Published online Oct 15, 2021. doi: 10.4239/wjd.v12.i10.1731
Peer-review started: June 28, 2021
First decision: July 15, 2021
Revised: July 24, 2021
Accepted: August 6, 2021
Article in press: August 6, 2021
Published online: October 15, 2021
Recently, specific immunometabolic profiles have been postulated in patients with schizophrenia, even before full-blown disease and independent of antipsychotic treatment. Proteomic profiling studies offer a promising potential for elucidating the cellular and molecular pathways that may be involved in the onset and progression of schizophrenia symptoms, and co-occurrent metabolic changes. In view of all this, we were intrigued to explore galectin-3 (Gal-3) as a glycan, and in our previous study, we measured its elevated levels in remission of schizophrenia. The finding may be a consequence of antipsychotic treatment and may have an impact on the onset of inflammation, the development of obesity, and the presumed cognitive changes in schizophrenia. In the animal study, it was shown that downregulation of Gal-3 was beneficial in insulin regulation of obesity and cognitive preservation. Strategies involving plasma exchange are discussed in this review, particularly in the context of Gal-3 elimination.
Core Tip: Atypical antipsychotic use can be associated with undesired metabolic effects. In that context, glycosylation has become a new target in the investigation of schizophrenia pathophysiology. As a glycan, galectin-3 (Gal-3) might be involved in the inflammation-insulin resistance-obesity cascade in schizophrenia, leading to cognitive changes. Eliminating Gal-3 influence may be beneficial in preserving cognition and reestablishing metabolic balance.