Weight Loss May Reverse Blunted Sympathetic Neural Responsiveness to Glucose Ingestion in Obese Metabolic Syndrome Subjects
- Nora E. Straznicky (Nora.Straznicky{at}bakeridi.edu.au),
- Gavin W. Lambert,
- Mariee T. McGrane,
- Kazuko Masuo,
- Tye Dawood,
- Paul J. Nestel,
- Nina Eikelis,
- Markus P. Schlaich,
- Murray D. Esler,
- Florentia Socratous,
- Reena Chopra and
- Elisabeth A. Lambert
- From the Human Neurotransmitters (NES, GWL, MTG, KM, TD, NE, MDE, RC and EAL), Cardiovascular Nutrition (PJN) and Neurovascular Hypertension and Kidney Disease (FS, MPS) Laboratories, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, AUSTRALIA
Abstract
Objective- To study the effects of weight loss on sympathetic nervous system responsiveness to glucose ingestion in obese metabolic syndrome (MetS) subjects, in whom such responses are reportedly blunted.
Research Design and Methods- Thirty four subjects, 19 insulin resistant (IR) and 15 insulin sensitive (IS), mean age 55 ± 1 yrs, BMI, 31.6 ± 0.6 kg/m2, who fulfilled ATP III MetS criteria participated. Simultaneous measurements of whole-body norepinephrine (NE) spillover rate, calf blood flow and intra-arterial blood pressure were made at times 0, 30, 60, 90, and 120 minutes post 75g glucose. The experiment was repeated after a 3-month hypocaloric diet with or without an exercise program.
Results- Body weight decreased by 8.1 ± 0.9 and 8.4 ± 1.1 kg, and resting NE spillover by 94 ± 31 and 166 ± 58 ng/min (P all ≤ 0.01), in IR and IS subjects respectively. Weight loss was accompanied by a marked increase in sympathetic responsiveness post-glucose, but only in IR subjects. In this subgroup, comparative increases in NE spillover rates at baseline and post weight loss averaged −3 ± 25 versus 73 ± 24 ng/min at 30 min (P=0.039), 36 ± 21 versus 115 ± 28 ng/min at 60 min (P=0.045), 9 ± 21 versus 179 ± 50 ng/min at 90 min (P<0.001) and 40 ± 48 versus 106 ± 39 ng/min at 120 min (P= 0.24).
Conclusions- Weight loss reverses blunted sympathetic responsiveness to glucose ingestion in insulin resistant metabolic syndrome subjects, which is relevant to postprandial energy utilization and body weight homeostasis.
Footnotes
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- Received November 16, 2008.
- Accepted January 24, 2009.
- Copyright © American Diabetes Association














