Aging, Depot Origin, and Preadipocyte Gene Expression

Abstract

Fat distribution changes with aging. Inherent changes in fat cell progenitors may contribute because fat cells turn over throughout life. To define mechanisms, gene expression was profiled in preadipocytes cultured from epididymal and perirenal depots of young and old rats. 8.4% of probe sets differed significantly between depots, particularly developmental genes. Only 0.02% differed with aging, despite using less stringent criteria than for comparing depots. Twenty-five genes selected based on fold change with aging were analyzed in preadipocytes from additional young, middle-aged, and old animals by polymerase chain reaction. Thirteen changed significantly with aging, 13 among depots, and 9 with both. Genes involved in inflammation, stress, and differentiation changed with aging, as occurs in fat tissue. Age-related changes were greater in perirenal than epididymal preadipocytes, consistent with larger declines in replication and adipogenesis in perirenal preadipocytes. Thus, age-related changes in preadipocyte gene expression differ among depots, potentially contributing to fat redistribution and dysfunction.

Biological aging alters circadian mechanisms in murine adipose tissue depots

“…Transcriptomic analyses of pre-adipocytes isolated from young (3 months) and old (30 months) rats have revealed similar outcomes (Cartwright et al 2010). …”

“…Pre-adipocytes obtained from the epididymal and retroperitoneal fat pads exhibited an 8.4% depotdependent difference in gene expression profiles; however, aging accounted for only a 0.02% difference in gene expression within each depot (Cartwright et al 2010). It is possible that the collagenase isolation and subsequent culture expansion of the pre-adipocytes from the young and old rats masked differences in their gene expression profiles.…”

JAK inhibition alleviates the cellular senescence-associated secretory phenotype and frailty in old age

“…Preadipocytes also were induced to become senescent by 27-30 serial passages, at which point cell proliferation was attenuated and more than 80% of cells exhibited SABG positivity. Preadipocytes were isolated from Brown Norway rats as previously described (66). HUVECs were purchased from ATCC.…”

Caloric restriction attenuates the age-associated increase of adipose-derived stem cells but further reduces their proliferative capacity

“…Based on this, one might suspect that the number and functioning of the stem cell population within adipose tissue might be altered in situations where fat mass changes dramatically. Supporting this prediction is the observation that aging causes substantial changes in the size and cellular composition of WAT (Cartwright et al 2010;Kirkland et al 1990Kirkland et al , 1994Kuk et al 2009). To date, the effects of aging on adipose stem/progenitor cells have only been studied in the non-specific heterogeneous SVF (Cartwright et al 2010;Kirkland et al 1990Kirkland et al , 1994 and has yet to be described in a more specific ASC population.…”

“…Supporting this prediction is the observation that aging causes substantial changes in the size and cellular composition of WAT (Cartwright et al 2010;Kirkland et al 1990Kirkland et al , 1994Kuk et al 2009). To date, the effects of aging on adipose stem/progenitor cells have only been studied in the non-specific heterogeneous SVF (Cartwright et al 2010;Kirkland et al 1990Kirkland et al , 1994 and has yet to be described in a more specific ASC population. Of additional interest is a diet that greatly reduces the amount of WAT, a diet chronically restricted in calories (caloric restriction (CR)), extends mean and maximal life span of mammals via its anti-aging effects (Anderson et al 2009;Mair and Dillin 2008;Weindruch 1996;Weindruch et al 1986).…”