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Oral glucose intake inhibits hypothalamic neuronal activity more effectively than glucose infusion

¹Image Sciences Institute, University Medical Center Utrecht, Utrecht; ²Department of Endocrinology and Metabolism, Leiden University Medical Center, Leiden; ³Department of Food and Chemical Risk Analysis, TNO Quality of Life, Zeist; ⁴Division of Human Nutrition, Wageningen University, Wageningen; and ⁵Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands

Submitted 13 April 2007 ; accepted in final form 11 June 2007

We previously showed that hypothalamic neuronal activity, as measured by the blood oxygen level-dependent (BOLD) functional MRI signal, declines in response to oral glucose intake. To further explore the mechanism driving changes in hypothalamic neuronal activity in response to an oral glucose load, we here compare hypothalamic BOLD signal changes subsequent to an oral vs. an intravenous (iv) glucose challenge in healthy humans. Seven healthy, normal-weight men received four interventions in random order after an overnight fast: 1) ingestion of glucose solution (75 g in 300 ml) or 2) water (300 ml), and 3) iv infusion of 40% glucose solution (0.5 g/kg body wt, maximum 35 g) or 4) infusion of saline (0.9% NaCl, equal volume). The BOLD signal was recorded as of 8 min prior to intervention (baseline) until 30 min after. Glucose infusion was associated with a modest and transient signal decline in the hypothalamus. In contrast, glucose ingestion was followed by a profound and persistent signal decrease despite the fact that plasma glucose levels were almost threefold lower than in response to iv administration. Accordingly, glucose ingestion tended to suppress hunger more than iv infusion (P < 0.1). We infer that neural and endocrine signals emanating from the gastrointestinal tract are critical for the hypothalamic response to nutrient ingestion.

functional magnetic resonance imaging; glucose homeostasis; insulin; incretins

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