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Acute inhibition of lipolysis does not affect postprandial suppression of endogenous glucose production

Lookup NU author(s): Dr Peter Carey, Dr Michael FirbankORCiD, Professor Roy Taylor

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Abstract

To test the hypothesis that intrahepatic availability of fatty acid could modify the rate of suppression of endogenous glucose production (EGP), acipimox or placebo was administered before and during a test meal. We used a modified isotopic methodology to measure EGP in 11 healthy subjects, and 1H magnetic resonance spectroscopic measurement of hepatic triglyceride stores was also undertaken. Acipimox suppressed plasma free fatty acids markedly before the meal (0.05 ± 0.01 mmol/l at -10 min, P = 0) and throughout the postprandial period (0.03 ± 0.01 mmol/l at 150 min). Mean peak plasma glucose was significantly lower after the meal on acipimox days (8.9 ± 0.4 vs. 10.1 ± 0.5 mmol/l, P < 0.01), as was mean peak serum insulin (653.1 ± 99.9 vs. 909 ± 118 pmol/l, P < 0.01). Fasting EGP was similar (11.15 ± 0.58 μmol·kg-1·min-1 placebo vs. 11.17 ± 0.89 mg·kg-1·min-1 acipimox). The rate of suppression of EGP after the meal was almost identical on the 2 test days (4.36 ± 1.52 vs. 3.69 ± 1.21 μmol·kg-1·min-1 at 40 min). There was a significant negative correlation between the acipimox-induced decrease in peak plasma glucose and liver triglyceride content r = -0.827, P = 0.002), suggesting that, when levels of liver fat were low, inhibition of lipolysis was able to affect glucose homeostasis. Acute pharmacological sequestration of fatty acids in triglyceride stores improves postprandial glucose homeostasis without effect on the immediate postprandial suppression of EGP. Copyright © 2005 the American Physiological Society.


Publication metadata

Author(s): Carey PE, Gerrard J, Cline GW, Dalla Man C, English PT, Firbank MJ, Cobelli C, Taylor R

Publication type: Article

Publication status: Published

Journal: American Journal of Physiology - Endocrinology and Metabolism

Year: 2005

Volume: 289

Issue: 6

Pages: E941-E947

ISSN (print): 0193-1849

ISSN (electronic): 1522-1555

Publisher: American Physiological Society

URL: http://dx.doi.org/10.1152/ajpendo.00195.2005

DOI: 10.1152/ajpendo.00195.2005

PubMed id: 15998660


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Funding

Funder referenceFunder name
Wellcome Trust
P01 DK 68229NIDDK NIH HHS
P30 DK 45735NIDDK NIH HHS

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