Thermal measurements support a role of the ABA/LANCL1-2 hormone/receptors system in thermogenesis.

Abstract

Abscisic acid (ABA) is a conserved 'stress hormone' in unicellular organisms, plants and animals. In mammals, ABA and its receptors LANCL1 and LANCL2 stimulate insulin-independent cell glucose uptake and oxidative metabolism: overexpression of LANCL1/2 increases, and their silencing conversely reduces, mitochondrial number, respiration and proton gradient dissipation in muscle cells and in brown adipocytes. We hypothesized that the ABA/LANCL hormone/receptors system could be involved in thermogenesis. Heat production by LANCL1/2-overexpressing versus double-silenced cells was compared in rat H9c2 cardiomyocytes with two different methods: differential temperature measurements using sensitive thermistor probes and differential isothermal calorimetry. Overexpressing cells generate an approximately double amount of thermal power compared with double-silenced cells, and addition of ABA further doubles heat production in overexpressing cells. With the temperature probes, we find a timescale of approximately 4 min for thermogenesis to 'turn on' after nutrient addition. We provide direct measurements of increased heat production triggered by the ABA/LANCL hormone receptors system. Combined with previous work on oxphos decoupling, these results support the role of the ABA/LANCL hormone receptors system as a hitherto unknown regulator of cell thermogenesis.