Exercise Attenuates CTGF Levels, Delaying the Onset of Fibrosis in the Aging Left Ventricle

Aging is associated with a progressive increase in collagen (i.e., fibrosis) in the aging heart. Fibrosis is associated with a stiffening of the heart and a decrease in heart function. Previous data (Kwak, 2008) showed that matrix metalloproteinase (MMP) activity in the aging heart is decreased linked to an elevation TIMP-1 (tissue inhibitor of MMPs-1); while exercise training increased TIMP-1 and reduced MMP expression. Connective tissue growth factor (CTGF) is an upstream inhibitor of TIMP-1 and is implicated in diabetes and heart failure. We hypothesized that exercise would decrease CTGF levels, thus reducing fibrosis in the aged left ventricle. Young (3 months) and old (31 months) male Fischer 344 × Brown Norway F1 hybrid (F344BNF1) rats were used for the study. The rats were randomly assigned to one of the following experimental groups (n=10/group): young sedentary controls (YS), young exercise trained (YE), old sedentary controls (OS), and old exercise trained (OE). Rats walked quickly on a motor-driven treadmill for 45 min/day, 5 days/wk, for 12 wks. Heart levels of CTGF were determined via Immunohistochemistry (IHC). CTGF was expressed more in the old group compared to the young group, as well as the sedentary group compared to the exercise group. Future studies will determine if CTGF is downstream of angiotensin II, TGF-beta, and oxidative stress in regulating MMPs and TIMP-1

The effects of exercise on caspase-independent mitochondrial proteins in regards to age-related apoptosis

Exercise may have protective factors in reducing oxidative stress, mitochondrial dysfunction and mitochondrial caspase-dependent apoptosis with aging. It is presently unclear whether the caspase-independent apoptosis via EndonucleaseG (EndoG) and Apoptosis Inducing Factor (AIF) translocation from the mitochondria to the nucleosome is effected by exercise in aging skeletal muscle. It is understood that in aging skeletal muscle EndoG and AIF do translocate from the mitochondria to the nucleosome. We hypothesize that exercise will attenuate the translocation of EndoG and AIF from the mitochondria to the nucleosome in aging white gastrocnemius muscle. Twenty-four Fischer Brown Norway rats were randomly assigned to four groups, young sedentary, old sedentary, young exercisers and old exercisers. The exercise consisted of treadmill training. The protein expression of EndoG and AIF were analyzed using western blot assays. In the old sedentary group, EndoG increased 86.4 % in the soluble fraction, but there was no change in the young groups. EndoG protein levels in the nucleosome fraction of young exercisers decreased 49 % when compared to young sedentary controls and old sedentary increased by 86.5 % when compared to young sedentary controls. With AIF changes in the soluble fraction were neglible. Protein levels of AIF in the nucleosome fraction increased 64 % in the old sedentary group compared to young sedentary controls. The data indicates that exercise was a protective factor against caspase-independent apoptosis by decreasing the translocation of EndoG and AIF to the nucleosome in aged skeletal muscle

New insight on the role of the oral mucosa in aroma release

International audienc

Interactions between aroma compounds and the oral mucosa could be responsible for aroma persistence

Interactions between aroma compounds and the oral mucosa could be responsible for aroma persistence. 4. international conference on food oral processing - “Food Oral Processing through life: interplay between food structure, sensory, pleasure and nutritional needs.

Role of mucosa and mucosal pellicle in aroma persistence

International audienc

Saliver pour mieux sentir ?: Actualité du CSGA publiée par Ludovic Piquemal sur l'internet du Centre INRA de Dijon

Ce mois-ci, sur le site de l’UMR, retrouvez (deux) actualité(s) : « Saliver pour mieux sentir », sur le rôle des enzymes salivaires dans les différences de perception interindividuelle : si nous ne sentons pas tous la même chose en mangeant un aliment, c’est en partie parce que nous ne salivons pas tous de la même façon ! Un article à lire ici (PDF). (...