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Introduction In fully compensated insulin resistance, there is a sufficient upregulation of insulin secretion whereas in glucose intolerance and type 2 diabetes this upregulation is inadequate (1) . Several mechanisms have been suggested to
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). PCOS is also associated with several comorbidities resulting in long-term sequelae ( 4 ) like insulin resistance (IR) ( 5 ), obesity ( 6 ) and metabolic syndrome ( 7 ). Although metabolic parameters are not included in the diagnostic criteria, they
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(defined as birth weight (BW) below 2500 g) has been proposed to lead to insulin resistance and type 2 diabetes (1, 2, 3, 4) . In studies of individuals born SGA at term (defined as BW SDS below −2 SDS), signs of insulin resistance have been detected in
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been observed in prospective studies of large PCOS cohorts of mostly obese women ( 2 , 3 ), since the two preconditions for T2DM development are encountered in PCOS. Specifically, profound insulin resistance (IR) constitutes a key player underlying
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‘Research of Age and Age-Associated Conditions’ Department, Laboratory of Bioinformatics, The ‘Russian Clinical Research Center for Gerontology’, ‘Chronic Noncommunicable Diseases Primary Prevention in the Healthcare System’ Department, Moscow Institute of Physics and Technology, National Research Centre for Preventive Medicine, National Research Centre for Preventive Medicine, Building 10, Petroverigskiy Lane, Moscow RF 101000, Russian Federation
‘Research of Age and Age-Associated Conditions’ Department, Laboratory of Bioinformatics, The ‘Russian Clinical Research Center for Gerontology’, ‘Chronic Noncommunicable Diseases Primary Prevention in the Healthcare System’ Department, Moscow Institute of Physics and Technology, National Research Centre for Preventive Medicine, National Research Centre for Preventive Medicine, Building 10, Petroverigskiy Lane, Moscow RF 101000, Russian Federation
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formula: (concentration of fasting blood glucose (mmol/l))×(concentration of fasting blood insulin (mU/l))/22.5. Insulin resistance (IR) was diagnosed if HOMA-IR >2.5 (11) . A 75 g OGTT was performed with blood glucose measurement before glucose intake
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Introduction Insulin resistance (IR) is the pathophysiological basis of metabolic diseases, such as type 2 diabetes mellitus (T2DM), metabolic syndrome (MetS) and nonalcoholic fatty liver disease (NAFLD) ( 1 , 2 , 3 , 4 ). Increased IR in T
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sensitivity: (1) the OGTT insulin sensitivity index of Matsuda and DeFronzo (IS OGTT ) ( 8 ); (2) the quantitative insulin sensitivity check index (QUICKI) model and (3) the homeostasis model of assessment for insulin resistance (HOMA-IR). The IS OGTT model
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Division of Internal Medicine, University Hospital of North Norway, Tromsø, Norway
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parameters, while the rest showed no effects or even adverse outcomes ( 14 ). In a meta-analysis by Poolsup et al . including 10 trials, no effect of vitamin D on insulin resistance was found in subjects with pre-diabetes ( 15 ). And finally, in a study from
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sensitivity in apparently healthy, middle-aged, centrally obese men . Diabetic Medicine 2009 26 19 – 27 . ( doi:10.1111/j.1464-5491.2008.02636.x ). 9 Diamanti-Kandarakis E Dunaif A . Insulin resistance and the polycystic ovary syndrome revisited
The Center for Biomedical Research, Tongji Hospital Research Building, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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gluconeogenesis. Specifically, in the long run, metabolic disorders that are responsible for insulin resistance may also, in turn, damage the insulin-secreting capability of islet β cells through the accumulation of proinflammatory cytokines and toxic lipids ( 1