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Anti-diabetic effect of quercetin in type 2 diabetes mellitus by regulating the microRNA-92b-3p/EGR1 axis.
Ke, R Q; Wang, Y; Hong, S H; Xiao, L X.
Afiliación
  • Ke RQ; Department of Endocrinology, First Affiliated Hospital of Gannan Medical University, Ganzhou City, Jiangxi Province, China.
  • Wang Y; Department of Endocrinology, First Affiliated Hospital of Gannan Medical University, Ganzhou City, Jiangxi Province, China.
  • Hong SH; Department of Endocrinology, First Affiliated Hospital of Gannan Medical University, Ganzhou City, Jiangxi Province, China.
  • Xiao LX; Department of Endocrinology, First Affiliated Hospital of Gannan Medical University, Ganzhou City, Jiangxi Province, China. xiaolixia981107@qmu-edu.cn.
J Physiol Pharmacol ; 74(2)2023 Apr.
Article en En | MEDLINE | ID: mdl-37453091
ABSTRACT
Insulin resistance (IR) is predominantly causal for type 2 diabetes mellitus (T2DM). To solve this problem, this study particularly determined the role of quercetin (Que) in controlling IR in T2DM mice. The T2DM mouse model was established, and given 20 mg/kg/d Que by gavage for 6 weeks, and the lentiviral vector that interfered with microRNA-92b-3p (miR-92b-3p) or early growth response 1 (EGR1) expression was injected into the tail vein of T2DM mice. Blood glucose homeostasis and histopathological changes in the pancreas were observed after the corresponding treatment. miR-92b-3p and EGR1 expressions were assessed in T2DM mice, as well as their interlink. In results we found that Que could improve IR and pancreatic histopathological changes in T2DM mice. Low miR-92b-3p and high EGR1 were expressed in T2DM mice, while Que could upregulate miR-92b-3p to target EGR1. Enhancing miR-92b-3p or reducing EGR1 could further improve IR and pancreatic histopathological changes in T2DM mice after Que administration. Nevertheless, silencing miR-92b-3p or overexpressing EGR1 contributed to the opposite results. We concluded that Que exerted anti-diabetic effects in T2DM mice by regulating the miR-92b-3p/EGR1 axis.
Asunto(s)

Texto completo: 1 Base de datos: MEDLINE Asunto principal: Resistencia a la Insulina / MicroARNs / Diabetes Mellitus Tipo 2 Idioma: En Revista: J Physiol Pharmacol Asunto de la revista: FARMACOLOGIA / FISIOLOGIA Año: 2023 Tipo del documento: Article

Texto completo: 1 Base de datos: MEDLINE Asunto principal: Resistencia a la Insulina / MicroARNs / Diabetes Mellitus Tipo 2 Idioma: En Revista: J Physiol Pharmacol Asunto de la revista: FARMACOLOGIA / FISIOLOGIA Año: 2023 Tipo del documento: Article