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Mathis Grossmann

70 years of clinical experience. On the other hand, in functional androgen deficiency due to axis suppression because of age-related comorbidities, treatment may aim for a specific health outcome, such as improvement of glucose metabolism, and

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Nami Kim, Jung Ok Lee, Hye Jeong Lee, Yong Woo Lee, Hyung Ip Kim, Su Jin Kim, Sun Hwa Park, Chul Su Lee, Sun Woo Ryoo, Geum-Sook Hwang, and Hyeon Soo Kim

Introduction In the muscles, glucose uptake occurs through two major pathways, namely insulin-dependent glucose uptake and non-insulin-dependent glucose uptake. In muscle cells, binding of insulin to insulin receptors increases the activation of the

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Hideyuki Takahashi, Yohei Kurose, Muneyuki Sakaida, Yoshihiro Suzuki, Shigeki Kobayashi, Toshihisa Sugino, Masayasu Kojima, Kenji Kangawa, Yoshihisa Hasegawa, and Yoshiaki Terashima

inhibits insulin secretion from rat pancreatic islets in a dose- and glucose-dependent manner ( Colombo et al. 2003 ) and from mouse islets in the presence of glucose ( Reimer et al. 2003 ). GHS-R antagonist and immunoneutralization of endogenous

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Bo Ahrén, Maria Sörhede Winzell, and Giovanni Pacini

versus i.v. glucose ( Elrick et al . 1964 , Perley & Kipnis 1967 ). This effect is partially achieved by gastrointestinal hormones that are released during meal ingestion and augment glucose-stimulated insulin secretion; the two most important being

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Fang Cai, Armen V Gyulkhandanyan, Michael B Wheeler, and Denise D Belsham

neuronal systems, through orexigenic or anorexigenic mechanisms. These neurons are modulated by circulating hormones, nutrient-derived signals, and cytokines. Specific neurons from the hypothalamus can sense nutrient-derived signals like glucose, and

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Alex Rafacho, Henrik Ortsäter, Angel Nadal, and Ivan Quesada

Introduction Glucocorticoids (GCs), such as cortisol in humans and corticosterone in rodents, are produced in the adrenal cortex and play a key role in the regulation of glucose homeostasis and nutrient metabolism. Synthetic GCs, which include

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Paula J Brunton, Katie M Sullivan, David Kerrigan, John A Russell, Jonathan R Seckl, and Amanda J Drake

al . 1998 , Welberg et al . 2000 , Lesage et al . 2004 , Brunton & Russell 2010 ) that later develop glucose intolerance ( Lindsay et al . 1996 b , Nyirenda et al . 1998 , Lesage et al . 2004 ), hypertension ( Benediktsson et al . 1993

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B Maiztegui, M I Borelli, M A Raschia, H Del Zotto, and J J Gagliardino

Introduction Glucose homeostasis depends on the balance between insulin levels and the response of peripheral tissues to insulin action; it can remain normal even when insulin action decreases due to a compensatory increase in β-cell insulin release

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Hyo-Sup Kim, Seung-Hyun Hong, Seung-Hoon Oh, Jae-Hyeon Kim, Myung-Shik Lee, and Moon-Kyu Lee

glucose levels ( Gutniak et al . 1992 , Nauck et al . 1993 , Thorens et al . 1993 ). Moreover, GLP1 increases the β-cell mass by inducing the differentiation and neogenesis of ductal cells into insulin-producing cells through regulation of PDX1

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Xuanchun Wang, Wei Gong, Yu Liu, Zhihong Yang, Wenbai Zhou, Mei Wang, Zhen Yang, Jie Wen, and Renming Hu

). Glucose is one of the most important factors by which the expression of genes in either β-cells or other cells of islets are regulated. Many glucose-responsive genes have been identified in β-cells or islets. Webb et al . (2000) identified glucose