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Glucose Ingestion Fails to Inhibit Hypothalamic Neuronal Activity in Patients With Type 2 Diabetes

  1. Solrun Vidarsdottir1,
  2. Paul A.M. Smeets2,
  3. Diane L. Eichelsheim1,
  4. Matthias J.P. van Osch3,
  5. Max A. Viergever2,
  6. Johannes A. Romijn1,
  7. Jeroen van der Grond3 and
  8. Hanno Pijl1
  1. 1Department of Endocrinology and Metabolism, Leiden University Medical Center, Leiden, The Netherlands
  2. 2Image Sciences Institute, University Medical Center Utrecht, Utrecht, the Netherlands
  3. 3Department of Radiology, Leiden University Medical Center, Leiden, the Netherlands
  1. Address correspondence and reprint requests to Hanno Pijl, MD, PhD, Leiden University Medical Center, Department of Endocrinology and Metabolic Disease, C4-83, P.O. Box 9600, 2300 RC, Leiden, Netherlands. E-mail: h.pijl{at}lumc.nl

Abstract

OBJECTIVE—The hypothalamus plays a critical role in the regulation of energy balance and fuel flux. Glucose ingestion inhibits hypothalamic neuronal activity in healthy humans. We hypothesized that hypothalamic neuronal activity in response to an oral glucose load would be altered in patients with type 2 diabetes.

RESEARCH DESIGN AND METHODS—In this randomized, single blind, case-control study, 7 type 2 diabetic men (BMI 27.9 ± 2.0 kg/m2) and 10 age-matched healthy men (BMI 26.1 ± 3.2 kg/m2) were scanned twice for 38 min on separate days using functional magnetic resonance imaging. After 8 min, they ingested either a glucose solution (75 g in 300 ml water) or water (300 ml).

RESULTS—Glucose ingestion resulted in a prolonged significant blood oxygen level–dependent signal decrease in the upper and lower hypothalamus in healthy subjects but not in diabetic patients.

CONCLUSIONS—Glucose ingestion fails to inhibit hypothalamic neuronal activity in patients with type 2 diabetes. Failure of neural circuits to properly adapt to nutrient ingestion may contribute to metabolic imbalance in type 2 diabetic patients.

Footnotes

  • Published ahead of print at http://diabetes.diabetesjournals.org on 1 August 2007. DOI: 10.2337/db07-0193.

    The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

    • Accepted July 1, 2007.
    • Received February 20, 2007.
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This Article

  1. Published online before print August 1, 2007, doi: 10.2337/db07-0193 Diabetes October 2007 vol. 56 no. 10 2547-2550
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