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Caloric Restriction Modulates Age‐related Inflammation and Lipid Accumulation through SREBP‐1 and PPARs in Skeletal Muscle
Author(s) -
Chung Hae Young,
Kim Ji Young,
Kim Dae Hyun,
Seo Arnold Young,
Leeuwenburgh Christiaan,
Yu Byung Pal
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.271
Subject(s) - endocrinology , adipose triglyceride lipase , medicine , lipolysis , skeletal muscle , lipid metabolism , adipose tissue , inflammation , triglyceride , white adipose tissue , lipid droplet , chemistry , biology , cholesterol
Evidence indicates that visceral lipid accumulation during aging may be the causal factor underlying age‐related inflammation. We present data on the age‐related changes of several key molecular factors involved in lipid metabolism: sterol regulatory element‐binding protein‐1 (SREBP‐1), peroxisome proliferators‐activated receptors (PPARs), adipose triglyceride lipase (ATGL), and parameters involved in lipid redistribution. Results indicate that the age‐related decreases in SREBP‐1 and PPARγ activities are correlated with decreased preadipocyte differentiation in white adipose tissue (WAT) of aged AL rats. In parallel, decreased WAT lipolysis was indicated by an age‐related decline of ATGL in AL adipose tissue. However, in skeletal muscle of aged AL rats, increased SREBP‐1 and triglyceride indicate lipid accumulation through decreased carnitine palmitoyltransferases‐1 activity. In addition, inflammatory factors significantly augmented in aged skeletal muscle, while CR significantly reversed these trends. We conclude that aging impacts on intra‐myocellular lipid accumulation through saturation of storage capacity of WAT leading to muscular inflammation and CR can modulate balance between storage capacity of WAT and lipid accumulation in skeletal muscle during aging. This work was supported by the Korea Science and Engineering Foundation (KOSEF) grant funded by the Korea government (MOST) (NO. 2007‐00376).