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Altered Temporal Organization of Plasma Insulin Oscillations in Chronic Renal Failure

Divisions of Pediatric Nephrology (R.F., M.S., O.M., F.S.) and Clinical Nephrology (E.R.), Faculty of Medicine, and Institute of Pharmacology and Toxicology (R.F.), Faculty of Clinical Medicine Mannheim, Ruperto-Carolus University, 69115 Heidelberg, Germany; and Department of Internal Medicine (J.D.V.), University of Virginia Health Sciences Center and General Clinical Research Center, Charlottesville, Virginia 22908

Address all correspondence and requests for reprints to: Franz Schaefer, M.D., Pediatric Nephrology Division, University Children’s Hospital, Im Neuenheimer Feld 150, 69120 Heidelberg, Germany. E-Mail: . franz_schaefer{at}med.uni-heidelberg.de

Abstract

Chronic renal failure (CRF) is associated with mechanistically unexplained impaired insulin sensitivity. Erratic insulin secretory patterns typify other states of insulin resistance. We sought to investigate possible alterations of plasma insulin oscillations in CRF. We assessed high- and low-frequency insulin and glucose oscillations in 7 male CRF patients and 11 controls by multiparametric deconvolution analysis and cluster analysis, approximate entropy (ApEn) statistic, and cross-ApEn statistics. Insulin sensitivity was appraised by euglycemic hyperinsulinemic clamps. Despite impaired glucose disappearance rates in CRF, fasting and 24-h mean insulin and glucose concentrations did not differ between patients and controls. However, patients showed a 2.5-fold increase of insulin elimination half-life, reduced frequency of both rapid (6.1 ± 0.4 vs. 7.1 ± 0.2 h^-1, P < 0.001) and slow oscillations of insulin release (0.54 ± 0.11 vs. 0.71 ± 0.1 h^-1, P < 0.001), lack of acceleration and paradoxically more orderly slow insulin and glucose pulses after meals, and increased temporal coupling between insulin and glucose patterns (cross-ApEn: 0.58 ± 0.13 vs. 1.37 ± 0.23, P < 0.001). Postprandial glucose intolerance was inferable by prolonged and amplified blood glucose excursions despite exaggerated insulin bursts of almost 3-fold higher area. In summary, CRF is associated with a complex disruption of the temporal organization of insulin release, which differs from abnormalities observed to date in other states of insulin resistance.

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