Endogenous peripheral hydrogen sulfide is propyretic: Its permissive role in brown adipose tissue thermogenesis in rats

Abstract

In recent years hydrogen sulfide (H₂S) has been reported as a gaseous modulator acting in several tissues in health and disease. In systemic inflammation animal models, plasma H₂S concentration increases in response to endotoxin (bacterial lipopolysaccharide, LPS). The most striking response in the acute phase reaction of systemic inflammation is fever, but reports of the peripheral action of H₂S on this thermoregulatory response are not found. We aimed at investigating whether endogenous systemic H₂S modulates LPS-induced fever. A temperature datalogger capsule was inserted in abdominal cavity of male Wistar rats (220–270 g) to record body core temperature. These animals received an intraperitoneal (ip) injection of a systemic H₂S inhibitor (propargylglycine; 50 or 75 mg kg⁻¹) immediately followed by an ip injection of LPS (50 or 2,500 μg kg⁻¹), and were exposed to different ambient temperatures (16, 22 or 27°C). At 22°C, but not at 27°C, propargylglycine at 75 mg kg⁻¹ significantly attenuated (P < 0.0001) LPS (50 μg kg⁻¹)-induced fever, indicating a modulatory (permissive) action of endogenous peripheral H₂S on brown adipose tissue (BAT) thermogenesis. Evidence on the modulatory role of peripheral H₂S in BAT thermogenesis was made stronger when we discarded (i) the possible influence of the gas on febrigenic signaling (when measuring plasma cytokines), and (ii) its interaction with the nitric oxide pathway, and mainly when (iii) we carried out physiological and pharmacological activations of BAT. Endogenous peripheral H₂S modulates (permits) BAT activity not only in fever but also maintaining thermal homeostasis in cold environments.

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