Aging results in paradoxical susceptibility of fat cell progenitors to lipotoxicity.

Aging results in paradoxical susceptibility of fat cell progenitors to lipotoxicity. Research Abstract Details 

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Aging results in paradoxical susceptibility of fat cell progenitors to lipotoxicity. Abstract Text:

Wen Guo,Tamar Pirtskhalava,Tamara Tchkonia,Weisheng Xie,Thomas Thomou,Jianrong Han,Tong Wang,Siu Wong,Andrew Cartwright,Fausto G Hegardt,Barbara E Corkey,James L Kirkland,

Aging is associated with metabolic syndrome, tissue damage by cytotoxic lipids, and altered fatty acid handling. Fat tissue dysfunction may contribute to these processes. This could result, in part, from age-related changes in preadipocytes, since they give rise to new fat cells throughout life. To test this hypothesis, preadipocytes cultured from rats of different ages were exposed to oleic acid, the most abundant fatty acyl moiety in fat tissue and the diet. At fatty acid concentrations at which preadipocytes from young animals remained viable, cells from old animals accumulated lipid in multiple small lipid droplets and died, with increased apoptotic index, caspase activity, BAX, and p53. Rather than inducing apoptosis, oleic acid promoted adipogenesis in preadipocytes from young animals, with appearance of large lipid droplets. CCAAT/enhancer-binding protein-alpha (C/EBPalpha) and peroxisome proliferator-activated receptor-gamma (PPARgamma) increased to a greater extent in cells from young than old animals after oleate exposure. Oleic acid, but not glucose, oxidation was impaired in preadipocytes and fat cells from old animals. Expression of carnitine palmitoyltransferase (CPT)-1, which catalyzes the rate-limiting step in fatty acid beta-oxidation, was not reduced in preadipocytes from old animals. At lower fatty acid levels, constitutively active CPT I expression enhanced beta-oxidation. At higher levels, CPT I was not as effective in enhancing beta-oxidation in preadipocytes from old as young animals, suggesting that mitochondrial dysfunction may contribute. Consistent with this, medium-chain acyl-CoA dehydrogenase expression was reduced in preadipocytes from old animals. Thus preadipocyte fatty acid handling changes with aging, with increased susceptibly to lipotoxicity and impaired fatty acid-induced adipogenesis and beta-oxidation.

Aging results in paradoxical susceptibility of fat cell progenitors to lipotoxicity. Publishing Authors By Initials

W Guo,T Pirtskhalava,T Tchkonia,W Xie,T Thomou,J Han,T Wang,S Wong,A Cartwright,FG Hegardt,BE Corkey,JL Kirkland,

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Aging results in paradoxical susceptibility of fat cell progenitors to lipotoxicity. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: American journal of physiology. Endocrinology and

VOLUME: 292

Page Numbers: E1041-51

Journal Abbreviation: Am. J. Physiol. Endocrinol. Me

ISSN: 0193-1849

DAY: 5

MONTH: 12

YEAR: 2006

Aging results in paradoxical susceptibility of fat cell progenitors to lipotoxicity. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901226

Aging results in paradoxical susceptibility of fat cell progenitors to lipotoxicity. Keywords Mesh Terms:

KEYWORDS: Stem Cells

MESH TERMS: physiology

Chemical & Substance for Abstract: Aging results in paradoxical susceptibility of fat cell progenitors to lipotoxicity. Information

Substance Name: Carnitine O-Palmitoyltransferase

Registry Number: EC 2.3.1.21

Grant and Affiliation Information for Aging results in paradoxical susceptibility of fat cell progenitors to lipotoxicity.

AFFILIATION: Evans Department of Medicine, Obesity Research Center, Boston University Medical Center, 88 E. Newton St., Boston, MA 02118, USA.

Country: United States

AGENCY: United States NIDDK

GRANT: DK-59261

ACRONYM: DK

MEDLINETA: Am J Physiol Endocrinol Metab

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