Intranasal Insulin Enhances Postprandial Thermogenesis and Lowers Postprandial Serum Insulin Levels in Healthy Men
- Christian Benedict1,2,
- Swantje Brede1,
- Helgi B. Schiöth2,
- Hendrik Lehnert3,
- Bernd Schultes4,
- Jan Born1 and
- Manfred Hallschmid1
- 1Department of Neuroendocrinology, University of Lübeck, Lübeck, Germany;
- 2Department of Neuroscience, Functional Pharmacology, Uppsala University, Uppsala, Sweden;
- 3Department of Internal Medicine I, University of Lübeck, Lübeck, Germany;
- 4Interdisciplinary Obesity Center, Kantonsspital St. Gallen, St. Gallen, Switzerland.
- Corresponding author: Christian Benedict, .
OBJECTIVE Animal studies indicate a prominent role of brain insulin signaling in the regulation of peripheral energy metabolism. We determined the effect of intranasal insulin, which directly targets the brain, on glucose metabolism and energy expenditure in humans.
RESEARCH DESIGN AND METHODS In a double-blind, placebo-controlled, balanced within-subject comparison, 19 healthy normal-weight men (18–26 years old) were intranasally administered 160 IU human insulin after an overnight fast. Energy expenditure assessed via indirect calorimetry and blood concentrations of glucose, insulin, C-peptide, and free fatty acids (FFAs) were measured before and after insulin administration and the subsequent consumption of a high-calorie liquid meal of 900 kcal.
RESULTS Intranasal insulin, compared with placebo, increased postprandial energy expenditure, i.e., diet-induced thermogenesis, and decreased postprandial concentrations of circulating insulin and C-peptide, whereas postprandial plasma glucose concentrations did not differ from placebo values. Intranasal insulin also induced a transient decrease in prandial serum FFA levels.
CONCLUSIONS Enhancing brain insulin signaling by means of intranasal insulin administration enhances the acute thermoregulatory and glucoregulatory response to food intake, suggesting that central nervous insulin contributes to the control of whole-body energy homeostasis in humans.
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- Received March 5, 2010.
- Accepted September 20, 2010.
- © 2011 by the American Diabetes Association.
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