najnowszych badań wskazują na związek między składem mikrobioty jelitowej a zaburzeniami psychicznymi u zwierząt (reakcja na przewlekły stres, depresja). Temat ten wymaga dalszych badań, szczególnie ze względu na wiążące się z nim potencjalne opcje terapeutyczne.

Dysfunction of the glutamatergic system, the main stimulating system in the brain, has a major role in pathogenesis of schizophrenia. The frontal white matter (WM) is partially composed of axons from glutamatergic pyramidal neurons and glia with glutamatergic receptors. The natural amino acid sarcosine, a component of a normal diet, inhibits the glycine type 1 transporter, increasing the glycine level. Thus, it modulates glutamatergic transmission through the glutamatergic ionotropic NMDA (N-methyl-d-aspartate) receptor, which requires glycine as a co-agonist. To evaluate the concentrations of brain metabolites (NAA, N-acetylaspartate; Glx, complex of glutamate, glutamine, and γ-aminobutyric acid (GABA); mI, myo-inositol; Cr, creatine; Cho, choline) in the left frontal WM, Proton Nuclear Magnetic Resonance (¹H-NMR) spectroscopy was used. Twenty-five patients randomly chosen from a group of fifty with stable schizophrenia (DSM-IV-TR) and dominant negative symptoms, who were receiving antipsychotic therapy, were administered 2 g of sarcosine daily for six months. The remaining 25 patients received placebo. Assignment was double blinded. ¹H-NMR spectroscopy (1.5 T) was performed twice: before and after the intervention. NAA, Glx and mI were evaluated as Cr and Cho ratios. All patients were also assessed twice with the Positive and Negative Syndrome Scale (PANSS). Results were compared between groups and in two time points in each group. The sarcosine group demonstrated a significant decrease in WM Glx/Cr and Glx/Cho ratios compared to controls after six months of therapy. In the experimental group, the final NAA/Cr ratio significantly increased and Glx/Cr ratio significantly decreased compared to baseline values. Improvement in the PANSS scores was significant only in the sarcosine group. In patients with schizophrenia, sarcosine augmentation can reverse the negative effect of glutamatergic system overstimulation, with a simultaneous beneficial increase of NAA/Cr ratio in the WM of the left frontal lobe. Our results further support the glutamatergic hypothesis of schizophrenia.

Ghrelin, a gastrointestinal peptide, is an endogenous ligand of growth hormone secretagogue receptor 1a (GHSR1a), which is mainly produced by X/A-like cells in the intestinal mucosa. Beyond its initial description as a growth hormone (GH) secretagogue stimulator of appetite, ghrelin has been revealed to have a wide range of physiological effects, for example, the modulation of inflammation; the improvement of cardiac performance; the modulation of stress, anxiety, taste sensation, and reward-seeking behavior; and the regulation of glucose metabolism and thermogenesis. Ghrelin secretion is altered in depressive disorders and metabolic syndrome, which frequently co-occur, but it is still unknown how these modifications relate to the physiopathology of these disorders. This review highlights the increasing amount of research establishing the close relationship between ghrelin, nutrition, microbiota, and disorders such as depression and metabolic syndrome, and it evaluates the ghrelinergic system as a potential target for the development of effective pharmacotherapies.