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Long‐Chain Glycosphingolipids Mediate Renal Aging

In the kidney, there is an age‐associated progressive deterioration in renal function even in the absence of obvious renal disease. Within the aged kidney, there are elevated levels of apoptosis, necrosis, and inflammation. These cellular processes have been shown to be mediated by sphingolipids. Thus, we hypothesized that alterations in kidney sphingolipids play a role in the declining kidney function that occurs during aging. To test this hypothesis, we measured the sphingolipid profile in young (3 mo), middle aged (9 mo) and old (17 mo) C57BL/6 male mice. Long‐chain hexosylceramides (HexCer) and lactosylceramides (LacCer) were elevated in kidneys from 17 mo. mice. The kidney is the source of the HexCer and LacCer as their levels are not elevated in the blood during aging. The increase in long‐chain LacCers is not exclusive to the kidney nor to mice, suggesting that long‐chain lactosylceramides may be biomarkers of aging. The only known intervention to extend lifespan in mammals is caloric restriction (CR), which attenuates kidney aging. Importantly, CR prevents the elevation in long‐chain renal LacCers during aging, suggesting that LacCer may mediate the aging process. Our data indicate a novel role for LacCer in renal aging and indicate that CR regulates sphingolipid metabolism in mammals. This work is supported by: the Veteran's Administration, ACS IRG, and the NIH/NCRR P20 RR17677 COBRE.