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  • In conclusion our results showed that

    2022-01-25

    In conclusion, our results showed that FFAR1 can mediate the effect of PIO in attenuating β-cell lipoapoptosis through anti-oxidative stress, which may be related to the activation of the PLCγ-ERK1/2-PPARγ pathway. Our study helps not only to distinguish the role played by FFAR1 in lipotoxicity, but also to provide the experimental evidence on reducing β-cell lipotoxic damage as well as understanding the molecular mechanism underlying PIO as an FFAR1 agonist in attenuating pancreatic β-cell lipoapoptosis. In future studies, it will be important to decipher the mechanism by which PPARγ regulates GPR40 expression, potentially at the level of gene transcription. The primary limitation of the current study is that it consists only of in vitro data, and further experimentation is needed to ascertain the relationship between PIO treatment and GPR40 expression in vivo, in both animals and humans.
    Author contributions
    Funding This study was supported by Grants from the National Natural Science Foundation of China (grant number 81270940), Chinese Medical Association clinical research special funds (grant number 12030460346), and Natural Science Foundation of Fujian Province (grant number ). Youth Foundation of Fujian Provincial Department of Health (grant number 2013-2-44).
    Conflict of interest
    Acknowledgments
    Short Communication Free fatty TCEP receptors (FFAR) play significant roles in energy metabolism (Brown et al., 2005; Ichimura et al., 2009). The receptor FFAR1 is involved in insulin secretion in humans (Meidute Abaraviciene et al., 2013). Activation of the receptor FFAR2 increases lipid accretion and reduces lipolysis in mice (Hong et al., 2005). Short-chain fatty acids activate FFAR2, whereas medium- and long-chain fatty acids are ligands for FFAR1 (Brown et al., 2003; Kim et al., 2013; Yonezawa et al., 2013). Functionalities of bovine FFAR1 and FFAR2 have been demonstrated. Initially, Wang et al. (2009) showed decreasing acetate-, propionate-, and butyrate-activated cyclic AMP using bovine FFAR2-transfected Chinese hamster ovary (CHO) cells. Hudson et al. (2012) established pharmacological differences between human and bovine FFAR2; for example, by using the extracellular signal-regulated kinase1/2 phosphorylation assay. Manosalva et al. (2015) cloned and characterized bovine FFAR1 by measuring intracellular calcium levels after receptor activation and demonstrated effects of receptor activation on production of bovine neutrophil reactive oxygen species. Friedrichs et al. (2014) observed the greatest mRNA abundance of FFAR1 in liver compared with other tissues, which decreased after parturition. The mRNA of FFAR2 in liver, which is not regulated during the peripartal period, is higher compared with that in muscle but comparable to that in subcutaneous adipose tissue. Protein data on both receptors in bovine liver is not available yet. Because of the general association of FFAR1 and FFAR2 with energy metabolism in other species, the ubiquitous importance of the signal transduction pathways used by these receptors, and the importance of their ligands for bovine liver metabolism, we hypothesize that both receptors could be involved in the regulation of liver metabolism of dairy cows during the peripartal period. The increasing synthesis of BHB postpartum is driven by increasing fatty acid concentrations but also by other intermediates such as lactate and ketogenic amino acids and could be related to individual differences in the gluconeogenic capacity with propionate as main precursor for gluconeogenesis, as discussed by McCarthy et al. (2015a). High concentrations of BHB postpartum are related to changes in the abundance of enzymes linked to the reduction of hepatic β-oxidation in bovine liver (Li et al., 2012). Simultaneously, with increasing ketone body formation and fatty acid concentrations, the gluconeogenic activity of the liver is decreased (Grummer, 1993; McCarthy et al., 2015b). A higher prevalence of subclinical ketosis is observed when BHB exceeds 1.2 mmol/L postpartum (Suthar et al., 2013).