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Beta cell function balanced insulin sensitivity following hyperglycemia
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Beta cell function following a hyperglycemic load properly compensated insulin sensitivity lost with kidney dysfunction in older men, preserving the net balance between the two, according to research published in the Journal of Clinical Endocrinology & Metabolism.
“Therapeutic and preventive strategies aiming at improving glucose tolerance in chronic kidney disease may benefit more if they are focused on improving insulin sensitivity rather than beta cell function,” the researchers wrote.
Ting Jia, MD, a postdoctoral research fellow at Karolinska Institutet, Stockholm, Sweden, and colleagues conducted a community-based cohort study investigating insulin release and glucose tolerance across kidney function strata.
The investigators studied 1,015 Swedish men aged 70 to 71 years without diabetes from the Uppsala Longitudinal Study of Adult Men.
To determine insulin sensitivity, beta cell function and glucose tolerance, a standardized oral glucose tolerance test (OGTT) and euglycaemic hyperinsulinemic clamp (HEGC) tests were administered. Cystatin C-algorithms were used to gauge kidney function and mixed models to identify causes of insulin secretion following hyperglycemic load.
Moderate-advanced kidney disease was observed in as many as 466 men (46%). Insulin sensitivity, based on HEGC, diminished across decreasing kidney function quartiles. Beta cell function indices were incrementally higher after OGTT, based on area under the curve for insulin release, the estimated first-phase insulin release and the insulinogenic index.
Oral disposition index and 2-hour post-load glucose tolerance did not differ across kidney function strata. Dynamic insulin release during OGTT was inversely related to kidney function, based on mixed models, correcting for individual insulin sensitivity or its risk factors.
“Our results indicate that beta cell function adequately compensates the loss of insulin sensitivity that occurs during the earlier stages of chronic kidney disease,” the researchers wrote. “Whether beta cell function is preserved also in individuals with more advanced stages of chronic kidney disease (stages 4 and 5) cannot be derived from this analysis and needs verification in future studies.”
Disclosure: This work was supported by the Swedish Research Council; one researcher reports support from the NIDDKD and the Veterans Administration Merit Award. One researcher reports being employed by Baxter Healthcare Corporation and another by Astellas.
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