Liraglutide treatment reduced interleukin-6 in adults with type 1 diabetes but did not improve established autonomic or polyneuropathy

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Liraglutide treatment reduced interleukin-6 in adults with type 1 diabetes but did not improve established autonomic or polyneuropathy. / Brock, Christina; Hansen, Christian Stevns; Karmisholt, Jesper; Møller, Holger Jon; Juhl, Anne; Farmer, Adam Donald; Drewes, Asbjørn Mohr; Riahi, Sam; Lervang, Hans Henrik; Jakobsen, Poul Erik; Brock, Birgitte.

In: British Journal of Clinical Pharmacology, Vol. 85, No. 11, 2019, p. 2512-2523.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Brock, C, Hansen, CS, Karmisholt, J, Møller, HJ, Juhl, A, Farmer, AD, Drewes, AM, Riahi, S, Lervang, HH, Jakobsen, PE & Brock, B 2019, 'Liraglutide treatment reduced interleukin-6 in adults with type 1 diabetes but did not improve established autonomic or polyneuropathy', British Journal of Clinical Pharmacology, vol. 85, no. 11, pp. 2512-2523. https://doi.org/10.1111/bcp.14063

APA

Brock, C., Hansen, C. S., Karmisholt, J., Møller, H. J., Juhl, A., Farmer, A. D., Drewes, A. M., Riahi, S., Lervang, H. H., Jakobsen, P. E., & Brock, B. (2019). Liraglutide treatment reduced interleukin-6 in adults with type 1 diabetes but did not improve established autonomic or polyneuropathy. British Journal of Clinical Pharmacology, 85(11), 2512-2523. https://doi.org/10.1111/bcp.14063

Vancouver

Brock C, Hansen CS, Karmisholt J, Møller HJ, Juhl A, Farmer AD et al. Liraglutide treatment reduced interleukin-6 in adults with type 1 diabetes but did not improve established autonomic or polyneuropathy. British Journal of Clinical Pharmacology. 2019;85(11):2512-2523. https://doi.org/10.1111/bcp.14063

Author

Brock, Christina ; Hansen, Christian Stevns ; Karmisholt, Jesper ; Møller, Holger Jon ; Juhl, Anne ; Farmer, Adam Donald ; Drewes, Asbjørn Mohr ; Riahi, Sam ; Lervang, Hans Henrik ; Jakobsen, Poul Erik ; Brock, Birgitte. / Liraglutide treatment reduced interleukin-6 in adults with type 1 diabetes but did not improve established autonomic or polyneuropathy. In: British Journal of Clinical Pharmacology. 2019 ; Vol. 85, No. 11. pp. 2512-2523.

Bibtex

@article{5fd5d2de3e80477dbfafc7a6052e9dc6,
title = "Liraglutide treatment reduced interleukin-6 in adults with type 1 diabetes but did not improve established autonomic or polyneuropathy",
abstract = "Aims: Type 1 diabetes can be complicated with neuropathy that involves immune-mediated and inflammatory pathways. Glucagon-like peptide-1 receptor agonists such as liraglutide, have shown anti-inflammatory properties, and thus we hypothesized that long-term treatment with liraglutide induced diminished inflammation and thus improved neuronal function. Methods: The study was a randomized, double-blinded, placebo-controlled trial of adults with type 1 diabetes and confirmed symmetrical polyneuropathy. They were randomly assigned (1:1) to receive either liraglutide or placebo. Titration was 6 weeks to 1.2–1.8 mg/d, continuing for 26 weeks. The primary endpoint was change in latency of early brain evoked potentials. Secondary endpoints were changes in proinflammatory cytokines, cortical evoked potential, autonomic function and peripheral neurophysiological testing. Results: Thirty-nine patients completed the study, of whom 19 received liraglutide. In comparison to placebo, liraglutide reduced interleukin-6 (−22.6%; 95% confidence interval [CI]: −38.1, −3.2; P =.025) with concomitant numerical reductions in other proinflammatory cytokines. However neuronal function was unaltered at the central, autonomic or peripheral level. Treatment was associated with −3.38 kg (95% CI: −5.29, −1.48; P <.001] weight loss and a decrease in urine albumin/creatinine ratio (−40.2%; 95% CI: −60.6, −9.5; P =.02). Conclusion: Hitherto, diabetic neuropathy has no cure. Speculations can be raised whether mechanism targeted treatment, e.g. lowering the systemic level of proinflammatory cytokines may lead to prevention or treatment of the neuroinflammatory component in early stages of diabetic neuropathy. If ever successful, this would serve as an example of how fundamental mechanistic principles are translated into clinical practice similar to those applied in the cardiovascular and nephrological clinic.",
keywords = "anti-inflammation, diabetic neuropathy, glucagon-like peptide-1 agonist, interleukin-6, liraglutide",
author = "Christina Brock and Hansen, {Christian Stevns} and Jesper Karmisholt and M{\o}ller, {Holger Jon} and Anne Juhl and Farmer, {Adam Donald} and Drewes, {Asbj{\o}rn Mohr} and Sam Riahi and Lervang, {Hans Henrik} and Jakobsen, {Poul Erik} and Birgitte Brock",
year = "2019",
doi = "10.1111/bcp.14063",
language = "English",
volume = "85",
pages = "2512--2523",
journal = "British Journal of Clinical Pharmacology",
issn = "0306-5251",
publisher = "Wiley-Blackwell",
number = "11",

}

RIS

TY - JOUR

T1 - Liraglutide treatment reduced interleukin-6 in adults with type 1 diabetes but did not improve established autonomic or polyneuropathy

AU - Brock, Christina

AU - Hansen, Christian Stevns

AU - Karmisholt, Jesper

AU - Møller, Holger Jon

AU - Juhl, Anne

AU - Farmer, Adam Donald

AU - Drewes, Asbjørn Mohr

AU - Riahi, Sam

AU - Lervang, Hans Henrik

AU - Jakobsen, Poul Erik

AU - Brock, Birgitte

PY - 2019

Y1 - 2019

N2 - Aims: Type 1 diabetes can be complicated with neuropathy that involves immune-mediated and inflammatory pathways. Glucagon-like peptide-1 receptor agonists such as liraglutide, have shown anti-inflammatory properties, and thus we hypothesized that long-term treatment with liraglutide induced diminished inflammation and thus improved neuronal function. Methods: The study was a randomized, double-blinded, placebo-controlled trial of adults with type 1 diabetes and confirmed symmetrical polyneuropathy. They were randomly assigned (1:1) to receive either liraglutide or placebo. Titration was 6 weeks to 1.2–1.8 mg/d, continuing for 26 weeks. The primary endpoint was change in latency of early brain evoked potentials. Secondary endpoints were changes in proinflammatory cytokines, cortical evoked potential, autonomic function and peripheral neurophysiological testing. Results: Thirty-nine patients completed the study, of whom 19 received liraglutide. In comparison to placebo, liraglutide reduced interleukin-6 (−22.6%; 95% confidence interval [CI]: −38.1, −3.2; P =.025) with concomitant numerical reductions in other proinflammatory cytokines. However neuronal function was unaltered at the central, autonomic or peripheral level. Treatment was associated with −3.38 kg (95% CI: −5.29, −1.48; P <.001] weight loss and a decrease in urine albumin/creatinine ratio (−40.2%; 95% CI: −60.6, −9.5; P =.02). Conclusion: Hitherto, diabetic neuropathy has no cure. Speculations can be raised whether mechanism targeted treatment, e.g. lowering the systemic level of proinflammatory cytokines may lead to prevention or treatment of the neuroinflammatory component in early stages of diabetic neuropathy. If ever successful, this would serve as an example of how fundamental mechanistic principles are translated into clinical practice similar to those applied in the cardiovascular and nephrological clinic.

AB - Aims: Type 1 diabetes can be complicated with neuropathy that involves immune-mediated and inflammatory pathways. Glucagon-like peptide-1 receptor agonists such as liraglutide, have shown anti-inflammatory properties, and thus we hypothesized that long-term treatment with liraglutide induced diminished inflammation and thus improved neuronal function. Methods: The study was a randomized, double-blinded, placebo-controlled trial of adults with type 1 diabetes and confirmed symmetrical polyneuropathy. They were randomly assigned (1:1) to receive either liraglutide or placebo. Titration was 6 weeks to 1.2–1.8 mg/d, continuing for 26 weeks. The primary endpoint was change in latency of early brain evoked potentials. Secondary endpoints were changes in proinflammatory cytokines, cortical evoked potential, autonomic function and peripheral neurophysiological testing. Results: Thirty-nine patients completed the study, of whom 19 received liraglutide. In comparison to placebo, liraglutide reduced interleukin-6 (−22.6%; 95% confidence interval [CI]: −38.1, −3.2; P =.025) with concomitant numerical reductions in other proinflammatory cytokines. However neuronal function was unaltered at the central, autonomic or peripheral level. Treatment was associated with −3.38 kg (95% CI: −5.29, −1.48; P <.001] weight loss and a decrease in urine albumin/creatinine ratio (−40.2%; 95% CI: −60.6, −9.5; P =.02). Conclusion: Hitherto, diabetic neuropathy has no cure. Speculations can be raised whether mechanism targeted treatment, e.g. lowering the systemic level of proinflammatory cytokines may lead to prevention or treatment of the neuroinflammatory component in early stages of diabetic neuropathy. If ever successful, this would serve as an example of how fundamental mechanistic principles are translated into clinical practice similar to those applied in the cardiovascular and nephrological clinic.

KW - anti-inflammation

KW - diabetic neuropathy

KW - glucagon-like peptide-1 agonist

KW - interleukin-6

KW - liraglutide

U2 - 10.1111/bcp.14063

DO - 10.1111/bcp.14063

M3 - Journal article

C2 - 31338868

AN - SCOPUS:85074744988

VL - 85

SP - 2512

EP - 2523

JO - British Journal of Clinical Pharmacology

JF - British Journal of Clinical Pharmacology

SN - 0306-5251

IS - 11

ER -

ID: 238962980