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Neuroscience. 2014 Jan 3;256:282-91. doi: 10.1016/j.neuroscience.2013.10.022. Epub 2013 Oct 23.

Sphingolipid profiles are altered in prefrontal cortex of rats under acute hyperglycemia.

Author information

1
Department of Experimental Pharmacology, Medical University of Bialystok, Szpitalna 37, 15-295 Bialystok, Poland.
2
Department of Physiology, Medical University of Bialystok, Mickiewicza 2c, 15-222 Bialystok, Poland.
3
Department of Experimental Pharmacology, Medical University of Bialystok, Szpitalna 37, 15-295 Bialystok, Poland. Electronic address: zfarmdosw@umb.edu.pl.

Abstract

Diabetes type 1 is a common autoimmune disease manifesting by insulin deficiency and hyperglycemia, which can lead to dementia-like brain dysfunctions. The factors triggering the pathological processes in hyperglycemic brain remain unknown. We reported in this study that brain areas with different susceptibility to diabetes (prefrontal cortex (PFC), hippocampus, striatum and cerebellum) revealed differential alterations in ceramide (Cer) and sphingomyelin (SM) profiles in rats with streptozotocin-induced hyperglycemia. Employing gas-liquid chromatography, we found that level of total Cer increased significantly only in the PFC of diabetic animals, which also exhibited a broad spectrum of sphingolipid (SLs) changes, such as elevations of Cer-C16:0, -C18:0, -C20:0, -C22:0, -C18:1, -C24:1 and SM-C16:0 and -C18:1. In opposite, only minor changes were noted in other examined structures. In addition, de novo synthesis pathway could play a role in generation of Cer containing monounsaturated fatty acids in PFC during hyperglycemia. In turn, simultaneous accumulation of Cers and their SM counterparts may suggest that overproduced Cers are converted to SMs to avoid excessive Cer-mediated cytotoxicity. We conclude that broad changes in SLs compositions in PFC induced by hyperglycemia may provoke membrane rearrangements in some cell populations, which can disturb cellular signaling and cause tissue damage.

KEYWORDS:

AD; Alzheimer disease; Cer; Cer synthases; CerSes; MUFA; PFC; SAFA; SL; SM; SPT; STZ; ceramide; ceramides; diabetes; monounsaturated fatty acids; myriocin; prefrontal cortex; saturated fatty acids; serine palmitoyltransferase; sphingolipid; sphingomyelin; sphingomyelins; streptozotocin

[Indexed for MEDLINE]

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