scholarly journals The relationship between insulin sensitivity and heart rate-corrected QT interval in patients with type 2 diabetes

2017 ◽  
Vol 9 (1) ◽  
Author(s):  
Xiao-hua Yang ◽  
Jian-bin Su ◽  
Xiu-lin Zhang ◽  
Li-hua Zhao ◽  
Feng Xu ◽  
...  
2015 ◽  
Vol 32 (9) ◽  
pp. 1221-1226 ◽  
Author(s):  
Y. Hashimoto ◽  
M. Tanaka ◽  
T. Senmaru ◽  
H. Okada ◽  
M. Hamaguchi ◽  
...  

Diabetes Care ◽  
2014 ◽  
Vol 37 (5) ◽  
pp. 1454-1461 ◽  
Author(s):  
Amanda J. Cox ◽  
Amir Azeem ◽  
Joseph Yeboah ◽  
Elsayed Z. Soliman ◽  
Shivani R. Aggarwal ◽  
...  

PLoS ONE ◽  
2017 ◽  
Vol 12 (8) ◽  
pp. e0183055 ◽  
Author(s):  
Jian-bin Su ◽  
Xiao-hua Yang ◽  
Xiu-lin Zhang ◽  
Hong-li Cai ◽  
Hai-yan Huang ◽  
...  

2013 ◽  
Vol 37 (3) ◽  
pp. 190 ◽  
Author(s):  
Jae Won Beom ◽  
Jung Min Kim ◽  
Eun Joo Chung ◽  
Ju Yeong Kim ◽  
Seung Yeong Ko ◽  
...  

2021 ◽  
Author(s):  
Elsa Vazquez Arreola ◽  
Robert L. Hanson ◽  
Clifton Bogardus ◽  
William C. Knowler

We assessed whether the relationship between insulin secretion and sensitivity predicted development of type 2 diabetes in American Indians participating in a longitudinal epidemiologic study. At baseline, when all subjects did not have diabetes, 1566 participants underwent oral tests and 420 had intravenous measures of glucose regulation with estimates of insulin secretion and sensitivity. Standardized major axis regression was used to study the relationship of secretion and sensitivity. Distances away from and along the regression line estimated compensatory insulin secretion and secretory demand, respectively. This relationship differed according to glucose tolerance and BMI categories. The distance away from the line is similar to the disposition index (DI) defined as the product of estimated secretion and sensitivity, but the regression line may differ from a line with constant DI (i.e., it is not necessarily hyperbolic). Subjects with the same DI but different levels of insulin secretion and sensitivity had different incidence rates of diabetes; lower sensitivity with higher secretory demand was associated with greater diabetes risk. Insulin secretion and insulin sensitivity, analyzed together, predict diabetes better than DI alone. Physiologically, this may reflect long-term risk associated with increased allostatic load resulting from the stimulation of insulin hypersecretion by increased glycemia.


2021 ◽  
Author(s):  
Elsa Vazquez Arreola ◽  
Robert L. Hanson ◽  
Clifton Bogardus ◽  
William C. Knowler

We assessed whether the relationship between insulin secretion and sensitivity predicted development of type 2 diabetes in American Indians participating in a longitudinal epidemiologic study. At baseline, when all subjects did not have diabetes, 1566 participants underwent oral tests and 420 had intravenous measures of glucose regulation with estimates of insulin secretion and sensitivity. Standardized major axis regression was used to study the relationship of secretion and sensitivity. Distances away from and along the regression line estimated compensatory insulin secretion and secretory demand, respectively. This relationship differed according to glucose tolerance and BMI categories. The distance away from the line is similar to the disposition index (DI) defined as the product of estimated secretion and sensitivity, but the regression line may differ from a line with constant DI (i.e., it is not necessarily hyperbolic). Subjects with the same DI but different levels of insulin secretion and sensitivity had different incidence rates of diabetes; lower sensitivity with higher secretory demand was associated with greater diabetes risk. Insulin secretion and insulin sensitivity, analyzed together, predict diabetes better than DI alone. Physiologically, this may reflect long-term risk associated with increased allostatic load resulting from the stimulation of insulin hypersecretion by increased glycemia.


2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Jiajia Wang ◽  
Wenjuan Li ◽  
Chuan Wang ◽  
Lingshu Wang ◽  
Tianyi He ◽  
...  

Background. More and more studies focus on the relationship between the gastrointestinal microbiome and type 2 diabetes, but few of them have actually explored the relationship between enterotypes and type 2 diabetes. Materials and Methods. We enrolled 134 patients with type 2 diabetes and 37 nondiabetic controls. The anthropometric and clinical indices of each subject were measured. Fecal samples of each subject were also collected and were processed for 16S rDNA sequencing. Multiple logistic regression analysis was used to determine the associations of enterotypes with type 2 diabetes. Multiple linear regression analysis was used to explore the relationship between lipopolysaccharide levels and insulin sensitivity after adjusting for age, BMI, TG, HDL-C, DAO, and TNF-α. The correlation analysis between factors and microbiota was identified using Spearman correlation analysis. The correlation analysis between factors was identified using partial correlation analysis. Results. Gut microbiota in type 2 diabetes group exhibited lower bacterial diversity compared with nondiabetic controls. The fecal communities from all subjects clustered into two enterotypes distinguished by the levels of Bacteroides and Prevotella. Logistic regression analysis showed that the Bacteroides enterotype was an independent risk factor for type 2 diabetes by decreasing insulin sensitivity. The levels of lipopolysaccharide and tumor necrosis factor-alpha were higher in the Bacteroides enterotype compared to the Prevotella enterotype. Partial correlation analysis showed that lipopolysaccharide was closely associated with diamine oxidase, tumor necrosis factor-alpha, and Gutt insulin sensitivity index after adjusting for multiple covariates. Furthermore, the level of lipopolysaccharide was found to be an independent risk factor for insulin sensitivity. Conclusions. We identified two enterotypes, Bacteroides and Prevotella, among all subjects. Our results showed that the Bacteroides enterotype was an independent risk factor for type 2 diabetes, which was due to increased levels of lipopolysaccharide causing decreased insulin sensitivity.


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