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. 2020 Jul 24;8(8):243.
doi: 10.3390/biomedicines8080243.

The Role of GPR120 Receptor in Essential Fatty Acids Metabolism in Schizophrenia

Joanna Rog  1 , Anna Błażewicz  2 , Dariusz Juchnowicz  3 , Agnieszka Ludwiczuk  4 , Ewa Stelmach  5 , Małgorzata Kozioł  6 , Michal Karakula  7 , Przemysław Niziński  2 , Hanna Karakula-Juchnowicz  1   8
Affiliations

The Role of GPR120 Receptor in Essential Fatty Acids Metabolism in Schizophrenia

Joanna Rog et al. Biomedicines. .

Abstract

A growing body of evidence confirms abnormal fatty acid (FAs) metabolism in the pathophysiology of schizophrenia. Omega-3 polyunsaturated fatty acids (PUFAs) are endogenous ligands of the G protein-coupled receptors, which have anti-inflammatory properties and are a therapeutic target in many diseases. No clinical studies are concerned with the role of the GPR120 signaling pathway in schizophrenia. The aim of the study was to determine the differences in PUFA nutritional status and metabolism between patients with schizophrenia (SZ group) and healthy individuals (HC group). The study included 80 participants (40 in the SZ group, 40 in the HC group). There were no differences in serum GPR120 and PUFA concentrations and PUFA intake between the examined groups. In the HC group, there was a relationship between FAs in serum and GPR120 concentration (p < 0.05): α-linolenic acid (ALA) (R = -0.46), docosahexaenoic acid (DHA) (R = -0.54), omega-3 PUFAs (R = -0.41), arachidonic acid (AA) (R = -0.44). In the SZ group, FA serum concentration was not related to GPR120 (p > 0.05). In the HC group, ALA and DHA serum concentrations were independently associated with GPR120 (p < 0.05) in the model adjusted for eicosapentaenoic acid (EPA) and accounted for 38.59% of GPR120 variability (p < 0.05). Our results indicate different metabolisms of FAs in schizophrenia. It is possible that the diminished anti-inflammatory response could be a component connecting GPR120 insensitivity with schizophrenia.

Keywords: FFAR4; G protein-coupled receptors; GPR120; long-chain fatty acids; nutritional psychiatry; omega-3; polyunsaturated fatty acids; schizophrenia.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

Figures

Figure 1
Figure 1
The scatter plot of the relationship between GPR120 and PUFA serum concentration in the SZ group. Spearman’s rank correlation coefficient was calculated.
Figure 2
Figure 2
The scatter plot of the relationship between GPR120 and PUFA serum concentration in the HC group. Spearman’s rank correlation coefficient was calculated.
Figure 3
Figure 3
The proposed mechanism of the connection between GPR120 insensitivity and impaired lipid metabolism in schizophrenia. In healthy individuals, GPR120 activation leads to anti-inflammatory effects. Natural ligands (DHA and ALA) stimulate GPR120–β-arrestin complex formation and drive phospholipase A2 (PLA2) activation. Pro-/anti-inflammatory homeostasis is maintained. In schizophrenia patients, GPR120 insensitivity leads to pro/anti-inflammatory imbalance. Natural ligands (DHA and ALA) are unable to stimulate GPR120–β-arrestin complex formation. Overactivity of PLA2 causes a switch to inflammatory pathway stimulation. Pro-/anti-inflammatory homeostasis is disturbed.
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