scholarly journals Body Iron Stores and Glucose Intolerance in Premenopausal Women: Role of hyperandrogenism, insulin resistance, and genomic variants related to inflammation, oxidative stress, and iron metabolism

Diabetes Care ◽  
2009 ◽  
Vol 32 (8) ◽  
pp. 1525-1530 ◽  
Author(s):  
M. A. Martinez-Garcia ◽  
M. Luque-Ramirez ◽  
J. L. San-Millan ◽  
H. F. Escobar-Morreale
2009 ◽  
Vol 54 (4) ◽  
pp. 268-274 ◽  
Author(s):  
Petr Syrovatka ◽  
Pavel Kraml ◽  
Jana Potockova ◽  
Lenka Fialova ◽  
Martin Vejrazka ◽  
...  

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2048-P
Author(s):  
BENJAMIN J. RYAN ◽  
DOUGLAS W. VAN PELT ◽  
LISA M. GUTH ◽  
ALISON LUDZKI ◽  
RACHEL A. GIOSCIA-RYAN ◽  
...  

Endocrinology ◽  
2010 ◽  
Vol 151 (11) ◽  
pp. 5157-5164 ◽  
Author(s):  
Thomas A. Bowman ◽  
Sadeesh K. Ramakrishnan ◽  
Meenakshi Kaw ◽  
Sang Jun Lee ◽  
Payal R. Patel ◽  
...  

Rats selectively bred for low aerobic running capacity exhibit the metabolic syndrome, including hyperinsulinemia, insulin resistance, visceral obesity, and dyslipidemia. They also exhibit features of nonalcoholic steatohepatitis, including chicken-wire fibrosis, inflammation, and oxidative stress. Hyperinsulinemia in these rats is associated with impaired hepatic insulin clearance. The current studies aimed to determine whether these metabolic abnormalities could be reversed by caloric restriction (CR). CR by 30% over a period of 2–3 months improved insulin clearance in parallel to inducing the protein content and activation of the carcinoembryonic antigen-related cell adhesion molecule 1, a main player in hepatic insulin extraction. It also reduced glucose and insulin intolerance and serum and tissue (liver and muscle) triglyceride levels. Additionally, CR reversed inflammation, oxidative stress, and fibrosis in liver. The data support a significant role of CR in the normalization of insulin and lipid metabolism in liver.


Metabolism ◽  
2002 ◽  
Vol 51 (6) ◽  
pp. 716-723 ◽  
Author(s):  
Asako Kageyama ◽  
Tsutomu Hirano ◽  
Haruaki Kageyama ◽  
Toshimasa Osaka ◽  
Yoshio Namba ◽  
...  

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Takehiko Kujiraoka ◽  
Yasushi Satoh ◽  
Makoto Ayaori ◽  
Yasunaga Shiraishi ◽  
Yuko Arai-Nakaya ◽  
...  

Background Insulin signaling comprises 2 major cascades, the IRS/PI3K/Akt and Ras/Raf/MEK/ERK pathways. Many studies on the tissue-specific effects of the former pathway had been conducted, however, the role of the latter cascade in tissue-specific insulin resistance had not been investigated. High glucose/fatty acid toxicity, inflammation and oxidative stress, all of which are associated with insulin resistance, can activate ERK. Liver plays a central role of metabolism and hepatosteatosis (HST) is associated with vascular diseases. The aim of this study is to elucidate the role of hepatic ERK2 in HST, metabolic remodeling and endothelial dysfunction. Methods Serum biomarkers of vascular complications in human were compared between subjects with and without HST diagnosed by echography for regular medical checkup. Next, we created liver-specific ERK2 knockout mice (LE2KO) and fed them with a high-fat/high-sucrose diet (HFHSD) for 20 weeks. The histological analysis, the expression of hepatic sarco/endoplasmic reticulum (ER) Ca 2+ -ATPase 2 (SERCA2) and glucose-tolerance/insulin-sensitivity (GT/IS) were tested. Vascular superoxide production and endothelial function were evaluated with dihydroethidium staining and isometric tension measurement of aorta. Results The presence of HST significantly increased HOMA-IR, an indicator of insulin resistance or atherosclerotic index in human. HFHSD-fed LE2KO revealed a marked exacerbation in HST and metabolic remodeling represented by the impairment of GT/IS, elevated serum free fatty acid and hyperhomocysteinemia without changes in body weight, blood pressure and serum cholesterol/triglyceride levels. In the HFHSD-fed LE2KO, mRNA and protein expressions of hepatic SERCA2 were significantly decreased, which resulted in hepatic ER stress. Induction of vascular superoxide production and remarkable endothelial dysfunction were also observed in them. Conclusions Hepatic ERK2 revealed the suppression of hepatic ER stress and HST in vivo , which resulted in protection from vascular oxidative stress and endothelial dysfunction. HST with hepatic ER stress can be a prominent risk of vascular complications by metabolic remodeling and oxidative stress in obese-related diseases.


Diabetes Care ◽  
2007 ◽  
Vol 30 (9) ◽  
pp. 2309-2313 ◽  
Author(s):  
M. Luque-Ramirez ◽  
F. Alvarez-Blasco ◽  
J. I. Botella-Carretero ◽  
R. Sanchon ◽  
J. L. San Millan ◽  
...  

2018 ◽  
Vol 41 (1) ◽  
pp. 92-98 ◽  
Author(s):  
Koichi Murano ◽  
Hirofumi Ogino ◽  
Tomofumi Okuno ◽  
Tomohiro Arakawa ◽  
Hitoshi Ueno

2007 ◽  
Vol 28 (1) ◽  
pp. 67-75 ◽  
Author(s):  
Adam Whaley-Connell ◽  
Vincent G. DeMarco ◽  
Guido Lastra ◽  
Camila Manrique ◽  
Ravi Nistala ◽  
...  

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