Adrenergic Regulation of Lipid Mobilization in Fishes; a Possible Role in Hypoxia Survival

Lipids are for fish the major energy source. The nutritional conditions of most species vary throughout the year considerably. Thus storage and mobilization of lipids have to be tightly controlled, yet little is known about its control. Though several hormones are known to have a lipolytic effect, short term regulation of lipolysis is known for catecholamines only. Catecholamines are usually released under stress conditions, including hypoxia. In mammals these hormones have a strong lipolytic action, causing high plasma fatty acids levels during hypoxia. In contrast to mammals, several fish species show a decrease of plasma FFA-levels during hypoxia and anoxia. However, some studies gave contrasting results when catecholamines were administrated to different fish species. The reason for this may be due to opposing effects of catecholamines on lipolysis in different tissues. From catecholamine administration experiments in cannulated carp there is evidence that norepinephrine inhibits lipolysis via β1- and β3- adrenoceptors while β2-adrenoceptors are involved in stimulation of lipolysis. Thus the opposite responses of different β-adrenoceptors may explain the conflicting in-vivo results obtained with fish. In vitro studies with adipocytes from different fish species confirm that activation of β-adrenoceptors suppresses lipolysis, while the opposite occurs in hepatocytes. Inhibiting β1- and β3- adrenoceptors in adipocytes were shown to be involved. Under hypoxia β-oxidation is inhibited, resulting in accumulation of fatty acids together with intermediates of the β-oxidation. This process may cause severe cellular damage in mammalian tissues, which ‘apparently’ does not occur in fishes. Fishes encounter (environmental) hypoxia on a regular basis, while for mammals hypoxia/anoxia is a pathological phenomenon. Hence the suppression of lipolysis in fishes under hypoxia (by β1- and β3- adrenoceptors) may be considered as a survival mechanism lost in higher vertebrates.