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פותח על ידי קלירמאש פתרונות בע"מ -
αMUPA mice: A transgenic model for longevity induced by caloric restriction
Year:
2005
Authors :
יהב, שלמה
;
.
Volume :
126
Co-Authors:
Miskin, R., Department of Biological Chemistry, The Weizmann Institute of Science, Rehovot 76100, Israel, Israel
Tirosh, O., Institute of Biochemistry, Food Science and Nutrition, Hebrew Univ. Jerusalem, R., Israel
Pardo, M., Institute of Biochemistry, Food Science and Nutrition, Hebrew Univ. Jerusalem, R., Israel
Zusman, I., Koret School of Veterinary Medicine, The Hebrew University of Jerusalem, Rehovot 76100, Israel, Israel
Schwartz, B., Institute of Biochemistry, Food Science and Nutrition, Hebrew Univ. Jerusalem, R., Israel
Yahav, S., Institute of Animal Science, Agricultural Research Organization, Bet Dagan, Israel, Israel
Dubnov, G., Department of Pharmaceutics, School of Pharmacy, Hebrew Univ. Jerusalem, J., Israel
Kohen, R., Department of Pharmaceutics, School of Pharmacy, Hebrew Univ. Jerusalem, J., Israel
Facilitators :
From page:
255
To page:
261
(
Total pages:
7
)
Abstract:
Caloric restriction (CR) is currently the only therapeutic intervention known to attenuate aging in mammals, but the underlying mechanisms of this phenomenon are still poorly understood. To get more insight into these mechanisms, we took advantage of the αMUPA transgenic mice that previously were reported to spontaneously eat less and live longer compared with their wild-type control mice. Currently, two transgenic lines that eat less are available, thus implicating the transgenic enzyme, i.e. the urokinase-type plasminogen activator (uPA), in causing the reduced appetite. This phenotypic change could have resulted from the ectopic transgenic expression that we detected in the adult αMUPA brain, or alternatively, from a transgenic interference in brain development. Here, we have summarized similarities and differences so far found between αMUPA and calorically restricted mice. Recently, we noted several changes in the αMUPA liver, at the mitochondrial and cellular level, which consistently pointed to an enhanced capacity to induce apoptosis. In addition, αMUPA mice showed a reduced level of serum IGF-1 and a reduced incidence of spontaneously occurring or carcinogen-induced tumors in several tissues. In contrast, αMUPA did not differ from wild type mice in the levels of low molecular weight antioxidants when compared in several tissues at a young or an old age. Overall, the αMUPA model suggests that fine-tuning of the threshold for apoptosis, possibly linked in part to modulation of serum IGF-1 and mitochondrial functions, could play a role in the attenuation of aging in calorically restricted mice. © 2004 Elsevier Ireland Ltd. All rights reserved.
Note:
Related Files :
Animal
Animals
antioxidants
apoptosis
Female
Genetics
metabolism
mice
obesity
phenotype
עוד תגיות
תוכן קשור
More details
DOI :
10.1016/j.mad.2004.08.018
Article number:
Affiliations:
Database:
סקופוס
Publication Type:
מאמר מתוך כינוס
;
.
Language:
אנגלית
Editors' remarks:
ID:
31958
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 01:06
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Scientific Publication
αMUPA mice: A transgenic model for longevity induced by caloric restriction
126
Miskin, R., Department of Biological Chemistry, The Weizmann Institute of Science, Rehovot 76100, Israel, Israel
Tirosh, O., Institute of Biochemistry, Food Science and Nutrition, Hebrew Univ. Jerusalem, R., Israel
Pardo, M., Institute of Biochemistry, Food Science and Nutrition, Hebrew Univ. Jerusalem, R., Israel
Zusman, I., Koret School of Veterinary Medicine, The Hebrew University of Jerusalem, Rehovot 76100, Israel, Israel
Schwartz, B., Institute of Biochemistry, Food Science and Nutrition, Hebrew Univ. Jerusalem, R., Israel
Yahav, S., Institute of Animal Science, Agricultural Research Organization, Bet Dagan, Israel, Israel
Dubnov, G., Department of Pharmaceutics, School of Pharmacy, Hebrew Univ. Jerusalem, J., Israel
Kohen, R., Department of Pharmaceutics, School of Pharmacy, Hebrew Univ. Jerusalem, J., Israel
αMUPA mice: A transgenic model for longevity induced by caloric restriction
Caloric restriction (CR) is currently the only therapeutic intervention known to attenuate aging in mammals, but the underlying mechanisms of this phenomenon are still poorly understood. To get more insight into these mechanisms, we took advantage of the αMUPA transgenic mice that previously were reported to spontaneously eat less and live longer compared with their wild-type control mice. Currently, two transgenic lines that eat less are available, thus implicating the transgenic enzyme, i.e. the urokinase-type plasminogen activator (uPA), in causing the reduced appetite. This phenotypic change could have resulted from the ectopic transgenic expression that we detected in the adult αMUPA brain, or alternatively, from a transgenic interference in brain development. Here, we have summarized similarities and differences so far found between αMUPA and calorically restricted mice. Recently, we noted several changes in the αMUPA liver, at the mitochondrial and cellular level, which consistently pointed to an enhanced capacity to induce apoptosis. In addition, αMUPA mice showed a reduced level of serum IGF-1 and a reduced incidence of spontaneously occurring or carcinogen-induced tumors in several tissues. In contrast, αMUPA did not differ from wild type mice in the levels of low molecular weight antioxidants when compared in several tissues at a young or an old age. Overall, the αMUPA model suggests that fine-tuning of the threshold for apoptosis, possibly linked in part to modulation of serum IGF-1 and mitochondrial functions, could play a role in the attenuation of aging in calorically restricted mice. © 2004 Elsevier Ireland Ltd. All rights reserved.
Scientific Publication
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