Protein tyrosine phosphatase 1B inhibits adipocyte differentiation and mediates TNFα action in obesity

Song, Dae‐Kyu; Chen, Yue; Li, Zhiyong; Guan, Yongjun; Zou, Da-jin; Miao, Chao‐Yu

doi:10.1016/j.bbalip.2013.05.006

Cited by 23 publications

(12 citation statements)

References 53 publications

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“…35 Furthermore, it was reported that PTP1B, IkB, and MAPKs are important proteins that inuence the IIS signaling pathway via activation of serine phosphorylated IRS-1. 17 The negative inuence of PTP1B on glucose and insulin homeostasis contributes to the development of diabetes, obesity 28 and other metabolic syndromes. 18 PTP1B is a potential screening target for anti-diabetic compounds.…”

Section: Discussionmentioning

confidence: 99%

Cichoric acid regulates the hepatic glucose homeostasis via AMPK pathway and activates the antioxidant response in high glucose-induced hepatocyte injury

et al. 2017

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Section: Discussionmentioning

confidence: 99%

Cichoric acid regulates the hepatic glucose homeostasis via AMPK pathway and activates the antioxidant response in high glucose-induced hepatocyte injury

et al. 2017

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“…We used the pLenti‐CMV‐EGFP‐3FLAG vector to encode β‐arrestin‐1 and in vitro transfection was carried out as described previously …”

Section: Methodsmentioning

confidence: 99%

Activating α7 nicotinic acetylcholine receptor inhibits NLRP3 inflammasome through regulation of β‐arrestin‐1

Peng

Shao

et al. 2017

CNS Neurosci Ther

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“…Among these are such protein kinases as c-Jun N-terminal kinase, IκB kinase, and MAPK, including extracellular signal-regulated kinase 1/2, play an important role. [57][58][59] Additionally, Song et al 60 showed more influence of TNF in the pathogenesis of complications of obesity. It has been shown that TNF reduces the differentiation of 3T3-L1 preadipocytes in vitro, probably due to the increase of PTP1B expression.…”

Section: Tumor-necrosis Factormentioning

confidence: 99%

Adipokines: biological functions and metabolically healthy obese profile

Pereira¹,

Alvarez-Leite²

2014

JRLCR

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Adipose tissue is an extremely active organ, and plays a fundamental role in the genesis of comorbidities associated with obesity. Since the discovery of leptin, an important focus has been assigned to adipose tissue as a key organ in the pathogenesis of metabolic disorders. The influence on the genesis of comorbidities associated with obesity is directly related to the pattern of adipokine secretion, the bioactive molecules produced on adipose tissue. The imbalance of adipokines consequent to the expansion of adipose tissue has been implicated in the development of the low-grade chronic inflammation seen in obesity. Adipokines act in a paracrine, autocrine, and endocrine fashion, influencing cytokine and chemokine secretions and hormonal and growth factors, as well as interfering with actions of insulin and lipid and glucose metabolism. The main adipokines include leptin, adiponectin, resistin, tumor-necrosis factor, interleukin 6, chemokine (C-C motif) ligand 2, interleukin 10, and transforming growth factor-β. The imbalance between pro-and anti-inflammatory adipokines on adipose tissue results in insulin resistance and the development of metabolic syndrome, type 2 diabetes, and cardiovascular disease. However, not all obese individuals develop these comorbidities or metabolic changes. Metabolically normal obese or metabolically healthy obese individuals have been the focus of research because of their absence of comorbidities. The profile of adipokines in adipose tissue of these individuals can be protective for the development of insulin resistance and metabolic disorders. This review emphasizes the roles of adipokines, the signaling pathways involved in the pathogenesis of inflammation and insulin resistance, and the profile found in metabolically healthy obese individuals.

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Protein tyrosine phosphatase 1B inhibits adipocyte differentiation and mediates TNFα action in obesity

Cited by 23 publications

References 53 publications

Cichoric acid regulates the hepatic glucose homeostasis via AMPK pathway and activates the antioxidant response in high glucose-induced hepatocyte injury

Cichoric acid regulates the hepatic glucose homeostasis via AMPK pathway and activates the antioxidant response in high glucose-induced hepatocyte injury

Activating α7 nicotinic acetylcholine receptor inhibits NLRP3 inflammasome through regulation of β‐arrestin‐1

Adipokines: biological functions and metabolically healthy obese profile

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