Aging skeletal muscle mitochondria in the rat: decreased uncoupling protein-3 content
Departments of 1 Nutrition, 2 Pharmacology and Medicine, Case Western Reserve University, and 3 Veterans Affairs Medical Research Center, Geriatric Research, Education and Clinical Center, Cleveland, Ohio 44106 The goal of the present study was to discern the cellular mechanism(s) that contribute...
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| Veröffentlicht in: | American journal of physiology: endocrinology and metabolism 2001-11, Vol.281 (5), p.E1054-E1062 |
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| container_title | American journal of physiology: endocrinology and metabolism |
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| creator | Kerner, Janos Turkaly, Peter J Minkler, Paul E Hoppel, Charles L |
| description | Departments of 1 Nutrition, 2 Pharmacology and
Medicine, Case Western Reserve University, and 3 Veterans
Affairs Medical Research Center, Geriatric Research, Education and
Clinical Center, Cleveland, Ohio 44106
The goal of the present study was to discern
the cellular mechanism(s) that contributes to the age-associated
decrease in skeletal muscle aerobic capacity. Skeletal muscle
mitochondrial content, a parameter of oxidative capacity, was
significantly lower (25 and 20% calculated on the basis of citrate
synthase and succinate dehydrogenase activities, respectively) in
24-mo-old Fischer 344 rats compared with 6-mo-old adult rats.
Mitochondria isolated from skeletal muscle of both age groups had
identical state 3 (ADP-stimulated) and ADP-stimulated maximal
respiratory rates and phosphorylation potential (ADP-to-O ratios) with
both nonlipid and lipid substrates. In contrast, mitochondria from 24-mo-old rats displayed significantly lower state 4 (ADP-limited) respiratory rates and, consequently, higher respiratory control ratios.
Consistent with the tighter coupling, there was a 68% reduction in
uncoupling protein-3 (UCP-3) abundance in mitochondria from elderly
compared with adult rats. Congruent with the respiratory studies, there
was no age-associated decrease in carnitine palmitoyltransferase I and
carnitine palmitoyltransferase II activities in isolated skeletal
muscle mitochondria. However, there was a small, significant decrease
in tissue total carnitine content. It is concluded that the in vivo
observed decrease in skeletal muscle aerobic capacity with advanced age
is a consequence of the decreased mitochondrial density. On the basis
of the dramatic reduction of UCP-3 content associated with decreased
state 4 respiration of skeletal muscle mitochondria from elderly rats,
we propose that an increased free radical production might contribute
to the metabolic compromise in aging.
aging; fuel utilization; carnitine palmitoyltransferase; carnitine |
| doi_str_mv | 10.1152/ajpendo.2001.281.5.e1054 |
| format | Article |
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Medicine, Case Western Reserve University, and 3 Veterans
Affairs Medical Research Center, Geriatric Research, Education and
Clinical Center, Cleveland, Ohio 44106
The goal of the present study was to discern
the cellular mechanism(s) that contributes to the age-associated
decrease in skeletal muscle aerobic capacity. Skeletal muscle
mitochondrial content, a parameter of oxidative capacity, was
significantly lower (25 and 20% calculated on the basis of citrate
synthase and succinate dehydrogenase activities, respectively) in
24-mo-old Fischer 344 rats compared with 6-mo-old adult rats.
Mitochondria isolated from skeletal muscle of both age groups had
identical state 3 (ADP-stimulated) and ADP-stimulated maximal
respiratory rates and phosphorylation potential (ADP-to-O ratios) with
both nonlipid and lipid substrates. In contrast, mitochondria from 24-mo-old rats displayed significantly lower state 4 (ADP-limited) respiratory rates and, consequently, higher respiratory control ratios.
Consistent with the tighter coupling, there was a 68% reduction in
uncoupling protein-3 (UCP-3) abundance in mitochondria from elderly
compared with adult rats. Congruent with the respiratory studies, there
was no age-associated decrease in carnitine palmitoyltransferase I and
carnitine palmitoyltransferase II activities in isolated skeletal
muscle mitochondria. However, there was a small, significant decrease
in tissue total carnitine content. It is concluded that the in vivo
observed decrease in skeletal muscle aerobic capacity with advanced age
is a consequence of the decreased mitochondrial density. On the basis
of the dramatic reduction of UCP-3 content associated with decreased
state 4 respiration of skeletal muscle mitochondria from elderly rats,
we propose that an increased free radical production might contribute
to the metabolic compromise in aging.
aging; fuel utilization; carnitine palmitoyltransferase; carnitine</description><identifier>ISSN: 0193-1849</identifier><identifier>EISSN: 1522-1555</identifier><identifier>DOI: 10.1152/ajpendo.2001.281.5.e1054</identifier><identifier>PMID: 11595663</identifier><language>eng</language><publisher>United States</publisher><subject>Adenosine Diphosphate - pharmacology ; Aging ; Animals ; Carnitine O-Palmitoyltransferase - metabolism ; Carrier Proteins - metabolism ; Citrate (si)-Synthase - metabolism ; Ion Channels ; Kinetics ; Male ; Mitochondria, Muscle - enzymology ; Mitochondria, Muscle - metabolism ; Mitochondrial Proteins ; Muscle, Skeletal - ultrastructure ; Oxidation-Reduction ; Oxidative Phosphorylation ; Oxygen Consumption ; Phosphorylation ; Rats ; Rats, Inbred F344 ; Space life sciences ; Succinate Dehydrogenase - metabolism ; Uncoupling Protein 3</subject><ispartof>American journal of physiology: endocrinology and metabolism, 2001-11, Vol.281 (5), p.E1054-E1062</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c467t-fe06f8a47caf0ab83079c71ac8e41f14f3be3b826b50d892d5313fbe1212d4753</citedby><cites>FETCH-LOGICAL-c467t-fe06f8a47caf0ab83079c71ac8e41f14f3be3b826b50d892d5313fbe1212d4753</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,3026,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11595663$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kerner, Janos</creatorcontrib><creatorcontrib>Turkaly, Peter J</creatorcontrib><creatorcontrib>Minkler, Paul E</creatorcontrib><creatorcontrib>Hoppel, Charles L</creatorcontrib><title>Aging skeletal muscle mitochondria in the rat: decreased uncoupling protein-3 content</title><title>American journal of physiology: endocrinology and metabolism</title><addtitle>Am J Physiol Endocrinol Metab</addtitle><description>Departments of 1 Nutrition, 2 Pharmacology and
Medicine, Case Western Reserve University, and 3 Veterans
Affairs Medical Research Center, Geriatric Research, Education and
Clinical Center, Cleveland, Ohio 44106
The goal of the present study was to discern
the cellular mechanism(s) that contributes to the age-associated
decrease in skeletal muscle aerobic capacity. Skeletal muscle
mitochondrial content, a parameter of oxidative capacity, was
significantly lower (25 and 20% calculated on the basis of citrate
synthase and succinate dehydrogenase activities, respectively) in
24-mo-old Fischer 344 rats compared with 6-mo-old adult rats.
Mitochondria isolated from skeletal muscle of both age groups had
identical state 3 (ADP-stimulated) and ADP-stimulated maximal
respiratory rates and phosphorylation potential (ADP-to-O ratios) with
both nonlipid and lipid substrates. In contrast, mitochondria from 24-mo-old rats displayed significantly lower state 4 (ADP-limited) respiratory rates and, consequently, higher respiratory control ratios.
Consistent with the tighter coupling, there was a 68% reduction in
uncoupling protein-3 (UCP-3) abundance in mitochondria from elderly
compared with adult rats. Congruent with the respiratory studies, there
was no age-associated decrease in carnitine palmitoyltransferase I and
carnitine palmitoyltransferase II activities in isolated skeletal
muscle mitochondria. However, there was a small, significant decrease
in tissue total carnitine content. It is concluded that the in vivo
observed decrease in skeletal muscle aerobic capacity with advanced age
is a consequence of the decreased mitochondrial density. On the basis
of the dramatic reduction of UCP-3 content associated with decreased
state 4 respiration of skeletal muscle mitochondria from elderly rats,
we propose that an increased free radical production might contribute
to the metabolic compromise in aging.
aging; fuel utilization; carnitine palmitoyltransferase; carnitine</description><subject>Adenosine Diphosphate - pharmacology</subject><subject>Aging</subject><subject>Animals</subject><subject>Carnitine O-Palmitoyltransferase - metabolism</subject><subject>Carrier Proteins - metabolism</subject><subject>Citrate (si)-Synthase - metabolism</subject><subject>Ion Channels</subject><subject>Kinetics</subject><subject>Male</subject><subject>Mitochondria, Muscle - enzymology</subject><subject>Mitochondria, Muscle - metabolism</subject><subject>Mitochondrial Proteins</subject><subject>Muscle, Skeletal - ultrastructure</subject><subject>Oxidation-Reduction</subject><subject>Oxidative Phosphorylation</subject><subject>Oxygen Consumption</subject><subject>Phosphorylation</subject><subject>Rats</subject><subject>Rats, Inbred F344</subject><subject>Space life sciences</subject><subject>Succinate Dehydrogenase - metabolism</subject><subject>Uncoupling Protein 3</subject><issn>0193-1849</issn><issn>1522-1555</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE9vFCEchonR2LX6FQwnbzMCM8yf3pqmVZMmXtozYeDHDpWBEZjofvuy2VV78cSB93l5eRDClNSUcvZZPq3gdagZIbRmA615DZTw9hXalWtWUc75a7QjdGwqOrTjBXqX0hMhpOcte4suSsnIu67ZocfrvfV7nH6AgywdXrakHODF5qDm4HW0EluP8ww4ynyFNagIMoHGm1dhW92RXmPIYH3VYBV8Bp_fozdGugQfzuclery7fbj5Wt1___Lt5vq-Um3X58oA6cwg215JQ-Q0NKQfVU-lGqClhrammaCZBtZNnOhhZJo3tDETUEaZbnveXKJPp96y4OcGKYvFJgXOSQ9hS6JndCTlryU4nIIqhpQiGLFGu8h4EJSIo1JxViqOSkVRKri4PSot6MfzG9u0gP4Hnh2WwNUpMNv9_MtGEOt8SDa4sD-Iu825B_id__S_aBarNgWu_w__3fRizjOEb5r4</recordid><startdate>20011101</startdate><enddate>20011101</enddate><creator>Kerner, Janos</creator><creator>Turkaly, Peter J</creator><creator>Minkler, Paul E</creator><creator>Hoppel, Charles L</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20011101</creationdate><title>Aging skeletal muscle mitochondria in the rat: decreased uncoupling protein-3 content</title><author>Kerner, Janos ; Turkaly, Peter J ; Minkler, Paul E ; Hoppel, Charles L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c467t-fe06f8a47caf0ab83079c71ac8e41f14f3be3b826b50d892d5313fbe1212d4753</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Adenosine Diphosphate - pharmacology</topic><topic>Aging</topic><topic>Animals</topic><topic>Carnitine O-Palmitoyltransferase - metabolism</topic><topic>Carrier Proteins - metabolism</topic><topic>Citrate (si)-Synthase - metabolism</topic><topic>Ion Channels</topic><topic>Kinetics</topic><topic>Male</topic><topic>Mitochondria, Muscle - enzymology</topic><topic>Mitochondria, Muscle - metabolism</topic><topic>Mitochondrial Proteins</topic><topic>Muscle, Skeletal - ultrastructure</topic><topic>Oxidation-Reduction</topic><topic>Oxidative Phosphorylation</topic><topic>Oxygen Consumption</topic><topic>Phosphorylation</topic><topic>Rats</topic><topic>Rats, Inbred F344</topic><topic>Space life sciences</topic><topic>Succinate Dehydrogenase - metabolism</topic><topic>Uncoupling Protein 3</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kerner, Janos</creatorcontrib><creatorcontrib>Turkaly, Peter J</creatorcontrib><creatorcontrib>Minkler, Paul E</creatorcontrib><creatorcontrib>Hoppel, Charles L</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of physiology: endocrinology and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kerner, Janos</au><au>Turkaly, Peter J</au><au>Minkler, Paul E</au><au>Hoppel, Charles L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aging skeletal muscle mitochondria in the rat: decreased uncoupling protein-3 content</atitle><jtitle>American journal of physiology: endocrinology and metabolism</jtitle><addtitle>Am J Physiol Endocrinol Metab</addtitle><date>2001-11-01</date><risdate>2001</risdate><volume>281</volume><issue>5</issue><spage>E1054</spage><epage>E1062</epage><pages>E1054-E1062</pages><issn>0193-1849</issn><eissn>1522-1555</eissn><abstract>Departments of 1 Nutrition, 2 Pharmacology and
Medicine, Case Western Reserve University, and 3 Veterans
Affairs Medical Research Center, Geriatric Research, Education and
Clinical Center, Cleveland, Ohio 44106
The goal of the present study was to discern
the cellular mechanism(s) that contributes to the age-associated
decrease in skeletal muscle aerobic capacity. Skeletal muscle
mitochondrial content, a parameter of oxidative capacity, was
significantly lower (25 and 20% calculated on the basis of citrate
synthase and succinate dehydrogenase activities, respectively) in
24-mo-old Fischer 344 rats compared with 6-mo-old adult rats.
Mitochondria isolated from skeletal muscle of both age groups had
identical state 3 (ADP-stimulated) and ADP-stimulated maximal
respiratory rates and phosphorylation potential (ADP-to-O ratios) with
both nonlipid and lipid substrates. In contrast, mitochondria from 24-mo-old rats displayed significantly lower state 4 (ADP-limited) respiratory rates and, consequently, higher respiratory control ratios.
Consistent with the tighter coupling, there was a 68% reduction in
uncoupling protein-3 (UCP-3) abundance in mitochondria from elderly
compared with adult rats. Congruent with the respiratory studies, there
was no age-associated decrease in carnitine palmitoyltransferase I and
carnitine palmitoyltransferase II activities in isolated skeletal
muscle mitochondria. However, there was a small, significant decrease
in tissue total carnitine content. It is concluded that the in vivo
observed decrease in skeletal muscle aerobic capacity with advanced age
is a consequence of the decreased mitochondrial density. On the basis
of the dramatic reduction of UCP-3 content associated with decreased
state 4 respiration of skeletal muscle mitochondria from elderly rats,
we propose that an increased free radical production might contribute
to the metabolic compromise in aging.
aging; fuel utilization; carnitine palmitoyltransferase; carnitine</abstract><cop>United States</cop><pmid>11595663</pmid><doi>10.1152/ajpendo.2001.281.5.e1054</doi></addata></record> |
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| issn | 0193-1849 1522-1555 |
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| source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Adenosine Diphosphate - pharmacology Aging Animals Carnitine O-Palmitoyltransferase - metabolism Carrier Proteins - metabolism Citrate (si)-Synthase - metabolism Ion Channels Kinetics Male Mitochondria, Muscle - enzymology Mitochondria, Muscle - metabolism Mitochondrial Proteins Muscle, Skeletal - ultrastructure Oxidation-Reduction Oxidative Phosphorylation Oxygen Consumption Phosphorylation Rats Rats, Inbred F344 Space life sciences Succinate Dehydrogenase - metabolism Uncoupling Protein 3 |
| title | Aging skeletal muscle mitochondria in the rat: decreased uncoupling protein-3 content |
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