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Increase in hepatic and decrease in peripheral insulin clearance characterize abnormal temporal patterns of serum

Kaoru Ohashi1, Masashi Fujii1,2, Shinsuke Uda3

  • 11Department of Biological Sciences, Graduate School of Science, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033 Japan.

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Summary

Type 2 diabetes mellitus (T2DM) involves altered insulin clearance. Increased hepatic insulin clearance reduces insulin amplitude, while decreased peripheral clearance prolongs its presence, impacting glucose homeostasis.

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Area of Science:

  • Metabolism and Endocrinology
  • Physiology
  • Diabetes Research

Background:

  • Insulin is crucial for glucose homeostasis; impaired insulin action leads to glucose intolerance and type 2 diabetes mellitus (T2DM).
  • T2DM pathogenesis is associated with abnormal temporal patterns of circulating insulin, specifically a decreased peak and sustained increase after glucose infusion.
  • The underlying mechanisms for these altered insulin patterns in T2DM remain largely unknown.

Purpose of the Study:

  • To investigate the mechanisms behind the abnormal temporal pattern of circulating insulin concentration in type 2 diabetes mellitus.
  • To elucidate the roles of hepatic and peripheral insulin clearance in T2DM pathogenesis.

Main Methods:

  • Development of a mathematical model to analyze insulin dynamics.
  • Utilizing hyperglycemic and hyperinsulinemic-euglycemic clamp techniques in 111 subjects (healthy and diabetic).

Main Results:

  • Hepatic insulin clearance significantly increases, while peripheral insulin clearance significantly decreases from healthy to T2DM states.
  • Increased hepatic insulin clearance attenuates the amplitude of circulating insulin concentrations.
  • Decreased peripheral insulin clearance alters insulin temporal patterns from transient to sustained.

Conclusions:

  • Opposing changes in hepatic and peripheral insulin clearance characterize the abnormal insulin temporal patterns observed in T2DM.
  • These findings offer new insights into T2DM pathogenesis.
  • Understanding these mechanisms may aid in developing improved T2DM treatments.