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Neil R Chappell, Beth Zhou, Amy K Schutt, William E Gibbons and Chellakkan S Blesson

/mL vs lean PCOS 55.08 ± 7.8 ng/mL for AMH). Lean PCOS mice were glucose intolerance but normal hemoglobin A1c levels Glucose values were consistently higher at 30 min (control 13.5 ± 0.5 mmol/L vs lean PCOS 15.5 ± 0.5 mmol/L, P  < 0.01), 60 min

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Shane M Regnier, Andrew G Kirkley, Daniel Ruiz, Wakanene Kamau, Qian Wu, Kurunthachalam Kannan and Robert M Sargis

) signaling ( 18 , 20 ). In recent studies, male C57BL/6 mice exposed to TF via a standard laboratory chow diet for 12 weeks exhibited increased adiposity, glucose intolerance and insulin resistance with concomitant impairments in adipose insulin sensitivity

Open access

Chenghao Piao, Xiaojie Wang, Shiqiao Peng, Xinyu Guo, Hui Zhao, Li He, Yan Zeng, Fan Zhang, Kewen Zhu and Yiwei Wang

Introduction Insulin sensitivity during pregnancy is reduced with the advancement of gestation. Thus, the demand for insulin is elevated to maintain the common blood sugar ( 1 ). Gestational diabetes mellitus (GDM) is characterized by glucose

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Mohammed S Albreiki, Benita Middleton and Shelagh M Hampton

hormonal responses in healthy young participants. Significantly higher glucose and insulin in the BL session suggests glucose intolerance and insulin insensitivity. Elevated NEFAs level in the DL session prior to the meal could either be due to the

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Aline Stangherlin Martins, Ann Kristine Jansen, Luiz Oswaldo Carneiro Rodrigues, Camila Maria Matos, Marcio Leandro Ribeiro Souza, Juliana Ferreira de Souza, Maria de Fátima Haueisen Sander Diniz, Sandhi Maria Barreto, Leonardo Mauricio Diniz, Nilton Alves de Rezende and Vincent Michael Riccardi

Studies indicate a lower occurrence of diabetes mellitus (DM) in patients with neurofibromatosis type 1 (NF1). Fasting blood glucose (FBG) level is the main criterion used to diagnose DM and glucose intolerance. Therefore, this study compared FBG level between adults with NF1 and non-NF1 controls. We selected clinical records of 57 out of 701 individuals attending the Neurofibromatosis Outpatient Reference Center of the Clinics Hospital of the Federal University of Minas Gerais in Brazil. The selected patients with NF1 were matched to non-NF1 controls selected from the Brazilian Longitudinal Study of Adult Health according to sex, age (range, 35–74 years) and BMI at a ratio of 1:3. In both groups, individuals with DM were excluded. Median FBG level in the NF1 group (86 mg/dl (range, 56–127 mg/dl)) was lower than that in the non-NF1 control group (102 mg/dl (range, 85–146 mg/dl)) (P<0.001). Prevalence of FBG level ≥100 mg/dl in the NF1 group (16%) was lower than that in the non-NF1 control group (63%) (P<0.05). The chance of a high FBG level was 89% lower in the NF1 group (odds ratio, 0.112; 95% CI, 0.067–0.188) (P<0.05). In conclusion, adults with NF1 showed a lower FBG level and a lower prevalence of high FBG level compared with non-NF1 controls.

Open access

Lilit Egshatyan, Daria Kashtanova, Anna Popenko, Olga Tkacheva, Alexander Tyakht, Dmitry Alexeev, Natalia Karamnova, Elena Kostryukova, Vladislav Babenko, Maria Vakhitova and Sergey Boytsov

deviation degree Patients without glucose intolerance, who had passed the preventive outpatient examination. Patients with prediabetes (preD) (impaired fasting glucose or impaired glucose tolerance or the level of HbA1c from 5.7 to 6.5%. Patients with newly

Open access

A V Dreval, I V Trigolosova, I V Misnikova, Y A Kovalyova, R S Tishenina, I A Barsukov, A V Vinogradova and B H R Wolffenbuttel

Endocrinology 2000 52 549 – 555 . ( doi:10.1046/j.1365-2265.2000.00986.x ). 5 Kreze A Kreze-Spirova E Mikulecky M . Risk factors for glucose intolerance in active acromegaly . Brazilian Journal of Medical and Biological Research 2001 34 1429

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Magdalene K Montgomery and Nigel Turner

in decreased substrate oxidation, further aggravating lipid accumulation. The debate about mitochondrial dysfunction and IR Mitochondrial dysfunction was first described in the context of glucose intolerance ∼40 years ago (15) , and the majority of

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L Ahlkvist, K Brown and B Ahrén

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

Open access

Ling-Jun Li, Izzuddin M Aris, Lin Lin Su, Yap Seng Chong, Tien Yin Wong, Kok Hian Tan and Jie Jin Wang

: (1) elevated BP: SBP ≥ 130 mmHg and/or DBP ≥ 85 mmHg or on anti-hypertensive medication; (2) abdominal obesity: waist circumference >88 cm; (3) dyslipidemia: TG ≥ 1.7 mmol/L or HDL < 1.3 mmol/L and (4) glucose intolerance: fasting plasma glucose ≥6