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Effect of short‐term dietary curcumin supplementation on mitochondrial regulatory proteins in muscle and brown adipose tissue of aged mice (1159.4)
Author(s) -
Wawrzyniak Nicholas,
Duarte Andrew,
Nguyen Linda,
Joseph AnnaMaria,
Layne Andrew,
Criswell David,
Adhihetty Peter
Publication year - 2014
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.28.1_supplement.1159.4
Subject(s) - mitochondrial biogenesis , curcumin , tfam , mitochondrion , brown adipose tissue , apoptosis , biology , mitochondrial dna , adipose tissue , endocrinology , microbiology and biotechnology , medicine , pharmacology , biochemistry , gene
Curcumin, a polyphenol found in the spice turmeric, is shown to have antioxidant and anti‐inflammatory properties in multiple tissues, but whether it alters mitochondrial biogenesis/apoptotic pathways is unknown. The aging process is associated with impaired mitochondrial function and elevated mitochondrial apoptotic susceptibility. Potential pharmacological and/or neutraceutical therapeutic interventions capable of improving mitochondrial function, like curcumin, have been postulated to delay this process. Thus, we investigated whether short‐term (21d) dietary curcumin supplementation (5% diet) altered mitochondrial biogenesis in muscle and brown adipose tissue (BAT) of aged mice (24 month; C57BL/6) compared to control diet mice (n=4‐6/group). While curcumin supplementation increased the mitochondrial content markers cytochrome c (14%) and COX Vb (26%) and enhanced the mitochondrial regulators Tfam (25%) and NRF‐1 (14%) in BAT, it suppressed and/or caused no change in these mitochondrial indices in muscle. In contrast, curcumin treatment evoked significant decreases (P<0.05) in the pro‐apoptotic BAX protein in both BAT (20%) and muscle (55%). Our data indicate short‐term curcumin treatment in aged mice causes tissue‐specific mitochondrial biogenesis adaptations in BAT and muscle while potentially suppressing mitochondrial apoptotic susceptibility in both tissues.