Measurement of Insulin Resistance and Beta-Cell Function: The HOMA and CIGMA Approach

2015 ◽  
pp. 66-75 ◽  
Author(s):  
R. C. Turner ◽  
J. C. Levy ◽  
A. S. Rudenski ◽  
M. Hammersley ◽  
R. Page
Keyword(s):  
Insulin Resistance ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function

Insulin resistance and beta cell function in aboriginals with type 2 diabetes in Atlantic Canada

2000 ◽  
Vol 50 ◽  
pp. 108 ◽  
Author(s):  
Meng H. Tan ◽  
Sethu Reddy ◽  
Jean Abram ◽  
Pantelis Andreou ◽  
Danita Volder
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Atlantic Canada

scholarly journals Sustained Improvements in Glucose Metabolism Late After Roux-En-Y Gastric Bypass Surgery in Patients with and Without Preoperative Diabetes

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Nils B. Jørgensen ◽  
Kirstine N. Bojsen-Møller ◽  
Carsten Dirksen ◽  
Christoffer Martinussen ◽  
Maria S. Svane ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Gastric Bypass ◽  
Glucose Metabolism ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Relative Change

Abstract To describe glucose metabolism in the late, weight stable phase after Roux-en-Y Gastric Bypass (RYGB) in patients with and without preoperative type 2 diabetes we invited 55 RYGB-operated persons from two existing cohorts to participate in a late follow-up study. 44 (24 with normal glucose tolerance (NGT)/20 with type 2 diabetes (T2D) before surgery) accepted the invitation (median follow-up 2.7 [Range 2.2–5.0 years]). Subjects were examined during an oral glucose stimulus and results compared to preoperative and 1-year (1 y) post RYGB results. Glucose tolerance, insulin resistance, beta-cell function and incretin hormone secretion were evaluated. 1 y weight loss was maintained late after surgery. Glycemic control, insulin resistance, beta-cell function and GLP-1 remained improved late after surgery in both groups. In NGT subjects, nadir glucose decreased 1 y after RYGB, but did not change further. In T2D patients, relative change in weight from 1 y to late after RYGB correlated with relative change in fasting glucose and HbA1c, whereas relative changes in glucose-stimulated insulin release correlated inversely with relative changes in postprandial glucose excursions. In NGT subjects, relative changes in postprandial nadir glucose correlated with changes in beta-cell glucose sensitivity. Thus, effects of RYGB on weight and glucose metabolism are maintained late after surgery in patients with and without preoperative T2D. Weight loss and improved beta-cell function both contribute to maintenance of long-term glycemic control in patients with type 2 diabetes, and increased glucose stimulated insulin secretion may contribute to postprandial hypoglycemia in NGT subjects.

Beta-cell function and insulin resistance evaluated by HOMA in pancreatic cancer subjects with varying degrees of glucose intolerance

Pancreatology ◽  
2005 ◽  
Vol 5 (2-3) ◽  
pp. 229-233 ◽  
Author(s):  
Suresh T. Chari ◽  
Mauricio Zapiach ◽  
Dhiraj Yadav ◽  
Robert A. Rizza
Keyword(s):  
Insulin Resistance ◽  
Pancreatic Cancer ◽  
Beta Cell ◽  
Glucose Intolerance ◽  
Beta Cell Function ◽  
Cell Function

scholarly journals Short adult stature predicts impaired beta-cell function, insulin resistance, glycemia and type 2 diabetes in Finnish men

2016 ◽  
pp. jc.2016-2933 ◽  
Author(s):  
Jagadish Vangipurapu ◽  
Alena Stančáková ◽  
Raimo Jauhiainen ◽  
Johanna Kuusisto ◽  
Markku Laakso
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Adult Stature

scholarly journals Comparison of Serum Copper, Selenium and Zinc Concentrations Among the States of Glucose Tolerance

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A319-A320
Author(s):  
Vishwanath Pattan ◽  
Maria Chang Villacreses ◽  
Rudruidee Karnchanasorn ◽  
Wei Feng ◽  
Raynald Samoa ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Trace Elements ◽  
Glucose Tolerance ◽  
Beta Cell ◽  
Trace Element ◽  
Beta Cell Function ◽  
Cell Function ◽  
Primary Source ◽  
Serum Concentrations ◽  
Cross Sectional

Abstract Trace element is essential for the proper growth, development, and physiology of the organism and the primary source of trace element is dietary intake. Among trace elements, the role of copper (Cu), selenium (Se), and zinc (Zn) in the pathogenesis of diabetes have been widely recognized. However, there is little information available about these 3 trace elements across the different states of glucose tolerance. We examined associations between serum levels of trace elements - Cu, Zn, and Se with various stages of glucose tolerance in a representative, cross-sectional sample of US adults. Our sample included 5,087 adults (≥20 years) with available serum concentrations of Cu, Zn and Se as well as states of glucose tolerance, defined by history, HbA1c, fasting, and 2-hour plasma glucose concentrations. Serum concentrations of trace elements were compared with glucose tolerance status with the consideration of covariates. Regression analyses was used to examine the relationship of trace elements with HOMA-IR, HOMA-B, and BMI in non-diabetic subjects with the consideration of appropriate covariates. Serum Se (P<0.0001) and Zn (P<0.0001) concentrations differed significantly among 3 groups based on the states of glucose tolerance, while no difference was noted in serum Cu concentration. In non-diabetic subjects, serum Cu concentration was positively correlated with BMI (P<0.0001) with a possible compensatory increased beta cell function (P=0.018). Serum Se concentration was negatively correlated with insulin resistance (P=0.016) but not with beta cell function or BMI. Serum Zn concertation was negatively correlated with beta cell function (P=0.0023) and BMI (P=0.018), but not with insulin resistance. We found that a higher serum concentration of trace elements was associated with negative glucose and fuel homeostasis in a non-deficiency population possibly through different mechanisms. Although the casual relationship remains to be elucidated, we recommend against trace element supplementation in a non-deficiency population.

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