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Feng Wang, Lu Wang, Yifeng Wang, Dai Li, Tianpeng Hu, Manyi Sun and Ping Lei

-kinase (PI3K)/Akt-induced CREB activation exhibits neuroprotective effects ( Srivastava et al . 2018 ) and also improves cognitive function in rats ( Yang et al . 2018 ). Insulin-like growth factor-1 (IGF-1) is a polypeptide which is closely related

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Sriram Gubbi, Gabriela Farias Quipildor, Nir Barzilai, Derek M Huffman and Sofiya Milman

Introduction The growth hormone/insulin-like growth factor 1 (GH/IGF1) signaling pathway, also referred to as the somatotropic axis, has been extensively implicated in the aging process ( Bartke et al . 2003 , Kenyon 2010 , Barzilai et al

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Thalijn Liliana Catharina Wolters, Mihai Gheorghe Netea, Adrianus Rudolfus Marinus Maria Hermus, Johannes Willem Adriaan Smit and Romana Teodora Netea-Maier

significant. * P  < 0.05; ** P  < 0.01. IGF1, insulin-like growth factor 1; IL, interleukin; LPS, lipopolysaccharide; PBMC, peripheral blood mononuclear cell; P3C, Pam3Cys; RPMI, Roswell Park Memorial Institute (medium); TNF alpha, tumour necrosis factor alpha

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Rhonda D Kineman, Mercedes del Rio-Moreno and André Sarmento-Cabral

Introduction Although many tissues produce insulin-like growth factor-1 (IGF1), it is now recognized that the hepatocyte is the primary source of circulating IGF1 ( Sjogren et al . 1999 , Yakar et al . 1999 , LeRoith 2008 ). Despite the

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Richard C Lindsey, Charles H Rundle and Subburaman Mohan

:// ) 10.1210/endo-128-1-73 1846117 Chen C-Y Tseng K-Y Lai Y-L Chen Y-S Lin F-H Lin S 2017 Overexpression of insulin-like growth factor 1 enhanced the osteogenic capability of aging bone marrow mesenchymal stem

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Xin-wei Chen, Ye-hong Li, Meng-jun Zhang, Zhou Chen, Dian-shan Ke, Ying Xue and Jian-ming Hou

stress and age-related osteopenia in rats . Chinese Journal of Osteoporosis 2 .. Zhang W Shen X Wan C Zhao Q Zhang L Zhou Q Deng L 2012 Effects of insulin and insulin-like growth factor 1 on osteoblast proliferation and

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Ulas Ozkurede, Rishabh Kala, Cameron Johnson, Ziqian Shen, Richard A Miller and Gonzalo G Garcia

mice treated with rapamycin ( Zhou & Huang 2010 ) or calorie restriction ( Cummings & Lamming 2017 ). Mutants with lower growth hormone and insulin-like growth factor 1 (GH/IGF1) signaling, including Snell dwarf (DW), GH receptor deletion (GHR−/−) and

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Tingyuan Ren, Yuping Zhu, Xuejuan Xia, Yongbo Ding, Jing Guo and Jianquan Kan

This study aimed to evaluate the protein metabolism effect of Zanthoxylum alkylamides and to explore the potential mechanism in streptozotocin (STZ)-induced diabetic rats. Diabetic rats were orally treated with 2, 4 and 8 mg per kg bw of alkylamides daily for 28 days. Alkylamides decreased the relative weight of the liver and food intake, significantly increased the relative skeletal muscle weight and significantly decreased the blood urea nitrogen levels. Insulin, insulin-like growth factor 1, total protein (TP) and albumin (ALB), globular proteins and ALB proteins/globulin protein levels in serum significantly increased. TP, RNA content and RNA/DNA ratio significantly increased in the skeletal muscle of diabetic rats. Real-time quantitative polymerase chain reaction results indicated that alkylamides significantly increased the mRNA expression of insulin receptor (InR), IGF1 and insulin-like growth factor 1 receptor (IGF1R) in the liver and skeletal muscle. Moreover, the mRNA and protein expression levels of PI3K, PKB and mTOR significantly increased, whereas those of atrogin-1, muscle ring finger 1 and FOXO in the skeletal muscle significantly decreased. Alkylamides may advance protein synthesis by the PI3K/PKB/mTOR signalling pathway and attenuate the catabolism of protein through the ubiquitin–proteasome pathway. Therefore, it was possible that alkylamides ameliorate protein metabolism disorders in diabetic rats by activating the mTOR pathway.

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Lena Espelage, Hadi Al-Hasani and Alexandra Chadt

The two closely related RabGAPs TBC1D1 and TBC1D4 are key signaling factors of skeletal muscle substrate utilization. In mice, deficiency in both RabGAPs leads to reduced skeletal muscle glucose transport in response to insulin and lower GLUT4 abundance. Conversely, Tbc1d1 and Tbc1d4 deficiency results in enhanced lipid use as fuel in skeletal muscle, through yet unknown mechanisms. In humans, variants in TBC1D1 and TBC1D4 are linked to obesity, insulin resistance and type 2 diabetes. While the specific function in metabolism of each of the two RabGAPs remains to be determined, TBC1D1 emerges to be controlling exercise endurance and physical capacity, whereas TBC1D4 may rather be responsible for maintaining muscle insulin sensitivity, muscle contraction, and exercise. There is growing evidence that TBC1D1 also plays an important role in skeletal muscle development, since it has been found to be associated to meat production traits in several livestock species. In addition, TBC1D1 protein abundance in skeletal muscle is regulated by both, insulin receptor and insulin-like growth factor-1 (IGF-1) receptor signaling. This review focuses on the specific roles of the two key signaling factors TBC1D1 and TBC1D4 in skeletal muscle metabolism, development and exercise physiology.

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Leon A Bach

Introduction Insulin-like growth factor 1 (IGF1) and IGF2 are essential for normal pre- and postnatal growth and development ( Clemmons 2007 , Pollak 2008 ). These peptide growth factors are synthesised in most tissues and circulate at nanomolar