Impact of insulin sensitivity, beta-cell function and glycaemic control on initiation of second-line glucose-lowering treatment in newly diagnosed type 2 diabetes

2017 ◽  
Vol 19 (6) ◽  
pp. 866-873 ◽  
Author(s):  
Wolfgang Rathmann ◽  
Klaus Strassburger ◽  
Brenda Bongaerts ◽  
Pavel Bobrov ◽  
Oliver Kuss ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Glycaemic Control ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Second Line ◽  
Newly Diagnosed ◽  
Glucose Lowering

Factors influencing beta-cell function and insulin sensitivity in patients with type 2 (non-insulin-dependent) diabetes

1984 ◽  
Vol 106 (4) ◽  
pp. 505-510 ◽  
Author(s):  
Leif Groop ◽  
Esa-Matti Tolppanen
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Glycaemic Control ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Fasting Blood Glucose ◽  
Age At Onset ◽  
Consistent Finding

Abstract. This study was designed to evaluate the influence of age, duration of diabetes, relative body weight and glycaemic control on beta-cell function and insulin sensitivity in 250 patients with onset of nonketotic diabetes between the age of 35 and 70 years (Type 2 diabetes). Beta-cell function was assessed by measuring serum C-peptide concentrations after I mg of glucagon iv. It was not influenced by age, age at onset of diabetes nor by the duration of the disease. This suggests that progressive deterioration of beta-cell function with time is not a consistent finding in Type 2 diabetes. Insulin sensitivity, measured as the glucose disappearance rate, KITT, in response to iv-insulin, was not significantly influenced by age or age at onset, but decreased consistently with the duration of the disease (P < 0.001). Beta-cell function was not correlated to fasting blood glucose and HbA1 concentrations. In contrast, there was a strong inverse relationship between glycaemic control and insulin sensitivity (P < 0.001) indicating that decreased insulin sensitivity contributes to poor glycaemic control in these patients. Attempts to improve glycaemic control in patients with Type 2 diabetes should therefore include means to improve insulin sensitivity.

Correlation of insulin resistance, beta cell function and insulin sensitivity with serum sFas and sFasL in newly diagnosed type 2 diabetes

2011 ◽  
Vol 50 (4) ◽  
pp. 511-518 ◽  
Author(s):  
Hemant Kumar ◽  
Manish Mishra ◽  
Surabhi Bajpai ◽  
Deepa Pokhria ◽  
Awadhesh Kumar Arya ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Newly Diagnosed

970-P: Comparative Assessment of the Effect of Vildagliptin and Metformin on Pancreatic Beta-Cell Function and Insulin Sensitivity in Newly Diagnosed Asian Indians with Type 2 Diabetes

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 970-P
Author(s):  
KRISHNAMOORTHY SATHEESH ◽  
CHAMUKUTTAN SNEHALATHA ◽  
ARUN NANDITHA ◽  
ARUN RAGHAVAN ◽  
RAMACHANDRAN VINITHA ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Beta Cell Function ◽  
Asian Indians ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
Comparative Assessment ◽  
Newly Diagnosed ◽  
Pancreatic Beta Cell Function

scholarly journals Beta cell function and insulin sensitivity in obese youth with maturity onset diabetes of youth mutations vs type 2 diabetes in TODAY: Longitudinal observations and glycemic failure

2020 ◽  
Vol 21 (4) ◽  
pp. 575-585
Author(s):  
Silva Arslanian ◽  
Laure El ghormli ◽  
Morey H. Haymond ◽  
Christine L. Chan ◽  
Steven D. Chernausek ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Maturity Onset Diabetes ◽  
Onset Diabetes ◽  
Obese Youth

scholarly journals Biomarkers of subclinical inflammation and increases in glycaemia, insulin resistance and beta-cell function in non-diabetic individuals: the Whitehall II study

2016 ◽  
Vol 175 (5) ◽  
pp. 367-377 ◽  
Author(s):  
Christian Herder ◽  
Kristine Færch ◽  
Maren Carstensen-Kirberg ◽  
Gordon D Lowe ◽  
Rita Haapakoski ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Fasting Insulin ◽  
Subclinical Inflammation ◽  
Increased Risk

Objective Higher systemic levels of pro-inflammatory biomarkers and low adiponectin are associated with increased risk of type 2 diabetes, but their associations with changes in glycaemic deterioration before onset of diabetes are poorly understood. We aimed to study whether inflammation-related biomarkers are associated with 5-year changes in glucose and insulin, HbA1c, insulin sensitivity and beta-cell function before the diagnosis of type 2 diabetes and whether these associations may be bidirectional. Design and methods We used multiple repeat measures (17 891 person-examinations from 7683 non-diabetic participants) from the Whitehall II study to assess whether circulating high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL6), IL1 receptor antagonist (IL1Ra) and adiponectin are associated with subsequent changes in glycaemia, insulin, insulin resistance and beta-cell function (based on oral glucose tolerance tests). We examined bidirectionality by testing if parameters of glucose metabolism at baseline are associated with changes in inflammation-related biomarkers. Results Higher hsCRP and IL6 were associated with increases in fasting insulin, insulin resistance and, for IL6, with beta-cell function after adjustment for confounders. Higher adiponectin was associated with decreases in fasting glucose, HbA1c, fasting insulin, insulin resistance and beta-cell function. The reverse approach showed that 2-h glucose and insulin sensitivity were associated with changes in IL1Ra. Fasting insulin and insulin resistance showed inverse associations with changes in adiponectin. Conclusions Subclinical inflammation is associated with development of increased glycaemia, insulin resistance and beta-cell function in non-diabetic individuals. These findings are consistent with the hypothesis that inflammation-related processes may increase insulin resistance and lead to a compensatory upregulation of beta-cell function.

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