disease ( Kelly & Jones 2013 b ). The hypogonadal–obesity cycle hypothesis was originally proposed by Cohen in 1999 to explain the relationship between low testosterone levels and metabolic disease. It was based on the finding that obesity impairs
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Ananda Malta, Júlio Cezar de Oliveira, Tatiane Aparecida da Silva Ribeiro, Laize Peron Tófolo, Luiz Felipe Barella, Kelly Valério Prates, Rosiane Aparecida Miranda, Ghada Elmhiri, Claudinéia Conationi da Silva Franco, Aryane Rodrigues Agostinho, Amanda Bianchi Trombini, Audrei Pavanello, Clarice Gravena, Latifa Abdennebi-Najar, and Paulo Cezar de Freitas Mathias
impacts on world health and links the action of poor nutrition at critical development stages with the onset of metabolic diseases later in life. Many metabolic diseases with high worldwide prevalence such as obesity, type 2 diabetes, and hypertension can
Jonathan M Mudry, Julie Massart, Ferenc L M Szekeres, and Anna Krook
and after 3 weeks of endurance training ( n =13). Results are mean± s.e.m. of fold of control. Discussion TWIST1 and TWIST2 expression is altered in adipose tissue in the context of metabolic disease and implicated in the regulation of cytokine
Galya Vassileva, Weiwen Hu, Lizbeth Hoos, Glen Tetzloff, Shijun Yang, Li Liu, Ling Kang, Harry R Davis, Joseph A Hedrick, Hong Lan, Timothy Kowalski, and Eric L Gustafson
the deletion of GPBAR1 has differential effect in males and females. Recently, GPBAR1 has emerged as a promising new target in metabolic disease. Although the relevance of our data to human GPBAR1 biology is not yet established, our findings of a
Yanli Miao, Haojie Qin, Yi Zhong, Kai Huang, and Caijun Rao
asprosin mainly focused on glucose homeostasis ( Li et al. 2019 ), it has been reported that asprosin is related to a range of metabolic diseases such as non-alcoholic fatty liver disease ( Ke et al. 2020 ), insulin resistance ( Yuan et al. 2020
Thomas Nicholson, Chris Church, Kostas Tsintzas, Robert Jones, Leigh Breen, Edward T Davis, David J Baker, and Simon W Jones
implications for the treatment of metabolic diseases such as type 2 diabetes ( Bluher 2014 , Bluher & Mantzoros 2015 ). It has long been established that the accumulation of abdominal fat (central adiposity) is associated with insulin resistance ( Pratley et
Juliane K Czeczor, Amanda J Genders, Kathryn Aston-Mourney, Timothy Connor, Liam G Hall, Kyoko Hasebe, Megan Ellis, Kirstie A De Jong, Darren C Henstridge, Peter J Meikle, Mark A Febbraio, Ken Walder, and Sean L McGee
been considered in the context of AD, only recently have they been examined in the context of whole body metabolism and metabolic disease states. Interestingly, a number of AD animal models with increased circulating Aβ levels are reported to
Kenshiro Shikano, Eiko Iwakoshi-Ukena, Takaya Saito, Yuki Narimatsu, Atsuki Kadota, Megumi Furumitsu, George E Bentley, Lance J Kriegsfeld, and Kazuyoshi Ukena
current state of knowledge cannot fully account for dysregulation of energy balance resulting in obesity, other unidentified factors and/or mechanisms likely play a role in the onset and progression of metabolic disease. As part of a search for novel
Laura D Brown
metabolic diseases in adulthood. Therefore, the objectives of this article are to i) review the fundamentals of fetal myogenesis; ii) review the experimental studies showing that fetal undernutrition from maternal dietary restriction or placental
Charlotte Lawson, Jose M Vicencio, Derek M Yellon, and Sean M Davidson
Introduction It is well established that patients with metabolic diseases, in particular insulin resistance and type 2 diabetes mellitus (T2DM), are more than twice as likely to develop accelerated cardiovascular disease (CVD) including
