scholarly journals Fasting Plasma Glucose and Incidence of Diabetes --- Implication for the Threshold for Impaired Fasting Glucose: Results from the Population-Based Omiya MA Cohort Study

2009 ◽  
Vol 16 (6) ◽  
pp. 857-861 ◽  
Author(s):  
Masayuki Kato ◽  
Mitsuhiko Noda ◽  
Hiroshi Suga ◽  
Masahiko Matsumoto ◽  
Yasunori Kanazawa
2021 ◽  
Vol 9 (2) ◽  
pp. e002427
Author(s):  
Sangsulee Thamakaison ◽  
Thunyarat Anothaisintawee ◽  
Kanokporn Sukhato ◽  
Nattawut Unwanatham ◽  
Sasivimol Rattanasiri ◽  
...  

IntroductionThis ambidirectional cohort study aimed to assess the performance of combining hemoglobin A1c (HbA1c) to fasting plasma glucose (FPG) for estimation of progression rate to diabetes mellitus (DM) and to explore the risk factors of DM in patients with impaired fasting glucose (IFG).Research design and methodsPatients with IFG were eligible for this study. IFG was defined as FPG of 100–125 mg/dL. Progression rates to DM were estimated using Kaplan-Meier analysis. Risk factors of DM were explored by Cox regression analysis.Results3011 patients were enrolled with median follow-up time of 8 years (range: 6 months–29 years). Progression rates to DM in patients with FPG 100–109 mg/dL and 110–125 mg/dL were 2.64 and 4.79 per 100 person-years. After adjusting covariables, compared with patients with FPG 100–109 mg/dL plus normal HbA1c (<5.7%), hazard ratios (95% CI) of patients with FPG 110–125 plus normal HbA1c, FBG 100–109 plus abnormal HbA1c (5.7%–6.49%), and FPG 110–125 plus abnormal HbA1c were 5.89 (2.37 to 14.63), 16.30 (8.59 to 30.92), and 33.84 (16.41 to 69.78), respectively. Body mass index ≥27.5 kg/m2, serum triglyceride level ≥150 mg/dL, family history of DM, and low level of high-density lipoprotein-cholesterol were independently associated with risk of DM in patients with IFG.ConclusionsPatients with both IFG and abnormal HbA1c had higher risk of DM than patients with IFG alone. Therefore, performing HbA1c in combination with FPG helps to identify subgroups of people with IFG at highest risk of DM. These patients should have the highest priority in diabetes prevention programs, especially in countries with low and limited resources.


2010 ◽  
Vol 163 (4) ◽  
pp. 573-583 ◽  
Author(s):  
Petr Wohl ◽  
Eva Krušinová ◽  
Martin Hill ◽  
Simona Kratochvílová ◽  
Kateřina Zídková ◽  
...  

ObjectiveTelmisartan improves glucose and lipid metabolism in rodents. This study evaluated the effect of telmisartan on insulin sensitivity, substrate utilization, selected plasma adipokines and their expressions in subcutaneous adipose tissue (SAT) in metabolic syndrome.Design and methodsTwelve patients with impaired fasting glucose completed the double-blind, randomized, crossover trial. Patients received telmisartan (160 mg/day) or placebo for 3 weeks and vice versa with a 2-week washout period. At the end of each period, a hyperinsulinemic euglycemic clamp (HEC) combined with indirect calorimetry was performed. During HEC (0, 30, and 120 min), plasma levels of adipokines were measured and a needle biopsy (0 and 30 min) of SAT was performed.ResultsFasting plasma glucose was lower after telmisartan compared with placebo (P<0.05). There were no differences in insulin sensitivity and substrate utilization. We found no differences in basal plasma adiponectin, resistin and tumour necrosis factor α (TNFα), but an increase was found in basal leptin, after telmisartan treatment. Insulin-stimulated plasma adiponectin (P<0.05), leptin and resistin (P<0.001) were increased, whereas TNFα was decreased (P<0.05) after telmisartan treatment. Expression of resistin, but not adiponectin, TNFα and leptin was increased after telmisartan treatment.ConclusionsDespite the decrease in fasting plasma glucose, telmisartan does not improve insulin sensitivity and substrate utilization. Telmisartan increases plasma leptin as well as insulin-stimulated plasma adiponectin, leptin and resistin, and decreases plasma TNFα during HEC. Changes in plasma adipokines cannot be explained by their expressions in SAT. The changes in plasma adipokines might be involved in the metabolic effects of telmisartan in metabolic syndrome.


2014 ◽  
Vol 20 (8) ◽  
pp. 584-592 ◽  
Author(s):  
Hassan Khan ◽  
Setor K. Kunutsor ◽  
Jussi Kauhanen ◽  
Sudhir Kurl ◽  
Eiran Z. Gorodeski ◽  
...  

Diabetes ◽  
2017 ◽  
Vol 66 (9) ◽  
pp. 2495-2502 ◽  
Author(s):  
Muhammad Abdul-Ghani ◽  
Hussein Al Jobori ◽  
Giuseppe Daniele ◽  
John Adams ◽  
Eugenio Cersosimo ◽  
...  

2008 ◽  
Vol 17 (3) ◽  
pp. 164-169 ◽  
Author(s):  
Serkan Cay ◽  
Sezgin Ozturk ◽  
Senay Funda Biyikoglu ◽  
Ramazan Atak ◽  
Yucel Balbay ◽  
...  

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