NDLI: Different adaptive traits to cold exposure in young senescence-accelerated mice

Please wait, while we are loading the content...

Basal and glucocorticoid induced changes of hepatic glucocorticoid receptor during aging: relation to activities of tyrosine aminotransferase and tryptophan oxygenase

Different adaptive traits to cold exposure in young senescence-accelerated mice

Increased phosphorylation and decreased level of IκBα during aging in rat liver

Could carnosine suppress zinc-mediated proteasome inhibition and neurodegeneration? Therapeutic potential of a non-toxic but non-patentable dipeptide

Ageing and the extinction of large animals

Biogerontology : Volume 6, Issue 1, January 2005

Biogerontology : Volume 5

Biogerontology : Volume 4

Biogerontology : Volume 3

Biogerontology : Volume 2

Biogerontology : Volume 1

Different adaptive traits to cold exposure in young senescence-accelerated mice

Content Provider	Springer Nature Link
Author	Yamashita, Yoshiri Chiba, Yoichi Xia, Chen Hirayoshi, Kazuri Satoh, Mamoru Saitoh, Yuko Shimada, Atsuyoshi Nakamura, Eitaro Hosokawa, Masari
Copyright Year	2005
Abstract	A reduced adaptation to cold is a prominent feature in aged mammals, including humans. The accelerated senescence-prone strain of mice (SAMP) has been studied as an animal model for several age-associated disorders and in the acceleration of senescence. Recent studies revealed that SAMP strains have dysfunctional hyperactive mitochondria and are under a higher oxidative stress status from a young age. To investigate whether young SAMP mice show impaired cold adaptation abilities, we performed cold-exposure experiments. There were no strain differences in baseline body temperature and lowest reached temperature during cold exposure. SAMP1 mice took longer times to reach their lowest temperature in comparison to SAMR1 mice. SAMR1 mice showed an elevation in temperature following cold exposure, whereas SAMP1 mice did not. Behavioral observations demonstrated that SAMP1 mice moved more actively than SAMR1 during cold exposure. However, mRNA levels of uncoupling protein 1 (UCP1), a heat generating protein, as well as plasma norepinephrine levels, were higher in SAMP1 than in SAMR1 mice. This newly found physiological phenotype in SAMP1 mice provides us with a tool to clarify the genetic mechanism which accelerates the senescence process and helps us develop medical means which will bring mankind to a healthy old age.
Starting Page	133
Ending Page	139
Page Count	7
File Format	PDF
ISSN	13895729
Journal	Biogerontology
Volume Number	6
Issue Number	2
e-ISSN	15736768
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2005-01-01
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	body temperature cold exposure senescence-accelerated mouse (SAM) spontaneous motor activity (SMA) uncoupling protein 1 (UCP1) Geriatrics/Gerontology Cell Biology Developmental Biology
Content Type	Text
Resource Type	Article
Subject	Aging Gerontology Geriatrics and Gerontology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Elevated Oxidative Stress in the Brain of Senescence-accelerated Mice at 5 Months of Age

The senescence-accelerated mouse (SAM-P8) as a model for the study of vascular functional alterations during aging

Cell death in the Purkinje cells of the cerebellum of senescence accelerated mouse (SAMP8)

Changes of brain activity in the aged SAMP mouse

Vitamin D treatment of senescence accelerated mice (SAM-P/6) induces several regulators of stromal cell plasticity

Suppression of the aging-associated decline in physical performance by a combination of resveratrol intake and habitual exercise in senescence-accelerated mice

Increase in tetrahydrobiopterin concentration with aging in the cerebral cortex of the senescence-accelerated mouse prone 10 strain caused by abnormal regulation of tetrahydrobiopterin biosynthesis

Long-term wheel running changes on sensorimotor activity and skeletal muscle in male and female mice of accelerated senescence.

Melatonin can improve insulin resistance and aging-induced pancreas alterations in senescence-accelerated prone male mice (SAMP8).

Different adaptive traits to cold exposure in young senescence-accelerated mice

Similar Documents

Elevated Oxidative Stress in the Brain of Senescence-accelerated Mice at 5 Months of Age

The senescence-accelerated mouse (SAM-P8) as a model for the study of vascular functional alterations during aging

Cell death in the Purkinje cells of the cerebellum of senescence accelerated mouse (SAMP8)

Changes of brain activity in the aged SAMP mouse

Vitamin D treatment of senescence accelerated mice (SAM-P/6) induces several regulators of stromal cell plasticity

Suppression of the aging-associated decline in physical performance by a combination of resveratrol intake and habitual exercise in senescence-accelerated mice

Increase in tetrahydrobiopterin concentration with aging in the cerebral cortex of the senescence-accelerated mouse prone 10 strain caused by abnormal regulation of tetrahydrobiopterin biosynthesis

Long-term wheel running changes on sensorimotor activity and skeletal muscle in male and female mice of accelerated senescence.

Melatonin can improve insulin resistance and aging-induced pancreas alterations in senescence-accelerated prone male mice (SAMP8).

Different adaptive traits to cold exposure in young senescence-accelerated mice