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Relevance of Sympathetic Nervous System Activation in Obesity and Metabolic Syndrome
Open accessAbstract
Sympathetic tone is well recognised as being implicit in cardiovascular control. It is less readily acknowledged that activation of the sympathetic nervous system is integral in energy homeostasis and can exert profound metabolic effects. Accumulating data from animal and human studies suggest that central sympathetic overactivity plays a pivotal role in the aetiology and complications of several metabolic conditions that can cluster to form the Metabolic Syndrome (MetS). Given the known augmented risk for type 2 diabetes, cardiovascular disease, and premature mortality associated with the MetS understanding the complex pathways underlying the metabolic derangements involved has become a priority. Many factors have been proposed to contribute to increased sympathetic nerve activity in metabolic abnormalities including obesity, impaired baroreflex sensitivity, hyperinsulinemia, and elevated adipokine levels. Furthermore there is mounting evidence to suggest that chronic sympathetic overactivity can potentiate two of the key metabolic alterations of the MetS, central obesity and insulin resistance. This review will discuss the regulatory role of the sympathetic nervous system in metabolic control and the proposed pathophysiology linking sympathetic overactivity to metabolic abnormalities. Pharmacological and device-based approaches that target central sympathetic drive will also be discussed as possible therapeutic options to improve metabolic control in at-risk patient cohorts.
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“The SNS increases in response to caloric surplus, with norepinephrine activating β-adrenergic receptors, particularly in BAT. This stimulates UCP1 in BAT mitochondria, generating heat through uncoupled respiration.”
From Beyond Calories: Individual Metabolic and Hormonal Adaptations Driving Variability in Weight Management—A State-of-the-Art Narrative Review (2024) · cites this paper as [39]
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Toprak, Ö., Kurt, H., Sarı, Y., Şarkış, C., Us, H., & Kırık, A. (2017) · Kidney & Blood Pressure Research · doi:10.1159/000468530 · Cited by 29,772
Alberti, K. G. M. M., Eckel, R. H., Grundy, S. M., Zimmet, P. Z., Cleeman, J. I., Donato, K. A., Fruchart, J.-C., James, W. P. T., Loria, C. M., & Smith, S. C. (2009) · Circulation · doi:10.1161/circulationaha.109.192644 · Cited by 14,860
Diagnosis and Classification of Diabetes Mellitus
American Diabetes Association (2010) · Diabetes Care · doi:10.2337/dc11-s062 · Cited by 14,094
The metabolic syndrome—a new worldwide definition
Alberti, K. G. M., Zimmet, P., & Shaw, J. (2005) · The Lancet · doi:10.1016/s0140-6736(05)67402-8 · Cited by 9,352
Diagnosis and classification of diabetes mellitus
American Diabetes Association (2010) · Diabetes Care · doi:10.2337/dc10-s062 · Cited by 5,491
Maffei, M., Halaas, J., Ravussin, E., Pratley, R. E., Lee, G. H., Zhang, Y., Fei, H., Kim, S., Lallone, R., Ranganathan, S., et al. (1995) · Nature Medicine · doi:10.1038/nm1195-1155 · Cited by 3,725
Krum, H., Schlaich, M., Whitbourn, R., Sobotka, P. A., Sadowski, J., Bartus, K., Kapelak, B., Walton, A., Sievert, H., Thambar, S., et al. (2009) · The Lancet · doi:10.1016/s0140-6736(09)60566-3 · Cited by 2,108
Self-citationMalik, S., Wong, N. D., Franklin, S. S., Kamath, T. V., L'Italien, G. J., Pio, J. R., & Williams, G. R. (2004) · Circulation · doi:10.1161/01.cir.0000140677.20606.0e · Cited by 1,837
Ford, E. S. (2005) · Diabetes Care · doi:10.2337/diacare.28.7.1769 · Cited by 1,718
Turning off the signal: desensitization of β‐adrenergic receptor function
Hausdorff, W. P., Caron, M. G., & Lefkowitz, R. J. (1990) · The FASEB Journal · doi:10.1096/fasebj.4.11.2165947 · Cited by 1,259
Research works printed but not linked: 7
- 1986, Quarterly Journal of Medicine, 61, 1081
- 1995, The American Journal of Physiology, 269, R222
- 10.1210/en.133.4.1753 · DOI
- 1992, The Journal of Clinical Investigation, 90, 27
- 2008, Jounral of Hypertension, 26, S347
- 1998, Blood Pressure, Supplement, 7, 5
- 2010, Arterial Hypertension (Greek), 19, 32
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Leggio, M., Lombardi, M., Caldarone, E., Severi, P., D’Emidio, S., Armeni, M., Bravi, V., Bendini, M. G., & Mazza, A. (2017) · Hypertension Research · doi:10.1038/hr.2017.75 · Cited by 319
Heart Failure With Preserved Ejection Fraction and Diabetes
McHugh, K., DeVore, A. D., Wu, J., Matsouaka, R. A., Fonarow, G. C., Heidenreich, P. A., Yancy, C. W., Green, J. B., Altman, N., & Hernandez, A. F. (2019) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2018.11.033 · Cited by 313
SGLT2 Inhibitor–Induced Sympathoinhibition
Herat, L. Y., Magno, A. L., Rudnicka, C., Hricova, J., Carnagarin, R., Ward, N. C., Arcambal, A., Kiuchi, M. G., Head, G. A., Schlaich, M. P., et al. (2020) · JACC: Basic to Translational Science · doi:10.1016/j.jacbts.2019.11.007 · Cited by 233
“There is clear evidence to indicate that obesity, metabolic syndrome, and type 2 diabetes are associated with chronic activation of sympathetic nervous tone (7,8).”
BackgroundSelf-citationRole of the sympathetic nervous system in regulation of the sodium glucose cotransporter 2
Matthews, V. B., Elliot, R. H., Rudnicka, C., Hricova, J., Herat, L., & Schlaich, M. P. (2017) · Journal of Hypertension · doi:10.1097/hjh.0000000000001434 · Cited by 222
“Sympathetic activity is upregulated in obesity and type 2 diabetes and associated with perturbed glucose homeostasis, as recently reviewed in detail [5,6].”
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Metadata
- Authors
- Thorp, A. A., & Schlaich, M. P.
- Affiliations
- Baker Heart and Diabetes Institute (AU)
- Corresponding author
- Schlaich, Markus P.
- ORCID
- Schlaich, Markus P.
- Venue
- Journal of Diabetes Research
- Publisher
- Wiley
- Published
- 2015
- Volume
- 2015
- Pages
- 1-11
- ISSN
- 2314-6745 (ISSN-L)
- 2314-6753
- PMC
- PMC4430650
- OpenAlex
- W2066041574
- Cited by
- 425
- References
- 101
- Citations by year
- 2026: 28 · 2025: 42 · 2024: 36 · 2023: 44 · 2022: 40 · 2021: 45 · 2020: 48 · 2019: 40 · 2018: 33 · 2017: 31 · 2016: 32 · 2015: 5
- FWCI
- 4.38
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Diabetes Research (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- UWA Profiles and Research Repository (UWA) (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Health and Medical Research Council
- Victorian Government’s Operational Infrastructure Support Program
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- sympathetic nervous system, sympathetic hyperactivity, obesity, metabolic syndrome, energy homeostasis, abdominal obesity, insulin resistance, baroreflex sensitivity, hyperinsulinemia, adipokines, type 2 diabetes, cardiovascular disease, sympathetic activity, device therapy
- MeSH terms
- Animals, Humans, Obesity, Sympathetic Nervous System, Metabolic Syndrome
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