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Mark C Turner, Neil R W Martin, Darren J Player, Richard A Ferguson, Patrick Wheeler, Charlotte J Green, Elizabeth C Akam, and Mark P Lewis

). Hyperinsulinaemia has been causally linked to the onset of diabetes in the early stages of the insulin resistance and in type 2 diabetes mellitus ( Corkey 2012 , Templeman et al. 2017 ), negatively affecting insulin-sensitive tissues such as liver, adipose and

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Louise K Metcalfe, Greg C Smith, and Nigel Turner

Insulin resistance and lipid metabolism Obesity and diabetes are metabolic conditions of increasingly widespread significance to modern populations. The global scale and gravity of their impacts on general health, life expectancy and quality

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Bo Zhou, Huixia Li, Jiali Liu, Lin Xu, Qinyue Guo, Hongzhi Sun, and Shufang Wu

-deficient mice exhibited resistance to diet-induced obesity and insulin insensitivity through the modulation of inflammation, whereas adipocytes exposed to PGRN have increased susceptibility to be insulin-resistant and those effects can be normalized with

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Tae Woo Jung, Yoon Hee Chung, Hyoung-Chun Kim, A M Abd El-Aty, and Ji Hoon Jeong

macrophages and T cells that infiltrate adipose tissue stimulate inflammation, which is thought to alter adipose tissue function, leading to metabolic disorders and systemic insulin resistance ( Olefsky & Glass 2010 , Sun et al . 2012 ). Various

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Jun Zhou, Qilong Wang, Ye Ding, and Ming-Hui Zou

Introduction Insulin resistance, a hallmark of obesity and fundamental cause of type 2 diabetes, is characterized by a diminished ability of insulin to regulate glucose homeostasis in insulin-sensitive organs including liver, skeletal muscle, and

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Huixia Li, Zhuanmin Zhang, Dongxu Feng, Lin Xu, Fang Li, Jiali Liu, Xinxin Jin, Zhuang Qian, Xiaomin Kang, and Hongzhi Sun

homeostasis and an increase in serum PGRN levels that were closely related to measures of adiposity, metabolic parameters, inflammatory marker and insulin resistance indices ( Hossein-Nezhad et al . 2012 , Alissa et al . 2017 ), potentially contributing to

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Lan Xu, Wenting Wang, Xinyue Zhang, Hanni Ke, Yingying Qin, Li You, Weiping Li, Gang Lu, Wai-Yee Chan, Peter C K Leung, Shidou Zhao, and Zi-Jiang Chen

of Reproduction 85 62 – 69 . ( https://doi.org/10.1095/biolreprod.110.088815 ) 10.1095/biolreprod.110.088815 21311036 Aguirre V Uchida T Yenush L Davis R White MF 2000 The c-Jun NH(2)-terminal kinase promotes insulin resistance during

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Hisashi Masuyama and Yuji Hiramatsu

Introduction Normal human pregnancy is characterized by mild fasting hypoglycemia, postprandial hyperglycemia, and hyperinsulinemia ( Cunningham et al . 2010 ). These responses are consistent with a pregnancy-induced state of insulin resistance

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Jian-Hua Chen, Maria Segni, Felicity Payne, Isabel Huang-Doran, Alison Sleigh, Claire Adams, UK10K Consortium, David B Savage, Stephen O'Rahilly, Robert K Semple, and Inês Barroso

Introduction Insulin action and linear growth are intimately linked, with crosstalk between insulin action and growth hormone/IGF1 signalling at multiple levels in liver and other tissues. This is attested to by the insulin resistance reported in

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Yanjun Liu, Yuichi Nakagawa, Ying Wang, Limei Liu, Hongwei Du, Wei Wang, Xiuhai Ren, Kabirullah Lutfy, and Theodore C Friedman

Introduction Excess glucocorticoid (GC) production (Cushing's syndrome) induces obesity and insulin resistance via activation of intracellular GC receptor (GR; Rizza et al . 1982 , Friedman et al . 1993 ). The GR belongs to a cytoplasmic nuclear