Stanniocalcin 1 effects on the renal gluconeogenesis pathway in rat and fish

Schein, Vanessa; Kucharski, Luiz Carlos; Guerreiro, Pedro; Martins, Tiago Leal; Morgado, Isabel; Power, Deborah M.; Canário, Adelino V.M.; Silva, Roselis Sm M. da

doi:10.1016/j.mce.2015.07.010

Cited by 17 publications

(10 citation statements)

References 70 publications

(87 reference statements)

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“…In addition, pro-STC1 treatments increased significantly the concentration of glutamine and glutamate which can enter the CAC or can be used for gluconeogenesis. This is in line with a recent report showing increased STC1-stimulated gluconeogenesis from 14 C-glutamine in sea bass kidney slices 22 . The significant increase in BCAAs in sea bass liver 24 h after the pro-STC1 treatment, possibly also originated from muscle.…”

Section: Discussionsupporting

confidence: 93%

“…However, STC binding is widespread in tissue, including mitochondria membranes of hepatocytes, myocytes and nephron cells, which together with the reported electron-transport chain stimulation suggests a role in cellular energy metabolism 20,21 . This is supported by recent in vitro studies which demonstrated STC1 modulation of renal gluconeogenesis in rat and fish 22 and lipogenesis in rat white retroperitoneal adipose tissue 23 .…”

Section: Introductionsupporting

confidence: 64%

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STC1 and PTHrP Modify Carbohydrate and Lipid Metabolism in Liver of a Teleost Fish

Bock

Silva

et al. 2019

Sci Rep

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Stanniocalcin 1 (STC1) and parathyroid hormone-related protein (PTHrP) are calciotropic hormones in vertebrates. Here, a recently hypothesized metabolic role for these hormones is tested on European sea bass treated with: (i) teleost PTHrP(1–34), (ii) PTHrP(1–34) and anti-STC1 serum (pro-PTHrP groups), (iii) a PTHrP antagonist PTHrP(7–34) or (iv) PTHrP(7–34) and STC1 (pro-STC1 groups). Livers were analysed using untargeted metabolic profiling based on proton nuclear magnetic resonance (1H-NMR) spectroscopy. Concentrations of branched-chain amino acid (BCAA), alanine, glutamine and glutamate increased in pro-STC1 groups suggesting their mobilization from the muscle to the liver for degradation and gluconeogenesis from alanine and glutamine. In addition, only STC1 treatment decreased the concentrations of succinate, fumarate and acetate, indicating slowing of the citric acid cycle. In the pro-PTHrP groups the concentrations of glucose, erythritol and lactate decreased, indicative of gluconeogenesis from lactate. Taurine, trimethylamine, trimethylamine N-oxide and carnitine changed in opposite directions in the pro-STC1 versus the pro-PTHrP groups, suggesting opposite effects, with STC1 stimulating lipogenesis and PTHrP activating lipolysis/β-oxidation of fatty acids. These findings suggest a role for STC1 and PTHrP related to strategic energy mechanisms that involve the production of glucose and safeguard of liver glycogen reserves for stressful situations.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionsupporting

confidence: 64%

STC1 and PTHrP Modify Carbohydrate and Lipid Metabolism in Liver of a Teleost Fish

Bock

Silva

et al. 2019

Sci Rep

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“…The function of STC1 was found to uncouple the process of oxidative phosphorylation via an increased expression of mitochondrial UCP2 [ 42 ] to reduce ATP synthesis [ 26 , 27 ]. Moreover, the effect of STC1 on the stimulation of gluconeogenesis in rat and fish kidneys was suggested [ 43 ], which is the endergonic process to consume cellular ATP. The reduced cellular ATP levels could be perceived by the key regulator in the cellular energy metabolism, AMPK a sensor of ADP/AMP/ATP ratio [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of STC1 overexpression on tumorigenicity and metabolism of hepatocellular carcinoma

Leung

Wong

2017

Oncotarget

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Stanniocalcin-1 (STC1) is a paracrine factor associated with inflammation and carcinogenesis. Using clinicopathological data, we previously reported that a greater expression of STC1 in hepatocellular carcinoma (HCC) was significantly correlated with smaller tumor size. The underlying mechanism on the correlation is not known. In this study, using a metastatic HCC cell-line (MHCC-97L, P) and lentiviral vector mediated-STC1 overexpression, the inoculation of STC1-overexpressing MHCC-97L (S1) cells in a nude mice xenograft model demonstrated reductions in tumor mass and volume. As compared with P cells, S1 cells exhibited epithelial phenotype with significantly lower plating efficiency and reduced migratory and proliferative potential. Using coulter counter for cell-sizing, S1 cells (17.6 μm) were significantly smaller than P cells (19.6 μm). Western blot analysis revealed that S1 cells exhibited reduced expression level of phosphorylated ribosomal protein S6 (p-rpS6). Moreover, an inhibition of the upstream kinase p70S6K was evident with the dephosphorylation of Thr389 in the linker domain of the kinase. The inhibition of p70S6K/p-rpS6 pathway was accompanied with reduced cellular ATP level and increase of p-AMPK in S1 cells. Significantly lower rates of glycolysis and extracellular O2 consumption in S1 cells exhibited a lower cellular energy status. Since a faster rate of ATP production is essential to support cancer growth and metastasis, the present study identified the effect of STC1-overexpression on reducing energy metabolism, leading to an activation of AMPK pathway but an inhibition of p70S6K/p-rpS6 signaling to reduce tumor growth.

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“…After the pre-incubation time, WRAT (300 ± 10 mg) slices were incubated for 60 min in flasks sealed with caps in [9,10]. Following incubation, the tissue slices were immediately homogenized in chloroform:methanol (2:1, v/v).…”

Section: Conversion Of 14 C-glucose To 14 C-lipidsmentioning

confidence: 99%

Stanniocalcin 1 Enhances Carbon Flux from Glucose to Lipids in White Retroperitoneal Adipose Tissue in the Fed Rat

Cozer

Trapp

Marques

et al. 2016

Lipids

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The present work assesses in vitro the role of human Stanniocalcin 1 (hSTC-1) in glucose metabolism in white retroperitoneal adipose tissue (WRAT) from fed rat. In the fed state, hSTC1 increases the incorporation of C from glucose into lipids in the rat WRAT. The increase in lipogenesis capacity supports the hypothesis that the activity of the glycerol-3-phosphate-generating pathway (glycolysis) from glucose is regulated by hSTC-1. The effect of hSTC-1 on de novo fatty acid synthesis and on glucose oxidation in WRAT is supported by an 85 % increase inCO production from C-glucose. The incubation of WRAT in the presence of hSTC-1 maintained the ADP/ATP ratio close to the control group. The presence of hSTC-1 in the incubation medium did not inhibit the lipolytic effect of epinephrine. In conclusion, hSTC-1 is one of the hormonal factors that control glucose metabolism in WRAT in the fed state.

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Stanniocalcin 1 effects on the renal gluconeogenesis pathway in rat and fish

Cited by 17 publications

References 70 publications

STC1 and PTHrP Modify Carbohydrate and Lipid Metabolism in Liver of a Teleost Fish

STC1 and PTHrP Modify Carbohydrate and Lipid Metabolism in Liver of a Teleost Fish

Effects of STC1 overexpression on tumorigenicity and metabolism of hepatocellular carcinoma

Stanniocalcin 1 Enhances Carbon Flux from Glucose to Lipids in White Retroperitoneal Adipose Tissue in the Fed Rat

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