scholarly journals Greater Glycemic Burden Is Associated with Further Poorer Glycemic Control in Newly-Diagnosed Type 2 Diabetes Mellitus Patients

Nutrients ◽  
2022 ◽  
Vol 14 (2) ◽  
pp. 320
Author(s):  
Wei-Lun Wen ◽  
Hui-Chun Huang ◽  
Hsiu-Chu Lin ◽  
Wan-Ching Lo ◽  
Szu-Chia Chen ◽  
...  

Aims: hyperglycemia impairs pancreatic β-cell function instantly, also known as glucotoxicity. It is unknown whether this insult is temporary or sustained, and little real-world evidence needs to reflect the relationship between hyperglycemic burden, per se, and glycemic durability. Materials and Methods: a retrospective observational cohort study was conducted to recruit newly-diagnosed type 2 diabetes mellitus (T2DM) patients. Durability was defined as the episode from first glycated hemoglobin A1c (HbA1c) below 7.0% to where it exceed 8.0% (with treatment failure) or where study ended (without treatment failure). Glycemic burden was defined with the area above a burden value line (HbA1c = 6.5%) but under the HbA1c curve (AUC), and it was then divided into two compartments with the demarcation timepoint once HbA1c was treated below or equal to 7.0%; the former AUC’ represented the initial insult; the latter AUC” represented the residual part. Multivariable regression models assessed factors associated with durability in whole participants and two distinct subgroups: patients with baseline HbA1c > 7.0% or ≤7.0%. Results: 1048 eligible participants were recruited and analyzed: 291 patients with treatment failure (durability 26.8 ± 21.1 months); 757 patients without treatment failure (durability 45.1 ± 31.8 months). Besides age, glycemic burden was the only constant determinant in the two subgroups. AUC’ or AUC” increased treatment failure, respectively, in baseline HbA1c > 7.0% or ≤7.0% subgroup [per 1%/90 days hazard ratio (95% confidence interval): 1.026 (1.018–1.034) and 1.128 (1.016–1.253)]. Other determinants include baseline HbA1c, initial OAD, and education level. Conclusions: in patients with newly-diagnosed T2DM, glycemic durability was negatively associated with greater glycemic burden.

2016 ◽  
Vol 101 (2) ◽  
pp. 572-580 ◽  
Author(s):  
Sharmistha Roy Chowdhury ◽  
Rebecca L. Thomas ◽  
Gareth J. Dunseath ◽  
Rajesh Peter ◽  
D. Aled Rees ◽  
...  

2020 ◽  
Vol 70 (12) ◽  
pp. 4217-4223 ◽  

When discussing insulin resistance and insulin sensitivity, data from literature focuses on obese and overweight patients. In our study on, 110 patients with normal body-mass index with newly diagnosed type 2 diabetes mellitus, with the help of glucose tolerance test, we explored insulin resistance, sensitivity, early insulin secretion and β-cell function assessed by using the following indexes: HOMA-IR, ISI, IGI and HOMA-β. We compared the results from our reference group with a control group of 109 overweight patients with newly diagnosed type 2 diabetes mellitus. Normal weight patients had a statistically significant lower HOMA-IR index than overweight patients (2.65 vs. 3.55, p<0.01), however in both groups HOMA-IR was above the cut-off value of 2.5. HOMA-β was statistically significant lower in normal weight patients than in overweight patients (55.08 vs 65.36, p<0.01). ISI index was in an inverse proportional relationship with HOMA-IR, statistically significant higher in normal weight individuals (5.97 vs.3.48, p<0.01). IGI index was not statistically significant lower in normal weight patients (3.63 vs.3.95, p=0.07). It is important to observe that although they have a normal BMI these patients are insulin-resistant confirming the hypothesis of metabolic obese normal weight patients that develop type 2 diabetes mellitus. The indexes that correlate with HbA1c in normal weight patients, predicting glucose status, are HOMA-β (negative correlation), ISI (positive correlation) and IGI index (negative correlation). Keywords: insulin, β-cell, glycated hemoglobin, type 2 diabetes mellitus


2017 ◽  
Vol 19 (11) ◽  
pp. 1625-1629 ◽  
Author(s):  
Juris J. Meier ◽  
Nina Schenker ◽  
Melanie Kahle ◽  
Freimut Schliess ◽  
Christoph Kapitza ◽  
...  

2010 ◽  
Vol 31 (2) ◽  
pp. 261-261
Author(s):  
Alexander M. Owyang ◽  
Kathrin Maedler ◽  
Lisa Gross ◽  
Johnny Yin ◽  
Lin Esposito ◽  
...  

ABSTRACT Recent evidence suggests that IL-1β-mediated glucotoxicity plays a critical role in type 2 diabetes mellitus. Although previous work has shown that inhibiting IL-1β can lead to improvements in glucose control and β-cell function, we hypothesized that more efficient targeting of IL-1β with a novel monoclonal antibody, XOMA 052, would reveal an effect on additional parameters affecting metabolic disease. In the diet-induced obesity model, XOMA 052 was administered to mice fed either normal or high-fat diet (HFD) for up to 19 wk. XOMA 052 was administered as a prophylactic treatment or as a therapy. Mice were analyzed for glucose tolerance, insulin tolerance, insulin secretion, and lipid profile. In addition, the pancreata were analyzed for β-cell apoptosis, proliferation, and β-cell mass. Mice on HFD exhibited elevated glucose and glycated hemoglobin levels, impaired glucose tolerance and insulin secretion, and elevated lipid profile, which were prevented by XOMA 052. XOMA 052 also reduced β-cell apoptosis and increased β-cell proliferation. XOMA 052 maintained the HFDinduced compensatory increase in β-cell mass, while also preventing the loss in β-cell mass seen with extended HFD feeding. Analysis of fasting insulin and glucose levels suggests that XOMA 052 prevented HFD-induced insulin resistance. These studies provide new evidence that targeting IL-1β in vivo could improve insulin sensitivity and lead to β-cell sparing. This is in addition to previously reported benefits on glycemic control. Taken together, the data presented suggest that XOMA 052 could be effective for treating many aspects of type 2 diabetes mellitus.


2021 ◽  
Vol 12 ◽  
Author(s):  
Ha Young Yoon ◽  
Min Hye Lee ◽  
Yubin Song ◽  
Jeong Yee ◽  
Gonjin Song ◽  
...  

BackgroundThe ATP-binding cassette transporter A1 (ABCA1) is likely associated with the risk of type 2 diabetes mellitus (T2DM) via β cell function modification, but the evidence on the association remains unclear. This study aimed to investigate the relationship between the ABCA1 69C&gt;T polymorphism and the risk of T2DM through a systematic review and meta-analysis.Materials and MethodsThe PubMed, Web of Science, and Embase databases were searched for qualified studies published until August 2020. Studies that included the association between the ABCA1 69C&gt;T polymorphism and the risk of T2DM were reviewed. The odds ratios (ORs) and 95% confidence intervals (CIs) were evaluated.ResultsWe analyzed data from a total of 10 studies involving 17,742 patients. We found that the CC or CT genotype was associated with increased risk of T2DM than the TT genotype (OR, 1.41; 95% CI, 1.02-1.93). In the Asian population, the C allele carriers had a higher risk of T2DM than those with the TT genotype; the ORs of the CC and CT genotypes were 1.80 (95% CI, 1.21-2.68) and 1.61 (95% CI, and 1.29-2.01), respectively.ConclusionsThis meta-analysis confirmed that the ABCA1 69C&gt;T genotype showed a decrease risk of T2DM compared to the CC or CT genotypes.


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