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these findings indicate that intestinal L cells are responsive to PANDER, and elevated PANDER levels impair GLP-1 production in vitro and in vivo.
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PANDER strongly impacts hepatic lipid metabolism across metabolic states and may induce a selective hepatic insulin resistant phenotype via the LXR pathway.
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in-vitro and in-vivo glucose is a potent stimulator of the PANDER promoter within the liver and this response may be facilitated by ChREBP.
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F3MB(PANDER) decreases mice hepatic triglyceride and is associated with decreased DGAT1 expression
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X-ray crystal structure of the mouse FAM3B protein.
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these results demonstrated that the JNK-mediated signaling mechanism of palmitic acid -induced beta-cell apoptosis involves up-regulated expression of PANDER and activation of caspase-3.
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Data suggest a new link between the endocrine and immune systems and provide useful information for further investigating the physiological functions of PANDER and its involvement in inflammation-related pancreatic disorders.
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Palmitic acid induces the expression of PANDER and the apoptosis of beta-TC3 cells while glucagon-like peptide-1 counteracts the above effects through an activation of Akt signaling.
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PANDER promotes lipogenesis and compromises insulin signaling in the liver by increasing FOXO1 activity.
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Findings further indicate PANDER impacts glycemic levels and may represent a potential but complicated therapeutic target.
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A paracrine/endocrine effect of insulin on Pander release and a potential glucose-regulatory role for Pander.
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we provide evidence that identifies PANDER as a regulator of hepatic glucose metabolism, where it amplifies hepatic cAMP and cAMP-response element-binding protein signaling to induce gluconeogenic gene expression and glucose output.
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Potential role of PANDER in the pancreatic beta-cell for regulation or facilitation of insulin secretion, shown in PANDER knockout mice.
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In conclusion, Ad-PANDER infection is as effective as truncated recombinant PANDER to induce betaTC3 cell and mouse islet apoptosis.
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Because FAM3B (PANDER) mRNA expression is up-regulated by IFNgamma, a cytokine implicated in the pathogenesis of type 1 diabetes, PANDER may contribute to the pathogenesis of beta-cell death. (FAM3B)
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Tissue-specific and glucose-responsive expression of FAM3B promoter were studied.
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Because PANDER (FAM3B) is expressed by pancreatic beta-cells and in response to glucose in a similar way to those of insulin, PANDER may be involved in glucose homeostasis
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PANDER is a potential PDX-1 target gene and the A box sites within the promoter region are critical for basal and glucose-stimulated PANDER expression.
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liver is a target for PANDER, and PANDER may be involved in the progression of diabetes by regulating hepatic insulin signaling pathways.
