Glucose ingestion fails to inhibit hypothalamic neuronal activity in patients with type 2 diabetes mellitus
- Solrun Vidarsdottir1,
- Paul A.M. Smeets2,
- Diane L. Eichelsheim1,
- Matthias J.P. van Osch3,
- Max A. Viergever2,
- Johannes A. Romijn1,
- Jeroen van der Grond3 and
- Hanno Pijl (h.pijl{at}lumc.nl)1
- 1 Department of Endocrinology and Metabolism, Leiden University Medical Center, Leiden, The Netherlands
- 2 Image Sciences Institute, University Medical Center Utrecht, Utrecht, The Netherlands
- 3 Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands
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 mellitus.
Research Design and Methods: In this randomized, single blind, case-control study, 7 male patients with type 2 diabetes mellitus (BMI 27.9 ± 2.0 kg/m2) and 10 healthy (BMI 26.1 ± 3.2 kg/m2), age-matched men participated. Subjects were scanned twice for 38 minutes 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 (BOLD) signal decrease in the upper and lower hypothalamus in healthy men, but not in patients with diabetes.
Conclusions: Glucose ingestion fails to inhibit hypothalamic neuronal activity in patients with type 2 diabetes mellitus. Failure of neural circuits to properly adapt to nutrient ingestion may contribute to metabolic imbalance in DM2 patients.
Footnotes
-
- Received February 20, 2007.
- Accepted July 1, 2007.
- Copyright © American Diabetes Association
