Combining different pharmaceuticals may be beneficial when treating disorders with complex neurobiology, including alcohol use disorder (AUD). The gut-brain peptides amylin and GLP-1 may be of potential interest as they individually reduce alcohol intake in rodents. While the combination of amylin receptor (AMYR) and glucagon-like peptide-1 receptor (GLP-1R) agonists have been found to decrease feeding and body weight in obese male rats synergistically, their combined impact on alcohol intake is unknown.

Therefore, the effect of the combination of an AMYR (salmon calcitonin (sCT)) and a GLP-1R (dulaglutide) agonist on alcohol intake in rats of both sexes was explored in two separate alcohol-drinking experiments. The first alcohol-drinking experiment evaluated the potential of adding sCT to an ongoing dulaglutide treatment, whereas the second alcohol-drinking experiment examined the effect when adding sCT and dulaglutide simultaneously.

When adding sCT to an ongoing dulaglutide treatment, a reduction in alcohol intake was observed in both male and female rats. However, when combining sCT and dulaglutide simultaneously, an initial reduction in alcohol intake was observed in rats of both sexes, whereas tolerance towards treatment was observed. In both alcohol-drinking experiments, this treatment combination consistently decreased food consumption and body weight in males and females. While the treatment combination did not affect inflammatory mediators, the gene expression of AMYR or GLP-1R, it changed fat tissue morphology.

Further investigation needs to be done on the combination of AMYR and GLP-1R agonists to assess their combined effects on alcohol intake.

There is a bi-directional biochemical communication pathway between the gastrointestinal tract and the central nervous system, referred to as the “gut–brain axis”. Studies show that bacteria in the gastrointestinal tract, including commensal, probiotic, or pathogenic, can affect brain’s function. Since there is a symbiotic relationship between gut microbiota and the brain, changes in its composition can lead to dysbiosis, which plays a role in many psychiatric disorders, such as depression and anxiety, and therefore becomes a potential therapeutic target.

To examine data from recent studies regarding the gut-brain axis and its relationship with psychiatric disorders, such as depression and anxiety.

Review of the most recent literature regarding the gut-brain axis and its relationship with depression and anxiety disorders. The research was carried out through the MedLine, PubMed, UptoDate, ScienceDirect, SciELO and SpringerLink databases, using the terms “gut-brain axis”, “depression” and “anxiety”, until December 2020.

There is a relationship between dysbiosis of microbiota and some psychiatric disorders, particularly depression. Symbiosis may be restored by purposefully manipulate the gut microbiota using therapies such as probiotics, therefore enhancing beneficial bacteria in the gastrointestinal tract and improving symptoms of depression.

Although probiotics can be used in the treatment of depression, further research is needed in order to carefully determine parameters such as the duration of treatment, dosage and drug interactions. Nonetheless, a better understanding of the gut-brain axis may arise new approaches on how we prevent and treat mental illnesses.

No significant relationships.

The gut microbiota constitute the largest and most diverse community in the body which is primarily responsible for the maintenance of the intestinal wall integrity and the protection against pathogens. Besides having an important role in the regulation of host energy metabolism, the gut microbiota can also influence neurodevelopment, modulate behavioral and might contribute to the development of psychiatry disorders.

The authors elaborated a narrative literature review to understand how gut microbiota can influence depression.

Using PubMed as the database, a research was conducted about how Gut Microbiota relates with Depression.

The microbiota-gut-brain axis encompasses the strong bidirectional communication between the gut microbiota and the CNS. Multiple mechanisms may be involved in this bilateral communication, including immune, endocrine and neural pathways. Permutations in the gut microbiome composition trigger microbial lipopolysaccharides production that activates inflammatory responses. Cytokines send signals to the vagus nerve, which links the process to the hypothalamic-pituitary-adrenal axis that consequently causes behavioral effects. Beyond this, gut microbiota have the capacity to produce many neurotransmitters and neuromodulators such as serotonin and can induce the secretion of the brain-derived neurotrophic factor, an important plasticity-related protein that promotes neuronal growth, development and survival.

Neuroinflammatory processes like those that occur in depression are deeply modulated by peripheral inflammatory stimuli, especially those from the intestinal microbiota. However, the knowledge is currently limited and the information available is not enough to understand the exact mechanisms. Therefore, more studies are required to show how gut microbiota influences the human brain.

No significant relationships.