Effects of stanniocalcin hormones on rat hepatic glucose homeostasis under fed and fasted conditions

Souza, Samir Khal de; Sarapio, Elaine Renner; Vogt, Éverton Lopes; Schein, Vanessa; Fabres, Rafael Bandeira; Model, Jorge Felipe Argenta; Lima, Matheus Vieira; Rocha, Débora Santos; Silva, Roselis Silveira Martins da

doi:10.1016/j.ygcen.2020.113661

Cited by 3 publications

(2 citation statements)

References 39 publications

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“…Sarapio et al (2019) revealed that STC2 could decrease triacylglycerol synthesis, reducing glyceride/glycerol generation from 14C-glucose, direct phosphorylation of glycerol and fatty acid synthesis from 14Cglucose in eWAT of fed rats [26]. Khal et al (2021) also demonstrated STC2 involvement in the mammalian liver gluconeogenesis pathway [27]. Joshi et al (2022) identified mouse STC2, a novel aryl hydrocarbon receptor (AhR) target gene regulated by endogenous AhR agonists and tryptophan metabolite cinnabaric acid (CA) as having a protective effect on cells with alcohol-induced liver injury [28].…”

Section: Introductionmentioning

confidence: 99%

STC2 Inhibits Hepatic Lipid Synthesis and Correlates with Intramuscular Fatty Acid Composition, Body Weight and Carcass Traits in Chickens

Cao,

Jia,

Xing

et al. 2024

Animals

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Stanniocalcin 2 (STC2) is a secreted glycoprotein involved in multiple biological processes. To systemically study the biological role of STC2 in chickens, phylogenetic tree analysis and conservation analysis were conducted. Association analysis between variations in the STC2 gene and the economic traits of Gushi-Anka F2 was conducted. The tissue expression patterns of STC2 expression in different chicken tissues and liver at different stages were detected. The biological role of STC2 in chicken liver was investigated through overexpression and interfering methods in the LMH cell line. Correlation analyses between STC2 expression and lipid components were conducted. (1) The phylogenetic tree displayed that chicken STC2 is most closely related with Japanese quail and most distantly related with Xenopus tropicalis. STC2 has the same identical conserved motifs as other species. (2) rs9949205 (T > C) found in STC2 intron was highly significantly correlated with chicken body weight at 0, 2, 4, 6, 8, 10 and 12 weeks (p < 0.01). Extremely significant correlations of rs9949205 with semi-evisceration weight (SEW), evisceration weight (EW), breast muscle weight (BMW), leg muscle weight (LMW), liver weight and abdominal fat weight (AFW) were revealed (p < 0.01). Significant associations between rs9949205 and abdominal fat percentage, liver weight rate, breast muscle weight rate and leg muscle weight rate were also found (p < 0.05). Individuals with TT or TC genotypes had significantly lower abdominal fat percentage and liver weight rate compared to those with the CC genotype, while their body weight and other carcass traits were higher. (3) STC2 showed a high expression level in chicken liver tissue, which significantly increased with the progression of age (p < 0.05). STC2 was observed to inhibit the content of lipid droplets, triglycerides (TG) and cholesterol (TC), as well the expression level of genes related to lipid metabolism in LMH cells. (4) Correlation analysis showed that the STC2 gene was significantly correlated with 176 lipids in the breast muscle (p < 0.05) and mainly enriched in omega-3 and omega-6 unsaturated fatty acids. In conclusion, the STC2 gene in chicken might potentially play a crucial role in chicken growth and development, as well as liver lipid metabolism and muscle lipid deposition. This study provides a scientific foundation for further investigation into the regulatory mechanism of the STC2 gene on lipid metabolism and deposition in chicken liver.

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Section: Introductionmentioning

confidence: 99%

STC2 Inhibits Hepatic Lipid Synthesis and Correlates with Intramuscular Fatty Acid Composition, Body Weight and Carcass Traits in Chickens

Cao,

Jia,

Xing

et al. 2024

Animals

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“…STC2 has a lower identity (approximately 35%) with STC1 and fish STC [10]. In contrast to fish STC, STC1 and STC2 are expressed in virtually all tissues and act primarily as paracrine/autocrine factors to regulate various biological functions such as apoptosis, inflammation, and oxidative stress responses [11,12]. In particular, in vitro analysis of rat aortic VSMCs has shown that knockdown or overexpression of STC2 causes acceleration and inhibition of phosphateinduced calcification, respectively [13].…”

Section: Introductionmentioning

confidence: 99%

Stanniocalcin 2 Is Upregulated by Calcium-Sensing Receptor and Protects Human Vascular Smooth Muscle Cells from High-Phosphate-Induced Apoptosis

Liu¹,

Zhang²,

Huang³

et al. 2022

Cardiorenal Med

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Introduction Apoptosis of vascular smooth muscle cells induced by hyperphosphatemia is a critical mechanism of chronic kidney disease-related vascular disorders. The present study investigated whether extracellular calcium-sensing receptor (CaSR) regulates stanniocalcin 2 (STC2) expression in HAoSMCs in vitro and whether induced STC2 protects HAoSMCs from high phosphate-induced apoptosis. Methods and Results The constitutive expression of STC2 was confirmed in cultured HAoSMCs. STC2 mRNA and protein levels were increased significantly by calcimimetic NPS R-568 at a concentration of 1 microM with or without high phosphate. Conversely, calcilytic NPS-2143 at a concentration of 1 microM resulted in significantly decreased STC2 mRNA levels regardless of whether high phosphate was present, but decreased STC2 protein levels were only found under the high phosphate condition. Confocal microscopy demonstrated colocalization of STC2 and plasma membrane or endoplasmic reticulum markers. STC2 overexpression significantly reduced caspase-3 levels in HAoSMCs with or without high phosphate, whereas STC2 silencing resulted in significantly increased caspase-3 levels. TUNEL staining revealed the same tendency. Similar to STC2 overexpression, NPS R-568 treatment significantly reduced caspase-3 levels in HAoSMCs, but STC2 silencing abolished the protective effect of NPS R-568, which was also supported by TUNEL staining. Conclusion This is the first evidence that STC2 is regulated by CaSR in HAoSMCs. CaSR activation and the subsequent STC2 increase have putative anti-apoptotic effects against high phosphate. Thus, calcimimetics are promising agents to treat vascular injury associated with uremia.

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Research Progress of Stanniocalcin 2

张¹

2022

ACM

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Effects of stanniocalcin hormones on rat hepatic glucose homeostasis under fed and fasted conditions

Cited by 3 publications

References 39 publications

STC2 Inhibits Hepatic Lipid Synthesis and Correlates with Intramuscular Fatty Acid Composition, Body Weight and Carcass Traits in Chickens

STC2 Inhibits Hepatic Lipid Synthesis and Correlates with Intramuscular Fatty Acid Composition, Body Weight and Carcass Traits in Chickens

Stanniocalcin 2 Is Upregulated by Calcium-Sensing Receptor and Protects Human Vascular Smooth Muscle Cells from High-Phosphate-Induced Apoptosis

Research Progress of Stanniocalcin 2

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