Muscle Sympathetic Nerve Activity in Response to Glucose Ingestion: Impact of Plasma Insulin and Body Fat

  1. Eric Ravussin
  1. Clinical Diabetes and Nutrition Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health Phoenix, Arizona
  2. Department of Nutrition and Metabolism, Heinrich Heine University Dusseldorf, Germany
  3. Department of Anesthesia and the Cardiovascular Center, College of Medicine, University of Iowa Iowa City, Iowa
  1. Address correspondence to Dr. Maximilian Spraul, Heinrich Heine Universita't. Abt. Ernährung und Stoffwechsel, Postfach 101007, Moorenstr. 5, 40001 Dusseldorf, Germany. No reprints available.

Abstract

Carbohydrate intake stimulates sympathetic nervous system activity in lean subjects, whereas in obese subjects, the results have been inconsistent. The aim of this study was to directly measure sympathetic neural outflow to skeletal muscle in response to a 75-g oral glucose tolerance test (OGTT) in 15 Pima Indian and 16 Caucasian men, matched for body fat and age, but covering a large range of body weight (57–113 kg) and body fat (4–41%). Fasting muscle sympathetic nerve activity (MSNA) correlated positively with body fat (r = 0.73; P = 0.001) in Caucasians but not in Pima Indians, whereas the increase in MSNA during the OGTT correlated negatively with the percentage of body fat (r = −0.38, P = 0.03) independently of race. In each subject, the increase in MSNA over time correlated positively with the increase in plasma insulin levels, but the slopes of these relationships were inversely related to the percentage of body fat (r = −0.52, P = 0.003) independently of race. In conclusion, obesity is associated with a higher fasting sympathetic neural outflow to muscle but a blunted increase in response to an oral glucose load despite a larger increase in plasma insulin levels. This blunted response may represent another feature of the obesity/insulin resistance syndrome.

  • Received May 19, 1993.
  • Revision received September 16, 1993.
  • Accepted September 16, 1993.
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