scholarly journals Inhibition of Renal Sodium–Glucose Cotransport With Empagliflozin Lowers Fasting Plasma Glucose and Improves β-Cell Function in Subjects With Impaired Fasting Glucose

Diabetes ◽  
2017 ◽  
Vol 66 (9) ◽  
pp. 2495-2502 ◽  
Author(s):  
Muhammad Abdul-Ghani ◽  
Hussein Al Jobori ◽  
Giuseppe Daniele ◽  
John Adams ◽  
Eugenio Cersosimo ◽  
...  
Keyword(s):  
Impaired Fasting Glucose ◽  
Plasma Glucose ◽  
Fasting Plasma Glucose ◽  
Cell Function ◽  
Fasting Glucose ◽  
Β Cell ◽  
Fasting Plasma ◽  
Β Cell Function ◽  
Sodium Glucose Cotransport

scholarly journals Antidepressant medication use and trajectories of fasting plasma glucose, glycated haemoglobin, β-cell function and insulin sensitivity: a 9-year longitudinal study of the D.E.S.I.R. cohort

2015 ◽  
Vol 44 (6) ◽  
pp. 1927-1940 ◽  
Author(s):  
Marine Azevedo Da Silva ◽  
Aline Dugravot ◽  
Beverley Balkau ◽  
Ronan Roussel ◽  
Frédéric Fumeron ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Plasma Glucose ◽  
Fasting Plasma Glucose ◽  
Cell Function ◽  
Glycated Haemoglobin ◽  
Β Cell ◽  
Fasting Plasma ◽  
Β Cell Function ◽  
Antidepressant Use

Abstract Background : Use of antidepressants is seen to be a risk factor for type 2 diabetes, even though the underlying mechanisms remain unclear. We examined whether antidepressant use was associated with change in fasting plasma glucose, glycated haemoglobin (HbA1c), β-cell function (HOMA2-%B) and insulin sensitivity (HOMA2-%S) over time. Methods : Participants in the French D.E.S.I.R. cohort study included over 4700 men (48.1%) and women, free of diabetes, aged 30–65 years at baseline in 1994–96 (D.E.S.I.R. 0), who were followed for 9 years at 3-yearly intervals (D.E.S.I.R. 3, 1997–99; 6, 2000–02; 9, 2003–05). Antidepressant use, fasting plasma glucose, HbA1c, HOMA2-%B and HOMA2-%S were assessed concurrently at four medical examinations. Linear mixed models were used to examine the cross-sectional and longitudinal associations of time-dependent antidepressant use with changes in these four biological parameters. Results : Mean fasting plasma glucose and HbA1c increased whereas HOMA2-%B and HOMA2-%S decreased over the follow-up. In a fully adjusted model, there were no differences in: mean fasting plasma glucose ( β  = 0.01 mmol/l, P  = 0.702); HbA1c ( β  = 0.01 %, P  = 0.738); HOMA2-%B ( β  = 0.00, P  = 0.812); or HOMA2-%S ( β  =−0.01, P  = 0.791) at baseline (1994–96) between antidepressant users and non-users. The interaction term with time also suggested no differences in the annual change in: fasting plasma glucose ( β  = 0.00 mmol/l, P  = 0.322); HbA1c ( β  = 0.00 %, P  = 0.496); HOMA2-%B ( β  = 0.00, P  = 0.609); or HOMA2-%S ( β  = 0.00, P  = 0.332) between antidepressant users and non-users. Similar associations were observed in analyses of type and cumulative use of antidepressants over follow-up. Conclusion : Our longitudinal data show that use of antidepressants is not associated with altered glucose metabolism, suggesting that the association between antidepressant use and diabetes reported by previous studies may not be causal. Detection bias or clinical ascertainment bias may account for much of this apparent association.

scholarly journals Weight Loss Improves β-Cell Function in People With Severe Obesity and Impaired Fasting Glucose: A Window of Opportunity

2019 ◽  
Vol 105 (4) ◽  
pp. e1621-e1630
Author(s):  
Amy E Rothberg ◽  
William H Herman ◽  
Chunyi Wu ◽  
Heidi B IglayReger ◽  
Jeffrey F Horowitz ◽  
...  
Keyword(s):  
Weight Loss ◽  
Insulin Secretion ◽  
Insulin Sensitivity ◽  
Impaired Fasting Glucose ◽  
Severe Obesity ◽  
Cell Function ◽  
Fasting Glucose ◽  
Β Cell ◽  
Obese People ◽  
Β Cell Function

Abstract Background In people with obesity, β-cell function may adapt to insulin resistance. We describe β-cell function in people with severe obesity and normal fasting glucose (NFG), impaired fasting glucose (IFG), and type 2 diabetes (T2DM), as assessed before, 3 to 6 months after, and 2 years after medical weight loss to describe its effects on insulin sensitivity, insulin secretion, and β-cell function. Methods Fifty-eight participants with body mass index (BMI) ≥ 35 kg/m2 (14 with NFG, 24 with IFG, and 20 with T2DM) and 13 normal weight participants with NFG underwent mixed meal tolerance tests to estimate insulin sensitivity (S[I]), insulin secretion (Φ), and β-cell function assessed as model-based Φ adjusted for S(I). All 58 obese participants were restudied at 3 to 6 months and 27 were restudied at 2 years. Results At 3 to 6 months, after a 20-kg weight loss and a decrease in BMI of 6 kg/m2, S(I) improved in all obese participants, Φ decreased in obese participants with NFG and IFG and tended to decrease in obese participants with T2DM, and β-cell function improved in obese participants with NFG and tended to improve in obese participants with IFG. At 2 years, β-cell function deteriorated in participants with NFG and T2DM but remained significantly better in participants with IFG compared to baseline. Conclusions Short-term weight loss improves β-cell function in participants with NFG and IFG, but β-cell function tends to deteriorate over 2 years. In participants with IFG, weight loss improves longer-term β-cell function relative to baseline and likely relative to no intervention, suggesting that obese people with IFG are a subpopulation whose β-cell function is most likely to benefit from weight loss.

scholarly journals Effect of telmisartan on selected adipokines, insulin sensitivity, and substrate utilization during insulin-stimulated conditions in patients with metabolic syndrome and impaired fasting glucose

2010 ◽  
Vol 163 (4) ◽  
pp. 573-583 ◽  
Author(s):  
Petr Wohl ◽  
Eva Krušinová ◽  
Martin Hill ◽  
Simona Kratochvílová ◽  
Kateřina Zídková ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Insulin Sensitivity ◽  
Impaired Fasting Glucose ◽  
Plasma Glucose ◽  
Fasting Plasma Glucose ◽  
Fasting Glucose ◽  
Substrate Utilization ◽  
Metabolic Effects ◽  
Plasma Adiponectin ◽  
Fasting Plasma

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.

scholarly journals A higher-carbohydrate, lower-fat diet reduces fasting glucose concentration and improves β-cell function in individuals with impaired fasting glucose

Metabolism ◽  
2012 ◽  
Vol 61 (3) ◽  
pp. 358-365 ◽  
Author(s):  
Barbara A. Gower ◽  
Laura Lee Goree ◽  
Paula C. Chandler-Laney ◽  
Amy C. Ellis ◽  
Krista Casazza ◽  
...  
Keyword(s):  
Impaired Fasting Glucose ◽  
Glucose Concentration ◽  
Cell Function ◽  
Fasting Glucose ◽  
Β Cell ◽  
Β Cell Function

Association of aortic pressures with fasting plasma glucose in patients with and without impaired fasting glucose

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

scholarly journals Effects of incretin-based therapies on β-cell function in type 1 diabetes mellitus: a systematic review and meta-analysis

2021 ◽  
Vol 49 (12) ◽  
pp. 030006052110663
Author(s):  
Yucheng Wu ◽  
Yu Lu ◽  
Shufang Yang ◽  
Qingqing Zhang
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Plasma Glucose ◽  
Fasting Plasma Glucose ◽  
Cell Function ◽  
Meta Analysis ◽  
Β Cell ◽  
C Peptide ◽  
Β Cell Function

Aim To assess the effects of incretin-based therapies on β-cell function in patients with type 1 diabetes mellitus (T1DM). Methods We searched the PubMed, Cochrane Library, Embase, and Web of Knowledge databases for eligible randomized clinical trials published up to July 2021. The inclusion criteria were patients with T1DM or latent autoimmune diabetes in adults, patients treated with dipeptidyl peptidase-4 inhibitors or glucagon like peptide-1 receptor agonists, and outcomes included one of the following: fasting plasma glucose, fasting C-peptide, postprandial C-peptide, C-peptide area under the curve (AUC), homeostasis model assessment for β cell function, and insulin resistance. The effects were analyzed using a random effect model with STATA 11.0. Results Eight trials including 427 participants were included in the final analysis. A pooled analysis found no significant difference in fasting plasma glucose, fasting C-peptide, postprandial C-peptide, or C-peptide AUC between patients treated with incretin-based therapies and placebo. The two trials that reported changes in 2-hour postprandial C-peptide and two of the four trials that reported changes in C-peptide AUC reported increases after incretin-based therapies. Conclusion This meta-analysis showed that incretin-based therapies did not preserve β-cell function in patients with T1DM.

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