2018
DOI: 10.3892/mmr.2018.9400
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miR‑338‑3p mediates gluconeogenesis via targeting of PP4R1 in hepatocytes

Abstract: Hyperglycaemia is a characteristic of type 2 diabetes. In hepatocytes, impaired insulin sensitivity leads to increased gluconeogenesis and decreased glycogenesis. MicroRNA (miR)‑338‑3p is associated with tumour necrosis factor (TNF)‑α‑induced suppression of hepatic glycogenesis via regulation of protein phosphatase 4 regulatory subunit 1 (PP4R1). However, the effect of miR‑338‑3p on gluconeogenesis in hepatocytes remains unknown. In a previous study, it was demonstrated that miR‑338‑3p is downregulated in the … Show more

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Cited by 6 publications
(3 citation statements)
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“…Consistently, another study further confirmed that inhibition of PP4R1 rescued the effect of TNF-α on the generation of glycogen and regulated the activation of the insulin signaling pathway, suggesting the crucial role of PP4R1 in T2DM [13]. Additionally, Wang et al also reported that downregulation of PP4R1 significantly attenuated the increased level of glucose production in murine liver cells after treatment with TNF-α, indicating that PP4R1 participants in the regulation of TNF-α-induced gluconeogenesis [14]. Considering the important role of hepatic insulin resistance in the occurrence of T2DM, we concluded that PP4R1 may be associated with the onset or development of T2DM.…”
Section: Introductionmentioning
confidence: 52%
See 1 more Smart Citation
“…Consistently, another study further confirmed that inhibition of PP4R1 rescued the effect of TNF-α on the generation of glycogen and regulated the activation of the insulin signaling pathway, suggesting the crucial role of PP4R1 in T2DM [13]. Additionally, Wang et al also reported that downregulation of PP4R1 significantly attenuated the increased level of glucose production in murine liver cells after treatment with TNF-α, indicating that PP4R1 participants in the regulation of TNF-α-induced gluconeogenesis [14]. Considering the important role of hepatic insulin resistance in the occurrence of T2DM, we concluded that PP4R1 may be associated with the onset or development of T2DM.…”
Section: Introductionmentioning
confidence: 52%
“…The impairment of insulin sensitivity in the liver can result in increased gluconeogenesis and decreased glycogenesis [30]. As previous evidence described, PP4R1 is involved in the regulation of TNF-α-induced gluconeogenesis, and PP4R1 downregulation inhibits glucose production in murine liver cells after treatment with TNF-α [14]. In the present study, PP4R1 was determined to be elevated in the serum of T2DM patients and had the potential to distinguish T2DM patients from healthy controls, which was supported by the previous evidence.…”
Section: Discussionmentioning
confidence: 78%
“…Mind éhezés, mind inzulinrezisztenciás állapot hatására megnő a SMEK1 és SMEK2 expressziós szintje a májban, amely megemelkedett glükóz szinthez vezet [136]. Inzulinrezisztencia modellekben TNFα kezelés hatására a PP4 expressziója és stabilitása csökken [137], amely a glikogén szintézis csökkenéséhez vezet [138].…”
Section: Metabolizmusunclassified