Relaxin Treatment Reverses Insulin Resistance in Mice Fed a High-Fat Diet

Bonner, Jeffrey S.; Lantier, Louise; Hocking, Kyle M.; Kang, Li; Owolabi, Mark; James, Freyja D.; Bracy, Deanna P.; Brophy, Colleen M.; Wasserman, David H.

doi:10.2337/db13-0033

Cited by 52Pregnancy-related medical researchAdipokines, Inflammation, and Metabolic DiseasesGrowth Hormone and Insulin-like Growth Factors

Relaxin Treatment Reverses Insulin Resistance in Mice Fed a High-Fat Diet

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Bonner, Jeffrey S., Lantier, Louise, Hocking, Kyle M., Kang, Li, Owolabi, Mark, James, Freyja D., Bracy, Deanna P., Brophy, Colleen M. +1 more·2013·Diabetes

DOI 10.2337/db13-0033PMC PMC3749347

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Abstract

The endogenous hormone relaxin increases vascular reactivity and angiogenesis. We demonstrate that acute relaxin infusion in lean C57BL/6J mice enhances skeletal muscle perfusion and augments muscle glucose uptake during a hyperinsulinemic-euglycemic clamp. However, an acute effect was absent in mice fed a high-fat (HF) diet for 13 weeks. In contrast, mice fed an HF diet for 13 weeks and continuously treated with relaxin for the final 3 weeks of the diet exhibited decreased fasting blood glucose. Insulin-stimulated whole-body glucose disappearance and percent suppression of hepatic glucose production are corrected by chronic relaxin. The increase in peripheral glucose utilization is a result of augmented in vivo skeletal muscle glucose uptake. Relaxin intervention improves endothelial-dependent vascular reactivity and induces a two-fold proliferation in skeletal muscle capillarity. The metabolic effects of the treatment are not attributed to changes in myocellular insulin signaling. Relaxin intervention reverses the accumulation of collagen III in the liver and collagen III and collagen IV in the heart; this is induced by HF feeding. These studies show the potential of relaxin in the treatment of diet-induced insulin resistance and vascular dysfunction. Relaxin provides a novel therapeutic approach targeting the extramyocellular barriers to insulin action, which are critical to the pathogenesis of insulin resistance.

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Vasodilators can partially prevent or reverse diet-induced insulin resistance in rodents.
“vasodilators can partially prevent159, 160 or reverse161 diet-induced insulin resistance in rodents.”
From The Vasculature in Prediabetes (2018) · cites this paper as [161]
Relaxin did not improve insulin action in isolated muscle, demonstrating the reliance on the microvascular for its insulin-sensitizing effect.
“Relaxin did not improve insulin action in isolated muscle, demonstrating the reliance on the microvascular for its insulin-sensitizing effect.”
From The Vasculature in Prediabetes (2018) · cites this paper as [161]
Relaxin administration caused endothelial relaxation and reversed insulin resistance in obese mice.
“Relaxin administration caused endothelial relaxation and reversed insulin resistance in obese mice.”
From The Vasculature in Prediabetes (2018) · cites this paper as [161]
Treatments that improve insulin action in rodent models of prediabetes normalize collagen levels and increase muscle capillaries.
“Treatments that improve insulin action in rodent models of prediabetes normalize collagen levels and increase muscle capillaries.”
From The Vasculature in Prediabetes (2018) · cites this paper as [161]

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Authors: Bonner, J. S., Lantier, L., Hocking, K. M., Kang, L., Owolabi, M., James, F. D., Bracy, D. P., Brophy, C. M., & Wasserman, D. H.
Affiliations: Vanderbilt University (US)
Corresponding author: Bonner, Jeffrey S.
ORCID: Lantier, Louise
Hocking, Kyle M.
Kang, Li
Wasserman, David H.
Venue: Diabetes
Publisher: American Diabetes Association
Published: 2013-08-15
Volume: 62
Issue: 9
Pages: 3251-3260
ISSN: 0012-1797 (ISSN-L)
1939-327X
DOI: 10.2337/db13-0033
PMC: PMC3749347
OpenAlex: W2156955670
Cited by: 52
References: 62
Citations by year: 2026: 1 · 2025: 1 · 2024: 6 · 2023: 2 · 2021: 3 · 2020: 6 · 2019: 4 · 2018: 8 · 2017: 4 · 2016: 10 · 2015: 4 · 2014: 3
FWCI: 5.79
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-nd
creativecommons.org/licenses/by-nc-nd/3.0/ (vor, 2937 d)
Locations: Diabetes (publishedVersion, cc-by-nc-nd)
Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
PubMed Central (publishedVersion, cc-by-nc-nd)
PubMed (publishedVersion)
Discovery Research Portal (University of Dundee) (publishedVersion)
Funders: National Institutes of Health (5p60dk020593-31)
National Institute of Diabetes and Digestive and Kidney Diseases (P60-DK020593, DK 20593, DK-054902, DK 059637, R01DK054902, R56DK054902, P30DK020593)
Topics: Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Pregnancy-related medical research
Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
Keywords: relaxin, insulin resistance, high-fat diet, skeletal muscle glucose uptake, hepatic glucose production, vascular reactivity, angiogenesis, muscle capillarization, endothelial dysfunction, collagen deposition, hyperinsulinemic-euglycemic clamp
MeSH terms: Animals, Blood Glucose, Glucose, Immunohistochemistry, Insulin Resistance, Male, Mice, Inbred C57BL, Relaxin, Immunoblotting, Muscle, Skeletal, Mice, Diet, High-Fat

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Relaxin Treatment Reverses Insulin Resistance in Mice Fed a High-Fat Diet

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