Further evidence supporting a potential role for ADH1B in obesity

Authors

Liza D. Morales, The University of Texas Rio Grande Valley
Douglas T. Cromack
Devjit Tripathy
Marcel Fourcaudot
Satish Kumar, The University of Texas Rio Grande Valley
Joanne E. Curran, The University of Texas Rio Grande ValleyFollow
Melanie A. Carless
Harald H. H. Goring, The University of Texas Rio Grande Valley
Shirley L. Hu, University of Texas Health at Houston
Juan C. Lopez-Alvarenga, The University of Texas Rio Grande ValleyFollow
Päivi Pajukanta
Kerrin S. Small
Rector Arya, The University of Texas Rio Grande Valley
Srinivas Mummidi, The University of Texas Rio Grande Valley
John Blangero, The University of Texas Rio Grande Valley
Ravindranath Duggirala, The University of Texas Rio Grande Valley
Christopher P. Jenkinson, The University of Texas Rio Grande Valley

Document Type

Article

Publication Date

1-21-2021

Abstract

Insulin is an essential hormone that regulates glucose homeostasis and metabolism. Insulin resistance (IR) arises when tissues fail to respond to insulin, and it leads to serious health problems including Type 2 Diabetes (T2D). Obesity is a major contributor to the development of IR and T2D. We previously showed that gene expression of alcohol dehydrogenase 1B (ADH1B) was inversely correlated with obesity and IR in subcutaneous adipose tissue of Mexican Americans. In the current study, a meta-analysis of the relationship between ADH1B expression and BMI in Mexican Americans, African Americans, Europeans, and Pima Indians verified that BMI was increased with decreased ADH1B expression. Using established human subcutaneous pre-adipocyte cell lines derived from lean (BMI < 30 kg m-2) or obese (BMI ≥ 30 kg m-2) donors, we found that ADH1B protein expression increased substantially during differentiation, and overexpression of ADH1B inhibited fatty acid binding protein expression. Mature adipocytes from lean donors expressed ADH1B at higher levels than obese donors. Insulin further induced ADH1B protein expression as well as enzyme activity. Knockdown of ADH1B expression decreased insulin-stimulated glucose uptake. Our findings suggest that ADH1B is involved in the proper development and metabolic activity of adipose tissues and this function is suppressed by obesity.

Comments

© The Author(s) 2021

Recommended Citation

Morales, L. D., Cromack, D. T., Tripathy, D., Fourcaudot, M., Kumar, S., Curran, J. E., Carless, M., Göring, H., Hu, S. L., Lopez-Alvarenga, J. C., Garske, K. M., Pajukanta, P., Small, K. S., Glastonbury, C. A., Das, S. K., Langefeld, C., Hanson, R. L., Hsueh, W. C., Norton, L., Arya, R., … Jenkinson, C. P. (2021). Further evidence supporting a potential role for ADH1B in obesity. Scientific reports, 11(1), 1932. https://doi.org/10.1038/s41598-020-80563-z

Creative Commons License

This work is licensed under a Creative Commons Attribution 4.0 International License.

Publication Title

Scientific Reports

DOI

10.1038/s41598-020-80563-z

Academic Level

faculty

Mentor/PI Department

Office of Human Genetics