Glycolipids are membrane lipids which act as cellular markers and also provide energy for the cells. The present study is an attempt to understand whether glycolipids can act as energy sources during fasting. To achieve this, we selected and subjected Anabas testudineus to short-term (15 days) and long-term (60 days) laboratory starvation. We estimated glycolipids biochemically using a standard protocol in six different tissues. Results showed a selective decline in glycolipid concentration in certain tissues, and also an increase was observed in some tissues. Short-term fasting led to a decline in glycolipids in tissues such as brain ( ), accessory respiratory organ ( ), pectoral and lateral line muscle. Liver and kidney ( ) reported an increase. Long term starvation also resulted in a decline in tissues such as liver ( ), kidney ( ), brain, and accessory respiratory organ. Muscle tissue, that is, both the pectoral ( ) and lateral line muscle ( ), showed an increase in the glycolipid fraction. This selective decline in glycolipid content of certain tissues suggests a possible utilization of these lipids during starvation and the significant upsurge observed in certain tissues suggests a simultaneous synthesis occurring along the degradation, probably reducing the oxidative stress created by ROS (reactive oxygen species). 1. Introduction Fish, during their life time, are capable of withstanding prolonged periods of natural starvation caused due to migration, reproduction and also during fish farming [1–3]. There are several instances where certain fish species have been reported to survive without food for several months or even for years as reported in case of silver eels which go without food for even four years [4, 5]. When the animal is in a state of food deprivation there are lines of evidence wherein the animal differentially utilizes proteins, carbohydrates, and lipids. Utilization of energy fuels is not uniform in all fish but is species dependent. In fish like Acipenser oxyrinchus and Oncorhynchus mykiss, parallel to glycogen mobilization, lipids are utilized initially and proteins are utilized as the last reserve [6]. In certain other fish species, liver glycogen stores are preserved and either protein is degraded via gluconeogenesis, or protein and lipid may be mobilized as energy substrates [6–8]. Apart from these regular energy substrates, other energy molecules such as glycolipids, which are membrane lipids which have glucose and galactose attached to the lipid unit [9], may also be considered as potential sources of energy by the starving
References
[1]
S. G. Hinch, S. J. Cooke, M. C. Healey, and A. P. Farrel, “Behavioural physiology of fish migrations: salmon as a model approach,” Fish Physiology, vol. 24, pp. 239–295, 2005.
[2]
K. M. Miller, A. D. Schulze, N. Ginther et al., “Salmon spawning migration: metabolic shifts and environmental triggers,” Comparative Biochemistry and Physiology D: Genomics and Proteomics, vol. 4, no. 2, pp. 75–89, 2009.
[3]
M. Furné, A. E. Morales, C. E. Trenzado et al., “The metabolic effects of prolonged starvation and refeeding in sturgeon and rainbow trout,” Journal of Comparative Physiology B, vol. 182, no. 1, pp. 63–76, 2012.
[4]
S. Abraham, H. J. M. Hansen, and F. N. Hansen, “The effect of prolonged fasting on total lipid synthesis and enzyme activities in the liver of the European eel (Anguilla anguilla),” Comparative Biochemistry and Physiology B, vol. 79, no. 2, pp. 285–289, 1984.
[5]
R. M. Love, The Chemical Biology of Fishes, Academic Press, London, UK, 1970.
[6]
I. Navarro and J. Gutierrez, “Fasting and starvation,” in Biochemistry and Molecular Biology of Fishes, Metabolic Biochemistry, P. W. Hochachka and T. P. Mommsen, Eds., vol. 4, pp. 393–434, Elsevier, Amsterdam, The Netherlands, 1995.
[7]
M. A. Sheridan and T. P. Mommsen, “Effects of nutritional state on in vivo lipid and carbohydrate metabolism of coho salmon, Oncorhynchus kisutch,” General and Comparative Endocrinology, vol. 81, no. 3, pp. 473–483, 1991.
[8]
T. E. Gillis and J. S. Ballantyne, “The effects of starvation on plasma free amino acid and glucose concentrations in lake sturgeon,” Journal of Fish Biology, vol. 49, no. 6, pp. 1306–1316, 1996.
[9]
http://www.nutriology.com/GLmetab.html.
[10]
T. A. Scherer, I. T. Lauredo, and W. M. Abraham, “Scavenging of reactive oxygen species by a glycolipid fraction of Mycobacterium avium serovar 2,” Free Radical Biology and Medicine, vol. 22, no. 3, pp. 561–565, 1997.
[11]
N. K. Raghuramulu, M. Nair, and Sundram,S. K., A Manual of Laboratory Techniques by National Institute of Nutrition, Indian Council of Medical Research, Andhra Pradesh, India, 1983.
[12]
J. N. Kanfer and S.-I. Hakomori, Hand Book of Lipid Research. Sphingo Lipid Biochemistry, vol. 3, Plenum Press, London, UK, 1983.
[13]
R. S. Batty and C. S. Wardle, “Restoration of glycogen from lactic acid in anaerobic swimming muscle of plaice, Plemonectes platessa L.,” Journal of Fish Biology, vol. 15, no. 5, pp. 509–519, 1979.
[14]
R. Scherz-Shouval, E. Shvets, E. Fass, H. Shorer, L. Gil, and Z. Elazar, “Reactive oxygen species are essential for autophagy and specifically regulate the activity of Atg4,” The European Molecular Biology Organization Journal, vol. 26, no. 7, pp. 1749–1760, 2007.
[15]
T. Yabu, S. Imamura, N. Mizusawa, K. Touhata, and M. Yamashita, “Induction of autophagy by amino acid starvation in fish cells,” Marine Biotechnology, vol. 14, no. 4, pp. 491–501, 2012.
