Insulin deficiency does not predict incident Type 2 diabetes
MedWire News: Results from a large Korean study suggest that measurement of blood glucose, but not homeostasis model assessment of β-cell function (HOMA-β), predicts future onset of Type 2 diabetes.
HOMA-β is an index of insulin secretory function calculated using measures of plasma glucose and insulin concentration. Previous studies have suggested that low HOMA-β is indicative of increased risk for Type 2 diabetes.
In this study, Ki-Chul Sung (Sungkyunkwan University School of Medicine, Seoul, South Korea) and team compared the ability of fasting plasma glucose (FPG) alone with HOMA-β to predict Type 2 diabetes in 12,924 Korean individuals.
The participants were free of diabetes at baseline in 2003 when FPG and insulin measurements were taken. The team divided the participants into three FPG categories: normal fasting glucose (NFG; blood glucose below 5.6 mmol/l), impaired fasting glucose (IFG)-100 (blood glucose 5.6–6.0 mmol/l), and IFG-110 (blood glucose 6.1–6.9 mmol/l).
The cohort was followed up until 2008 for incident Type 2 diabetes, during which time 234 individuals developed the condition.
The researchers found that 29% of the IFG-110 group (n=246) developed Type 2 diabetes over the study period compared with 5.0% and 0.3% of the IFG-100 (n=2546) and NFG (n=10,132) groups, respectively.
HOMA-β, in contrast, was higher in participants who developed Type 2 diabetes in the NFG group compared with those who did not, and similar in IFG-100 and IFG-110 patients who developed Type 2 diabetes compared with those who did not.
“We confirm that baseline glucose concentration is strongly associated with diabetes development, with 29% of individuals meeting the old IFG criteria (IFG-110) progressing to diabetes within 5 years,” conclude Sung et al.
“However, individuals who were at risk to develop diabetes were not characterized by insulin deficiency, as defined by absolute insulin concentration or HOMA-β,” they add.
“As pancreatic β-cell dysfunction has been established as a requisite defect in Type 2 diabetes, these findings likely highlight the inadequacies of fasting measures as surrogates for pancreatic function.”
The results of this study are published in the journal Diabetes Care.
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By Helen Albert