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Investigation of the relationship between betatrophin and certain key enzymes involved in carbohydrate and lipid metabolism in insulin-resistant mice

  • Funda Bulut Arikan EMAIL logo , Mustafa Ulas , Yasemin Ustundag , Hakan Boyunaga and Nermin Dindar Badem ORCID logo
Published/Copyright: March 6, 2023

Abstract

Objectives

The present study sought to examine the relationship of betatrophin with certain key enzymes, namely lactate dehydrogenase-5 (LDH5), citrate synthase (CS), and acetyl-CoA carboxylase-1 (ACC1), in insulin-resistant mice.

Methods

Eight-week-old male C57BL6/J mice were used in this study (experimental group n=10 and control group n=10). S961 was administered using an osmotic pump to induce insulin resistance in the mice. The betatrophin, LDH5, CS, and ACC1 expression levels were determined from the livers of the mice using the real-time polymerase chain reaction (RT-PCR) method. Moreover, biochemical parameters such as the serum betatrophin, fasting glucose, insulin, triglyceride, total cholesterol, and high-density lipoprotein (HDL) and low-density lipoprotein (LDL) cholesterol levels were analyzed.

Results

The betatrophin expression and serum betatrophin (p=0.000), fasting glucose, insulin, triglyceride (p≤0.001), and total cholesterol (p=0.013) levels were increased in the experimental group. In addition, the CS gene expression level was statistically significantly decreased in the experimental group (p=0.01). Although strong correlation was found between the expression and serum betatrophin and triglyceride levels, no correlation was found between the betatrophin gene expression and the LDH5, ACC1, and CS gene expression levels.

Conclusions

The betatrophin level appears to play an important role in the regulation of triglyceride metabolism, while insulin resistance increases both the betatrophin gene expression and serum levels and decreases the CS expression level. The findings suggest that betatrophin may not regulate carbohydrate metabolism through CS and LDH5 or lipid metabolism directly through the ACC1 enzyme.


Corresponding author: Funda Bulut Arikan, Assistant Professor, Faculty of Medicine, Department of Physiology, Kırıkkale University, Kırıkkale, Türkiye, E-mail:

Funding source: This study was supported by Scientific Research Projects Coordination Unit of Kırıkkale University.

Award Identifier / Grant number: Project number: 2015/43

  1. Research funding: This study was supported by Scientific Research Projects Coordination Unit of Kırıkkale University (project number: 2015/43).

  2. Author contribution: FBA, YU, MU and HB conceived and designed study. FBA, YU and NDB perform laboratory analysis and analysed data. FBA wrote manuscript. All authors have read and approved the final manuscript. All authors have accepted responsibility for the entire content of this manuscript and approved its submission.

  3. Competing interests: All Authors state no conflict of interest.

  4. Informed consent: Not applicable.

  5. Ethical approval: All ethical permissions required for animal experiments were obtained from Bogazici University (in Turkey) of Corporate Animal Experiments Local Ethics Board prior to commencement of the study. In addition, the study was performed in accordance with the requirements of the Institutional Guide for the Care and Use of Laboratory Animals, and the ethical treatment of all the experimental animals conformed to the guidelines issued by the Institutional Animal Care and Use Committee (IACUC).

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Received: 2022-11-15
Accepted: 2023-02-08
Published Online: 2023-03-06

© 2023 Walter de Gruyter GmbH, Berlin/Boston

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