Intranasal Insulin Suppresses Food Intake via Enhancement of Brain Energy Levels in Humans
- Kamila Jauch-Chara1⇓,
- Alexia Friedrich1,
- Magdalena Rezmer1,
- Uwe H. Melchert2,
- Harald G. Scholand-Engler1,2,
- Manfred Hallschmid3 and
- Kerstin M. Oltmanns1
- 1Department of Psychiatry and Psychotherapy, University of Luebeck, Luebeck, Germany
- 2Department of Neuroradiology, University of Luebeck, Luebeck, Germany
- 3Department of Neuroendocrinology, University of Luebeck, Luebeck, Germany
- Corresponding author: Kamila Jauch-Chara, .
Cerebral insulin exerts anorexic effects in humans and animals. The underlying mechanisms, however, are not clear. Because insulin physiologically facilitates glucose uptake by most tissues of the body and thereby fosters intracellular energy supply, we hypothesized that intranasal insulin reduces food consumption via enhancement of the neuroenergetic level. In a double-blind, placebo–controlled, within-subject comparison, 15 healthy men (BMI 22.2 ± 0.37 kg/m2) aged 22–28 years were intranasally administered insulin (40 IU) or placebo after an overnight fast. Cerebral energy metabolism was assessed by 31P magnetic resonance spectroscopy. At 100 min after spray administration, participants consumed ad libitum from a test buffet. Our data show that intranasal insulin increases brain energy (i.e., adenosine triphosphate and phosphocreatine levels). Cerebral energy content correlates inversely with subsequent calorie intake in the control condition. Moreover, the neuroenergetic rise upon insulin administration correlates with the consecutive reduction in free-choice calorie consumption. Brain energy levels may therefore constitute a predictive value for food intake. Given that the brain synchronizes food intake behavior in dependence of its current energetic status, a future challenge in obesity treatment may be to therapeutically influence cerebral energy homeostasis. Intranasal insulin, after optimizing its application schema, seems a promising option in this regard.
- Received January 6, 2012.
- Accepted March 27, 2012.
- © 2012 by the American Diabetes Association.
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