TY - JOUR
T1 - Obesity-induced oxidative stress, accelerated functional decline with age and increased mortality in mice
AU - Zhang, Yiqiang
AU - Fischer, Kathleen E.
AU - Soto, Vanessa
AU - Liu, Yuhong
AU - Sosnowska, Danuta
AU - Richardson, Arlan
AU - Salmon, Adam B.
N1 - Funding Information:
Animal studies were performed in the Healthspan and Functional Assessment Core of the San Antonio Nathan Shock Center of Excellence in the Basic Biology of Aging. This research was supported in part by funding from the American Federation for Aging Research (Y.Z. and A.B.S.), the Biomedical Laboratory Research & Development Service of the Veteran’s Affairs Office of Research and Development ( 1I01BX000547 to A.R.) and Geriatric Research Education and Clinical Center of the South Texas Veterans Healthcare System (A.B.S.).
PY - 2015/6/2
Y1 - 2015/6/2
N2 - Abstract Obesity is a serious chronic disease that increases the risk of numerous co-morbidities including metabolic syndrome, cardiovascular disease and cancer as well as increases risk of mortality, leading some to suggest this condition represents accelerated aging. Obesity is associated with significant increases in oxidative stress in vivo and, despite the well-explored relationship between oxidative stress and aging, the role this plays in the increased mortality of obese subjects remains an unanswered question. Here, we addressed this by undertaking a comprehensive, longitudinal study of a group of high fat-fed obese mice and assessed both their changes in oxidative stress and in their performance in physiological assays known to decline with aging. In female C57BL/6J mice fed a high-fat diet starting in adulthood, mortality was significantly increased as was oxidative damage in vivo. High fat-feeding significantly accelerated the decline in performance in several assays, including activity, gait, and rotarod. However, we also found that obesity had little effect on other markers of function and actually improved performance in grip strength, a marker of muscular function. Together, this first comprehensive assessment of longitudinal, functional changes in high fat-fed mice suggests that obesity may induce segmental acceleration of some of the aging process.
AB - Abstract Obesity is a serious chronic disease that increases the risk of numerous co-morbidities including metabolic syndrome, cardiovascular disease and cancer as well as increases risk of mortality, leading some to suggest this condition represents accelerated aging. Obesity is associated with significant increases in oxidative stress in vivo and, despite the well-explored relationship between oxidative stress and aging, the role this plays in the increased mortality of obese subjects remains an unanswered question. Here, we addressed this by undertaking a comprehensive, longitudinal study of a group of high fat-fed obese mice and assessed both their changes in oxidative stress and in their performance in physiological assays known to decline with aging. In female C57BL/6J mice fed a high-fat diet starting in adulthood, mortality was significantly increased as was oxidative damage in vivo. High fat-feeding significantly accelerated the decline in performance in several assays, including activity, gait, and rotarod. However, we also found that obesity had little effect on other markers of function and actually improved performance in grip strength, a marker of muscular function. Together, this first comprehensive assessment of longitudinal, functional changes in high fat-fed mice suggests that obesity may induce segmental acceleration of some of the aging process.
KW - Gait
KW - Grip strength
KW - Longevity
KW - Obesity
KW - Oxidation
KW - Respirometry
KW - Rotarod
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U2 - 10.1016/j.abb.2014.12.018
DO - 10.1016/j.abb.2014.12.018
M3 - Article
C2 - 25558793
AN - SCOPUS:84930542885
VL - 576
SP - 39
EP - 48
JO - Archives of Biochemistry and Biophysics
JF - Archives of Biochemistry and Biophysics
SN - 0003-9861
M1 - 6857
ER -