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Growth, metabolism, and blood pressure disturbances during aging in transgenic rats with altered brain renin-angiotensin systems
1 Hypertension and Vascular Disease Center and Physiology and Pharmacology Department, Wake Forest University School of Medicine, Winston-Salem, North Carolina 2 Charite, University Medicine Berlin, Berlin, Germany 3 Department of Physiology and Pharmacology, Ponce School of Medicine, Ponce, Puerto...
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| Published in: | Physiological genomics 2005-11, Vol.23 (3), p.311-317 |
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| container_title | Physiological genomics |
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| creator | Kasper, Sherry O Carter, Christy S Ferrario, Carlos M Ganten, Detlev Ferder, Leon F Sonntag, William E Gallagher, Patricia E Diz, Debra I |
| description | 1 Hypertension and Vascular Disease Center and Physiology and Pharmacology Department, Wake Forest University School of Medicine, Winston-Salem, North Carolina
2 Charite, University Medicine Berlin, Berlin, Germany
3 Department of Physiology and Pharmacology, Ponce School of Medicine, Ponce, Puerto Rico
Transgenic rats with targeted decreased glial expression of angiotensinogen (ASrAogen rats) did not show an increase in systolic pressure compared with Sprague-Dawley (SD) rats during aging (1569 wk of age). ASrAogen animals had lower body weights throughout the study, similar to reports for animals with systemic knockout of angiotensinogen or treated long term with renin-angiotensin system (RAS) blockers. Further characterization of indexes of growth and metabolism in ASrAogen rats compared with (mRen2)27 and SD rats, which express elevated versus normal brain and tissue angiotensin II levels, respectively, revealed that serum leptin was 100200% higher in SD and (mRen2)27 rats at 46 wk and 69 wk of age. Consistent with low serum leptin, ASrAogen rats had higher food intake (73%) compared with SD or (mRen2)27 rats. (mRen2)27 rats had higher resting insulin levels than ASrAogen rats at all ages. Insulin levels were constant during aging in ASrAogen rats, whereas an increase occurred in SD rats, leading to higher insulin levels at 46 and 69 wk of age compared with ASrAogen rats. IGF-1 was comparable among strains at all ages, but (mRen2)27 rats had longer and ASrAogen rats had shorter tail lengths versus SD rats at 15 wk of age. In conclusion, reduced expression of glial angiotensinogen blunts the age-dependent rise in insulin levels and weight gain, findings that mimic the effects of long-term systemic blockade of the RAS or systemic knockout of angiotensinogen. These data implicate glial angiotensinogen in the regulation of body metabolism as well as hormonal mechanisms regulating blood pressure.
insulin resistance; metabolic syndrome |
| doi_str_mv | 10.1152/physiolgenomics.00163.2005 |
| format | article |
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2 Charite, University Medicine Berlin, Berlin, Germany
3 Department of Physiology and Pharmacology, Ponce School of Medicine, Ponce, Puerto Rico
Transgenic rats with targeted decreased glial expression of angiotensinogen (ASrAogen rats) did not show an increase in systolic pressure compared with Sprague-Dawley (SD) rats during aging (1569 wk of age). ASrAogen animals had lower body weights throughout the study, similar to reports for animals with systemic knockout of angiotensinogen or treated long term with renin-angiotensin system (RAS) blockers. Further characterization of indexes of growth and metabolism in ASrAogen rats compared with (mRen2)27 and SD rats, which express elevated versus normal brain and tissue angiotensin II levels, respectively, revealed that serum leptin was 100200% higher in SD and (mRen2)27 rats at 46 wk and 69 wk of age. Consistent with low serum leptin, ASrAogen rats had higher food intake (73%) compared with SD or (mRen2)27 rats. (mRen2)27 rats had higher resting insulin levels than ASrAogen rats at all ages. Insulin levels were constant during aging in ASrAogen rats, whereas an increase occurred in SD rats, leading to higher insulin levels at 46 and 69 wk of age compared with ASrAogen rats. IGF-1 was comparable among strains at all ages, but (mRen2)27 rats had longer and ASrAogen rats had shorter tail lengths versus SD rats at 15 wk of age. In conclusion, reduced expression of glial angiotensinogen blunts the age-dependent rise in insulin levels and weight gain, findings that mimic the effects of long-term systemic blockade of the RAS or systemic knockout of angiotensinogen. These data implicate glial angiotensinogen in the regulation of body metabolism as well as hormonal mechanisms regulating blood pressure.
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2 Charite, University Medicine Berlin, Berlin, Germany
3 Department of Physiology and Pharmacology, Ponce School of Medicine, Ponce, Puerto Rico
Transgenic rats with targeted decreased glial expression of angiotensinogen (ASrAogen rats) did not show an increase in systolic pressure compared with Sprague-Dawley (SD) rats during aging (1569 wk of age). ASrAogen animals had lower body weights throughout the study, similar to reports for animals with systemic knockout of angiotensinogen or treated long term with renin-angiotensin system (RAS) blockers. Further characterization of indexes of growth and metabolism in ASrAogen rats compared with (mRen2)27 and SD rats, which express elevated versus normal brain and tissue angiotensin II levels, respectively, revealed that serum leptin was 100200% higher in SD and (mRen2)27 rats at 46 wk and 69 wk of age. Consistent with low serum leptin, ASrAogen rats had higher food intake (73%) compared with SD or (mRen2)27 rats. (mRen2)27 rats had higher resting insulin levels than ASrAogen rats at all ages. Insulin levels were constant during aging in ASrAogen rats, whereas an increase occurred in SD rats, leading to higher insulin levels at 46 and 69 wk of age compared with ASrAogen rats. IGF-1 was comparable among strains at all ages, but (mRen2)27 rats had longer and ASrAogen rats had shorter tail lengths versus SD rats at 15 wk of age. In conclusion, reduced expression of glial angiotensinogen blunts the age-dependent rise in insulin levels and weight gain, findings that mimic the effects of long-term systemic blockade of the RAS or systemic knockout of angiotensinogen. These data implicate glial angiotensinogen in the regulation of body metabolism as well as hormonal mechanisms regulating blood pressure.
insulin resistance; metabolic syndrome</description><subject>Aging - physiology</subject><subject>Angiotensinogen - genetics</subject><subject>Animals</subject><subject>Animals, Genetically Modified</subject><subject>Blood Pressure - physiology</subject><subject>Body Weight - physiology</subject><subject>Brain - growth & development</subject><subject>Brain - metabolism</subject><subject>Heart Rate - physiology</subject><subject>Insulin - blood</subject><subject>Leptin - blood</subject><subject>Neuroglia - physiology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Renin-Angiotensin System - genetics</subject><subject>Renin-Angiotensin System - physiology</subject><subject>Tail - anatomy & histology</subject><subject>Tail - growth & development</subject><issn>1094-8341</issn><issn>1531-2267</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNp1kEFr3DAQhU1padKkf6GIHnqKt5Zly1YvpYQkLQR6Sc5Clse2iiy5Gpnt3vLTo81uKKQUwUjMfO9peFn2kRYbSuvy8zLt0Hg7gvOz0bgpCsrZpiyK-lV2SmtG87Lkzev0LkSVt6yiJ9k7xF-Jq5q2fpudUE5ZcmpPs4eb4LdxuiAzRNV5a3C-IMr1pLPe92QJgLgGIL3BuIZOOQ1I-jUYNxI17qtxJAblMK1jNAkqItmaOBFlIwRIRkElJKSpy5UbjY_gMHVwhxFmPM_eDMoivD_eZ9n99dXd5ff89ufNj8tvt7muaBNzVg20q1hHe6b5wBgXvOIdG1hLBdRKN43ohSiFGFJPtLpjWvGaayi1UGqg7Cz7dPBdgv-9AkY5G9RgrXLgV5S8bWnDeZXALwdQB48YYJBLMLMKO0kLuc9fvshfPuUv9_kn8YfjL2s3Q_9Xegw8AewATGactibAs5sfd_8Yl0ymQ_fLf_2_6nq19g7-xJfyZ7Vc-oE9AsdJtW8</recordid><startdate>20051117</startdate><enddate>20051117</enddate><creator>Kasper, Sherry O</creator><creator>Carter, Christy S</creator><creator>Ferrario, Carlos M</creator><creator>Ganten, Detlev</creator><creator>Ferder, Leon F</creator><creator>Sonntag, William E</creator><creator>Gallagher, Patricia E</creator><creator>Diz, Debra I</creator><general>Am Physiological Soc</general><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>20051117</creationdate><title>Growth, metabolism, and blood pressure disturbances during aging in transgenic rats with altered brain renin-angiotensin systems</title><author>Kasper, Sherry O ; 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2 Charite, University Medicine Berlin, Berlin, Germany
3 Department of Physiology and Pharmacology, Ponce School of Medicine, Ponce, Puerto Rico
Transgenic rats with targeted decreased glial expression of angiotensinogen (ASrAogen rats) did not show an increase in systolic pressure compared with Sprague-Dawley (SD) rats during aging (1569 wk of age). ASrAogen animals had lower body weights throughout the study, similar to reports for animals with systemic knockout of angiotensinogen or treated long term with renin-angiotensin system (RAS) blockers. Further characterization of indexes of growth and metabolism in ASrAogen rats compared with (mRen2)27 and SD rats, which express elevated versus normal brain and tissue angiotensin II levels, respectively, revealed that serum leptin was 100200% higher in SD and (mRen2)27 rats at 46 wk and 69 wk of age. Consistent with low serum leptin, ASrAogen rats had higher food intake (73%) compared with SD or (mRen2)27 rats. (mRen2)27 rats had higher resting insulin levels than ASrAogen rats at all ages. Insulin levels were constant during aging in ASrAogen rats, whereas an increase occurred in SD rats, leading to higher insulin levels at 46 and 69 wk of age compared with ASrAogen rats. IGF-1 was comparable among strains at all ages, but (mRen2)27 rats had longer and ASrAogen rats had shorter tail lengths versus SD rats at 15 wk of age. In conclusion, reduced expression of glial angiotensinogen blunts the age-dependent rise in insulin levels and weight gain, findings that mimic the effects of long-term systemic blockade of the RAS or systemic knockout of angiotensinogen. These data implicate glial angiotensinogen in the regulation of body metabolism as well as hormonal mechanisms regulating blood pressure.
insulin resistance; metabolic syndrome</abstract><cop>United States</cop><pub>Am Physiological Soc</pub><pmid>16131528</pmid><doi>10.1152/physiolgenomics.00163.2005</doi><tpages>7</tpages></addata></record> |
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| ispartof | Physiological genomics, 2005-11, Vol.23 (3), p.311-317 |
| issn | 1094-8341 1531-2267 |
| language | eng |
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| source | American Physiological Society:Jisc Collections:American Physiological Society Journals ‘Read Publish & Join’ Agreement:2023-2024 (Reading list); American Physiological Society Free |
| subjects | Aging - physiology Angiotensinogen - genetics Animals Animals, Genetically Modified Blood Pressure - physiology Body Weight - physiology Brain - growth & development Brain - metabolism Heart Rate - physiology Insulin - blood Leptin - blood Neuroglia - physiology Rats Rats, Sprague-Dawley Renin-Angiotensin System - genetics Renin-Angiotensin System - physiology Tail - anatomy & histology Tail - growth & development |
| title | Growth, metabolism, and blood pressure disturbances during aging in transgenic rats with altered brain renin-angiotensin systems |
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