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diseases. Further, a study ( 13 ) has revealed that GPC4 levels are related to BMI and insulin sensitivity in humans, and that GPC4 directly binds to insulin receptors in the liver, skeletal muscle, and adipose tissue to enhance insulin signaling. The
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partly due to the predominance of stimulating β-receptors over antilipolytic α-adrenoreceptors, and lower insulin receptor affinity of mesenteric omental adipocytes respectively (27, 29) . In addition to differences in lipolysis at different
Institute of Clinical Medicine, University of Oslo, Oslo, Norway
Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog, Norway
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Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog, Norway
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catecholamines that inhibit insulin secretion and increase insulin resistance ( 14 ). In addition, we suggest that insulin-related molecules partly mimicking insulin may block the insulin receptor, and thereby contribute to hyperglycaemia. Secondly, rare cases
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-stimulating hormone receptor ( FSHR ) gene polymorphisms, fat mass and obesity-associated ( FTO ) gene polymorphisms, insulin receptor ( IR ) and IR substrate ( IRS ) polymorphisms, vitamin D receptor ( VDR ) polymorphisms, methylenetetrahydrofolate reductase ( MTHFR
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also of great importance ( 2 ). Insulin interacts with receptors in the cell membrane. It thus stimulates signal transduction pathway. Insulin signaling molecules include insulin receptor substrate 1 (IRS1), phosphatidylinositol 3-kinase (PI3K), and
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shown that insulin receptor tyrosine kinase (IRTK) activity is influenced by physiological polyamines such as spermine which have similar effects with insulin ( 22 , 23 , 24 ). Thus, it is suggested that polyamines may play an important role in the
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/insulin-like growth factor-1 pathway, thereby promoting the proliferation and differentiation of thyroid cells ( 18 ). The expression of the insulin receptor gene increases in the early stages of thyroid carcinoma ( 19 ). Insulin may promote cell proliferation through
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tyrosine-autophosphorylated insulin receptor, then activate insulin receptor substrate 1 (IRS1), and finally stimulates glucose transport via activating GLUT-4 ( 22 ). Increased insulin levels and GLUT-4 translocation promote glucose uptake and energy
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Raphael Recanati Genetic Institute, Rabin Medical Center – Beilinson Hospital, Petach Tikva, Israel
Felsenstein Medical Research Center, Petach Tikva, Israel
Pediatric Genetics, Schneider Children’s Medical Center of Israel, Petach Tikva, Israel
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Jesse Z. and Sara Lea Shafer Institute for Endocrinology and Diabetes, Schneider Children’s Medical Center of Israel, Petach Tikva, Israel
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Shalom and VardaYoran Institute for Human Genome Research, Tel Aviv University, Tel Aviv, Israel
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Jesse Z. and Sara Lea Shafer Institute for Endocrinology and Diabetes, Schneider Children’s Medical Center of Israel, Petach Tikva, Israel
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receptors could result in a high content of hybrid receptors, composed of one αβ IGF1R hemireceptor linked to one αβ insulin receptor hemireceptor. Hybrid receptors containing the IR-B isoform are expressed predominantly in muscle and adipose tissue ( 29
Department of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan
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Toronto General Research Institute, University Health Network, Toronto, Ontario, Canada
Division of Endocrinology and Metabolism, Leadership Centre for Diabetes, Mount Sinai Hospital, Toronto, Ontario, Canada
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Department of Pathology, Humber River Regional Hospital, Toronto, Ontario, Canada
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that new concentrated glargine and biosimilar glargine would contribute to increasing the number of patients treated with glargine, the potential cancer-promoting effect of glargine requires more detailed investigation. Insulin receptor (IR) and