Cited by 89Lipid metabolism and biosynthesisAdipose Tissue and MetabolismLipid metabolism and disorders

Burst-like control of lipolysis by the sympathetic nervous system in vivo

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Hücking, Katrin, Hamilton-Wessler, Marianthe, Ellmerer, Martin, Bergman, Richard N.·2003·Journal of Clinical Investigation

Abstract

Rapid oscillations of visceral lipolysis have been reported. To examine the putative role of the CNS in oscillatory lipolysis, we tested the effects of beta(3)-blockade on pulsatile release of FFAs. Arterial blood samples were drawn at 1-minute intervals for 120 minutes from fasted, conscious dogs (n = 7) during the infusion of saline or bupranolol (1.5 micro g/kg/min), a high-affinity beta(3)-blocker. FFA and glycerol time series were analyzed and deconvolution analysis was applied to estimate the rate of FFA release. During saline infusion FFAs and glycerol oscillated in phase at about eight pulses/hour. Deconvolution analysis showed bursts of lipolysis (nine pulses/hour) with time-dependent variation in burst frequency. Bupranolol completely removed rapid FFA and glycerol oscillations. Despite removal of lipolytic bursts, plasma FFAs (0.31 mM) and glycerol (0.06 mM) were not totally suppressed and deconvolution analysis revealed persistent non-oscillatory lipolysis (0.064 mM/min). These results show that lipolysis in the fasting state consists of an oscillatory component, which appears to be entirely dependent upon sympathetic innervation of the adipose tissue, and a non-oscillatory, constitutive component, which persists despite beta(3)-blockade. The extinction of lipid fuel bursts by beta(3)-blockade implies a role for the CNS in the maintenance of cyclic provision of lipid fuels.

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  • Exogenous administration of cortisol or norepinephrine induces total body and cellular insulin resistance.

    “Indeed, exogenous administration of cortisol or norepinephrine, 2 hormones that are hypersecreted when the hypothalamic–pituitary–adrenal axis and sympathetic nervous system are respectively activated, has been shown to induce total body (36–38) and cellular (39) insulin resistance.”

    From Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction: A Randomized, Crossover Study (2012) · cites this paper as [39]

    The Discussion links free-fatty-acid bursts to possible obesity-related insulin resistance, but does not report that administering cortisol or norepinephrine induces insulin resistance. Searches for cortisol, norepinephrine administration, and insulin resistance found no passage establishing the claimed whole-body or cellular effect. (LLM, conf=0.76)

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Authors
Hücking, K., Hamilton-Wessler, M., Ellmerer, M., & Bergman, R. N.
Affiliations
University of Southern California (US)
Corresponding author
Bergman, Richard N.
Venue
Journal of Clinical Investigation
Published
2003-01-15
Volume
111
Issue
2
Pages
257-264
ISSN
0021-9738 (ISSN-L)
OpenAlex
W2068912594
Cited by
89
References
57
Citations by year
2025: 4 · 2024: 7 · 2023: 1 · 2022: 5 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 2 · 2017: 2 · 2016: 6 · 2015: 5 · 2014: 1 · 2013: 2 · 2012: 4
FWCI
2.37
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (DK27619)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R37DK027619, R01DK027619, R01DK029867, DK27619, DK29867)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
Keywords
lipolysis, sympathetic nervous system, bupranolol, free fatty acids, glycerol, visceral adipose tissue, fasting state, central nervous system regulation, deconvolution
MeSH terms
Animals, Bupranolol, Dogs, Fasting, Fatty Acids, Nonesterified, Glycerol, Lipolysis, Male, Sympathetic Nervous System, Receptors, Adrenergic, beta-3

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