Search Results
Search for other papers by Nicolás Gigena in
Google Scholar
PubMed
Search for other papers by Vanina A Alamino in
Google Scholar
PubMed
Search for other papers by María del Mar Montesinos in
Google Scholar
PubMed
Search for other papers by Magalí Nazar in
Google Scholar
PubMed
Search for other papers by Ruy A Louzada in
Google Scholar
PubMed
Search for other papers by Simone M Wajner in
Google Scholar
PubMed
Search for other papers by Ana L Maia in
Google Scholar
PubMed
Search for other papers by Ana M Masini-Repiso in
Google Scholar
PubMed
Search for other papers by Denise P Carvalho in
Google Scholar
PubMed
Search for other papers by Graciela A Cremaschi in
Google Scholar
PubMed
Search for other papers by Claudia G Pellizas in
Google Scholar
PubMed
Introduction Thyroid hormones (THs) are critical regulators of cellular differentiation, growth and metabolism. The thyroid secretes 100% of circulating thyroxine (T 4 ). However, it provides a low percentage of serum levels of the most
Search for other papers by A Boelen in
Google Scholar
PubMed
Search for other papers by J Kwakkel in
Google Scholar
PubMed
Search for other papers by W M Wiersinga in
Google Scholar
PubMed
Search for other papers by E Fliers in
Google Scholar
PubMed
Introduction Acute systemic illness induced by bacterial endotoxin (lipopoly saccharide; LPS) administration, results in altered peripheral and central thyroid hormone metabolism, so-called nonthyroidal illness (NTI; Papanicolaou
Transgenic Research Center, Northeast Normal University, Changchun, Jilin, China
Search for other papers by Yang Chen in
Google Scholar
PubMed
Search for other papers by Xin Li in
Google Scholar
PubMed
Search for other papers by Jing Zhang in
Google Scholar
PubMed
Search for other papers by Mingjiao Zhang in
Google Scholar
PubMed
Search for other papers by Salah Adlat in
Google Scholar
PubMed
Search for other papers by Xiaodan Lu in
Google Scholar
PubMed
Search for other papers by Dan Li in
Google Scholar
PubMed
Search for other papers by Honghong Jin in
Google Scholar
PubMed
Search for other papers by Chenhao Wang in
Google Scholar
PubMed
Search for other papers by Zin Mar Oo in
Google Scholar
PubMed
Search for other papers by Farooq Hayel in
Google Scholar
PubMed
Search for other papers by Quangang Chen in
Google Scholar
PubMed
Search for other papers by Xufeng Han in
Google Scholar
PubMed
Search for other papers by Renjin Chen in
Google Scholar
PubMed
Search for other papers by Xuechao Feng in
Google Scholar
PubMed
Search for other papers by Luqing Zhang in
Google Scholar
PubMed
Search for other papers by Yaowu Zheng in
Google Scholar
PubMed
et al. 1996 ). Carolina E. Hagberg et al. found that Vegfb and nuclear-encoded mitochondrial genes have coordinated expression ( Hagberg et al. 2010 ), suggesting a close relationship between VEGFB and energy metabolism. It is reported that
Institute of Medical Sciences, University of Toronto, Toronto, Ontario, Canada
Department of Pharmacology, University of Toronto, Toronto, Ontario, Canada
Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada
Banting & Best Diabetes Centre, Toronto, Ontario, Canada
Search for other papers by Margaret K Hahn in
Google Scholar
PubMed
Banting & Best Diabetes Centre, Toronto, Ontario, Canada
Department of Physiology, University of Toronto, Toronto, Ontario, Canada
Search for other papers by Adria Giacca in
Google Scholar
PubMed
Department of Physiology, University of Toronto, Toronto, Ontario, Canada
Search for other papers by Sandra Pereira in
Google Scholar
PubMed
Introduction Breakthroughs in metabolic research rely upon in vivo studies using animal models, usually rodents. Assessment of glucose metabolism in rodents is a key component of diabetes research. Although general guidelines for
Search for other papers by Malin Hedengran Faulds in
Google Scholar
PubMed
Search for other papers by Chunyan Zhao in
Google Scholar
PubMed
Search for other papers by Karin Dahlman-Wright in
Google Scholar
PubMed
Search for other papers by Jan-Åke Gustafsson in
Google Scholar
PubMed
acid (FFA) metabolism (adiponectin, lipases), affect insulin sensitivity (PPARγ, insulin receptor substrates), affect lipid metabolism (CD36, apolipoprotein E), and are related to inflammation (tumor necrosis factor-α, C-reactive protein (CRP); reviewed
Search for other papers by Firoozeh Salehzadeh in
Google Scholar
PubMed
Search for other papers by Anna Rune in
Google Scholar
PubMed
Search for other papers by Megan Osler in
Google Scholar
PubMed
Search for other papers by Lubna Al-Khalili in
Google Scholar
PubMed
. 2010 ), indicating an important role of testosterone in metabolism. Interestingly, estradiol replacement therapy in postmenopausal women may partially provide cardiovascular protection and is suggested to be both estrogen receptor (ER) dependent and
Search for other papers by Corine Martineau in
Google Scholar
PubMed
Search for other papers by Louise Martin-Falstrault in
Google Scholar
PubMed
Search for other papers by Louise Brissette in
Google Scholar
PubMed
Search for other papers by Robert Moreau in
Google Scholar
PubMed
contribute to a healthy environment for bones. The product of the Scarb1 gene, the scavenger receptor class B, type I (SR-BI) is recognized as a high-affinity HDL receptor ( Acton et al . 1996 ) and is known for its role in HDL metabolism ( Cuchel & Rader
Search for other papers by Cathy A Guo in
Google Scholar
PubMed
Search for other papers by Shaodong Guo in
Google Scholar
PubMed
hyperglycemia, insulin resistance, hyperinsulinemia, hyperlipidemia, oxidative stresses and inflammation ( Battiprolu et al . 2010 ). These factors can cause energy metabolism alteration, calcium mishandling, mitochondrial dysfunction, apoptosis and myocardial
Search for other papers by A Albalat in
Google Scholar
PubMed
Search for other papers by C Liarte in
Google Scholar
PubMed
Search for other papers by S MacKenzie in
Google Scholar
PubMed
Search for other papers by L Tort in
Google Scholar
PubMed
Search for other papers by J V Planas in
Google Scholar
PubMed
Search for other papers by I Navarro in
Google Scholar
PubMed
and lipid metabolism in adipose tissue ( Sethi & Hotamisligil 1999 ). In fact, some authors have suggested that TNFα produced by the adipocyte itself acts as a true adipostat ( Bulló-Bonet et al. 1999 ). Described effects of TNFα on lipid metabolism
Search for other papers by I. M. D. JACKSON in
Google Scholar
PubMed
Search for other papers by K. D. BUCHANAN in
Google Scholar
PubMed
Search for other papers by M. T. McKIDDIE in
Google Scholar
PubMed
Search for other papers by C. R. M. PRENTICE in
Google Scholar
PubMed
SUMMARY
Carbohydrate metabolism has been investigated in eight patients with Klinefelter's syndrome. Seven of the eight had a normal oral glucose tolerance curve; one patient had slightly impaired tolerance. Plasma insulin levels were measured in response to the glucose load and were normal in six and slightly abnormal in two patients; one of the latter had an early increased and the other a delayed insulin response. No definite conclusions are reached regarding the possibility of a significant association between Klinefelter's syndrome and diabetes mellitus.