Norathyriol reverses obesity- and high-fat-diet-induced insulin resistance in mice through inhibition of PTP1B

Ding, Hanying; Zhang, Yan; Xu, Chen; Hou, De‐Xing; Li, Jing; Zhang, Yujing; Wei, Peng; Zen, Ke; Zhang, Chenyu; Jiang, Xiaohong

doi:10.1007/s00125-014-3315-8

Cited by 29 publications

(23 citation statements)

References 29 publications

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“…Norathyriol and mangiferin demonstrated potent inhibition in α -glucosidase in vitro, and some references reported that these compounds also have many other bioactivities in diabetic pathways such as AMP-activated protein kinase [13], PPAR- α [14], and PTP1B [15]. Also mangiferin was found abundantly in natural source such as Rhizome of Common Anemarrhena , Mangifera indica L., and Mangosteen ( Garcinia mangostana ).…”

Section: Resultsmentioning

confidence: 99%

In Vitro and In Vivo Effects of Norathyriol and Mangiferin on α-Glucosidase

Shi

Yi-dan²,

Yuan

et al. 2017

Biochemistry Research International

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Norathyriol is a metabolite of mangiferin. Mangiferin has been reported to inhibit α-glucosidase. To the best of our knowledge, no study has been conducted to determine or compare those two compounds on inhibiting α-glucosidase in vitro and in vivo by far. In this study, we determined the inhibitory activity of norathyriol and mangiferin on α-glucosidase in vitro and evaluated their antidiabetic effect in diabetic mice. The results showed that norathyriol inhibited α-glucosidase in a noncompetitive manner with an IC50 value of 3.12 μM, which is more potent than mangiferin (IC50 = 358.54 μM) and positive drug acarbose (IC50 = 479.2 μM) in the zymological experiment. Both of norathyriol and mangiferin caused significant (p < 0.05) reduction in fasting blood glucose and the blood glucose levels at two hours after carbohydrate loading and it was interesting that mangiferin and norathyriol can make the decline of the blood glucose earlier than other groups ever including normal group in the starch tolerance test. However, norathyriol and mangiferin did not significantly influence carbohydrate absorption in the glucose tolerance test. Therefore, the antidiabetic effects of norathyriol and mangiferin might be associated with α-glucosidase, and norathyriol was more potent than mangiferin.

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Section: Resultsmentioning

confidence: 99%

In Vitro and In Vivo Effects of Norathyriol and Mangiferin on α-Glucosidase

Shi

Yi-dan²,

Yuan

et al. 2017

Biochemistry Research International

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“…To validate the role of PTP1B in delaying diabetic wound healing, a specific PTP1B inhibitor, FRJ, 14,30 was used. In this experiment, the PTP1B inhibitor was added to the wound every other day.…”

Section: Resultsmentioning

confidence: 99%

Protein Tyrosine Phosphatase 1B Impairs Diabetic Wound Healing Through Vascular Endothelial Growth Factor Receptor 2 Dephosphorylation

Zhang

Liu

et al. 2015

ATVB

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Objective Impaired wound healing is a major complication of diabetes mellitus. The mechanisms that govern wound healing, however, are complex and incompletely understood. In the present study, we determined the inhibitory role of protein tyrosine phosphatase 1B (PTP1B) in the process of diabetic wound healing. Approach and Results First, by comparing the wound healing process in PTP1B knockout (PTP1B−/−) mice, ob/ob mice and their wild-type littermates in the presence or absence of streptozotocin treatment, we showed that the inhibition of mouse wound healing in streptozotocin-induced diabetic conditions is because of the upregulation and activation of PTP1B. Second, the impaired wound healing in ob/ob mice and streptozotocin-treated wild-type mice was rescued by a PTP1B inhibitor. Third, PTP1B, which is upregulated under hyperglycemic condition, inhibited the tube formation, proliferation, and migration of human microvascular endothelial cells induced by vascular endothelial growth factor, whereas this inhibition was largely abolished by the PTP1B inhibitor. Finally, mechanism study further indicated that PTP1B likely suppressed the proliferation, migration, and tube formation of vascular endothelial cells through dephosphorylation of vascular endothelial growth factor receptor 2. Conclusions Our study demonstrated that PTP1B negatively modulated the diabetic wound healing process by dephosphorylating the endothelial cell vascular endothelial growth factor receptor 2 and that the specific inhibitor of PTP1B might serve as a potential novel therapeutic tool for diabetic wound healing.

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“…We also analyzed the effect of pharmacologic inhibition of PTP1B in reactive gliosis. Cotreatment with cytokines and the PTP1B inhibitor used at 10 lM as described 44 decreased by 2-fold GFAP protein levels in mouse retinal explants (Fig. 6A).…”

Section: Pharmacologic Inhibition Of Ptp1b Reduced Reactive Gliosis Imentioning

confidence: 89%

Inhibition of Protein Tyrosine Phosphatase 1B Improves IGF-I Receptor Signaling and Protects Against Inflammation-Induced Gliosis in the Retina

Arroba

Valverde

2015

Invest. Ophthalmol. Vis. Sci.

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Norathyriol reverses obesity- and high-fat-diet-induced insulin resistance in mice through inhibition of PTP1B

Abstract: Our results indicate that the small molecule norathyriol is a potent PTP1B inhibitor with good cell permeability and oral availability.

Cited by 29 publications

References 29 publications

In Vitro and In Vivo Effects of Norathyriol and Mangiferin on α-Glucosidase

In Vitro and In Vivo Effects of Norathyriol and Mangiferin on α-Glucosidase

Protein Tyrosine Phosphatase 1B Impairs Diabetic Wound Healing Through Vascular Endothelial Growth Factor Receptor 2 Dephosphorylation

Inhibition of Protein Tyrosine Phosphatase 1B Improves IGF-I Receptor Signaling and Protects Against Inflammation-Induced Gliosis in the Retina

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