TY - JOUR
T1 - Altered temporal organization of plasma insulin oscillations in chronic renal failure
AU - Feneberg, Reinhard
AU - Sparber, Monika
AU - Veldhuis, Johannes D.
AU - Mehls, Otto
AU - Ritz, Eberhard
AU - Schaefer, Franz
PY - 2002
Y1 - 2002
N2 - 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.
AB - 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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U2 - 10.1210/jcem.87.5.8453
DO - 10.1210/jcem.87.5.8453
M3 - Article
C2 - 11994326
AN - SCOPUS:0036092894
SN - 0021-972X
VL - 87
SP - 1965
EP - 1973
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
IS - 5
ER -