The obesity‐linked human lncRNA AATBC stimulates mitochondrial function in adipocytes

EMBO Reports · 24 authors, 16 centres

AI SUMMARY

FIDELITY 100%

This summary was generated by AI from a single paper. It has not been reviewed by a clinician and is not clinical advice. Verify against the source before acting on it.

AGENT 01 · STRUCTURED SUMMARY

TRACE TO SOURCE

“

TL;DR

This preclinical study used human adipocyte cell lines and mouse models to show that the long non-coding RNA AATBC, which is linked to obesity, enhances mitochondrial function and browning markers in adipocytes. AATBC expression was inversely correlated with obesity parameters in human adipose tissue cohorts.

Full summary

642 CHARS

This preclinical investigation explored the role of the human long non-coding RNA (lncRNA) AATBC in adipocyte function using hMADS cells, primary human adipocytes, and mouse models. The study found that AATBC stimulates mitochondrial fission, oxygen consumption, and the expression of browning markers in human adipocytes. In a mouse model where AATBC is naturally absent, viral expression of AATBC altered systemic parameters, including plasma triglyceride and leptin levels. Human adipose tissue analysis from three cohorts showed AATBC expression is correlated with a thermogenic phenotype and inversely correlated with obesity parameters.

STUDY TYPE

other

SPECIALTY

preclinical research

SUMMARISED BY

AI pipeline

FIDELITY CHECK

100% · A

ORIGINAL PAPER

PMC10561178

The obesity‐linked human lncRNA AATBC stimulates mitochondrial function in adipocytes

EMBO Reports

READ THE FULL PAPER

ABSTRACT

Abstract Adipocytes are critical regulators of metabolism and energy balance. While white adipocyte dysfunction is a hallmark of obesity‐associated disorders, thermogenic adipocytes are linked to cardiometabolic health. As adipocytes dynamically adapt to environmental cues by functionally switching between white and thermogenic phenotypes, a molecular understanding of this plasticity could help improving metabolism. Here, we show that the lncRNA Apoptosis associated transcript in bladder cancer (AATBC) is a human‐specific regulator of adipocyte plasticity. Comparing transcriptional profiles of human adipose tissues and cultured adipocytes we discovered that AATBC was enriched in thermogenic conditions. Using primary and immortalized human adipocytes we found that AATBC enhanced the thermogenic phenotype, which was linked to increased respiration and a more fragmented mitochondrial network. Expression of AATBC in adipose tissue of mice led to lower plasma leptin levels. Interestingly, this association was also present in human subjects, as AATBC in adipose tissue was inversely correlated with plasma leptin levels, BMI, and other measures of metabolic health. In conclusion, AATBC is a novel obesity‐linked regulator of adipocyte plasticity and mitochondrial function in humans. Keywords: adipocyte, mitochondrial dynamics, non‐coding RNA, obesity, thermogenesis Subject Categories: Metabolism, RNA Biology

CITATION EXPORT

Maude Giroud, Stefan Kotschi, Yun Kwon et al.. The obesity‐linked human lncRNA AATBC stimulates mitochondrial function in adipocytes. EMBO Reports. (2023). https://doi.org/10.15252/embr.202357600

AUTHORS

24 · 16 CENTRES

Maude Giroud, Stefan Kotschi, Yun Kwon, Ophélia Le Thuc, Anne Hoffmann, Manuel Gil‐Lozano, Michael Karbiener, Juan Carlos Higareda‐Almaraz, Sajjad Khani, Daniel Tews, Pamela Fischer‐Posovszky, Wenfei Sun, Hua Dong, Adhideb Ghosh, Christian Wolfrum, Martin Wabitsch, Kirsi A Virtanen, Matthias Blüher, Søren Nielsen, Anja Zeigerer, Cristina García‐Cáceres, Marcel Scheideler, Stephan Herzig, Alexander Bartelt

1 Institute for Diabetes and Cancer, Helmholtz Center Munich, Neuherberg, Germany
2 German Center for Diabetes Research, Neuherberg, Germany
3 Joint Heidelberg‐IDC Translational Diabetes Program, Inner Medicine 1, Heidelberg University Hospital, Heidelberg, Germany
4 Institute for Cardiovascular Prevention, Faculty of Medicine, Ludwig‐Maximilians‐University, Munich, Germany
5 Institute for Diabetes and Obesity, Helmholtz Center Munich, Neuherberg, Germany
6 Helmholtz Institute for Metabolic, Obesity and Vascular Research of the Helmholtz Zentrum München at the University of Leipzig and University Hospital Leipzig, Leipzig, Germany
7 Global Pathogen Safety, Baxter AG, Vienna, Austria
8 Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics and Adolescent Medicine, Ulm University Medical Center, Ulm, Germany
9 Institute of Food, Nutrition and Health, ETH Zürich, Schwerzenbach, Switzerland
10 Turku PET Centre, Turku University Hospital, Turku, Finland
11 Medical Department III – Endocrinology, Nephrology, Rheumatology, University of Leipzig Medical Center, Leipzig, Germany
12 The Centre of Inflammation and Metabolism and the Centre for Physical Activity Research, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
13 Medizinische Klinik and Poliklinik IV, Klinikum der Universität, Ludwig‐Maximilians‐Universität München, Munich, Germany
14 Chair Molecular Metabolic Control, Technical University Munich, Munich, Germany
15 German Center for Cardiovascular Research, Partner Site Munich Heart Alliance, Ludwig‐Maximilians‐University, Munich, Germany
16 Department of Molecular Metabolism & Sabri Ülker Center, Harvard T.H. Chan School of Public Health, Boston, MA, USA