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11β-hydroxysteroid dehydrogenase type 1 inhibitor attenuates high-fat diet induced cardiomyopathy

Min Huang1, Juan Liu1, Yunlu Sheng1

  • 1Department of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing 210029, People's Republic of China.

Journal of Molecular and Cellular Cardiology
|October 7, 2018
PubMed

Insights

High-fat diets cause cardiac hypertrophy by increasing 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Inhibiting 11β-HSD1 can prevent this cardiac remodeling and dysfunction.

Area of Science:

  • Cardiovascular biology
  • Endocrinology
  • Molecular medicine

Background:

  • High-fat diet (HFD) is known to induce cardiac hypertrophy.
  • The precise cellular and molecular mechanisms driving HFD-induced cardiac dysfunction remain unclear.
  • 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which amplifies local glucocorticoid activity, was investigated for its role.

Purpose of the Study:

  • To investigate the role of 11β-HSD1 in the pathogenesis of cardiac dysfunction induced by a high-fat diet.
  • To explore the potential of targeting 11β-HSD1 as a therapeutic strategy for HFD-induced cardiac hypertrophy.

Main Methods:

  • Male Wistar rats were fed either a normal chow diet (NC) or HFD.
  • Cardiac remodeling and function were assessed using echocardiography and histology.
  • Primary neonatal rat ventricular cardiomyocytes (NRCMs) were treated with palmitic acid (PA) or lentivirus to study 11β-HSD1's role in hypertrophy.
  • Genome microarray analysis was performed on NRCMs to elucidate underlying mechanisms.

Main Results:

  • Palmitic acid induced NRCM hypertrophy, upregulating 11β-HSD1 expression and leading to increased cell size and cardiac hypertrophy gene expression.
  • Inhibition of 11β-HSD1 (using BVT.2733) or deficiency of 11β-HSD1 significantly reduced cardiomyocyte size.
  • Glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) antagonists (RU486 and spironolactone) attenuated 11β-HSD1-induced cardiomyocyte hypertrophy.
  • Genome microarray identified cAMP and calcium signaling pathways as downstream effectors of 11β-HSD1 in cardiomyocyte hypertrophy.
  • In HFD-fed rats, BVT.2733 treatment attenuated cardiac hypertrophy and improved cardiac function.

Conclusions:

  • 11β-HSD1 plays a crucial role in regulating cardiac remodeling through both GR and MR pathways.
  • Pharmacological inhibition of 11β-HSD1 presents a potential therapeutic approach for preventing high-fat diet-induced cardiac hypertrophy.
Abstract

Keywords:
11β-HSD1Cardiac hypertrophyGlucocorticoid receptorMineralocorticoid receptorPalmitic acid

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