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J. Biol. Chem., Vol. 277, Issue 40, 37670-37677, October 4, 2002
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From the Akt is a serine-threonine kinase that mediates a
variety of cellular responses to external stimuli. During postnatal
development, Akt signaling in the heart was up-regulated when the heart
was rapidly growing and was down-regulated by caloric restriction, suggesting a role of Akt in nutrient-dependent regulation
of cardiac growth. Consistent with this notion, reductions in Akt,
70-kDa S6 kinase 1, and eukaryotic initiation factor 4E-binding protein 1 phosphorylation were observed in mice with cardiac-specific deletion
of insulin receptor gene, which exhibit a small heart phenotype. In
contrast to wild type animals, caloric restriction in these mice had
little effect on Akt phosphorylation in the heart. Furthermore, forced
expression of Akt1 in these hearts restored 70-kDa S6 kinase 1 and
eukaryotic initiation factor 4E-binding protein 1 phosphorylation to
normal levels and rescued the small heart phenotype. Collectively,
these results indicate that Akt signaling mediates
insulin-dependent physiological heart growth during
postnatal development and suggest a mechanism by which heart size is
coordinated with overall body size as the nutritional status of the
organism is varied.
Akt Signaling Mediates Postnatal Heart Growth in Response to
Insulin and Nutritional Status*
§¶,
,,, and§¶¶
Molecular Cardiology/Whitaker
Cardiovascular Institute, Boston University School of Medicine,
Boston, Massachusetts 02118, § Division of Cardiovascular
Research, St. Elizabeth's Medical Center, Boston, Massachusetts 02135, Program in Human Molecular Biology and Genetics, University of
Utah School of Medicine, Salt Lake City, Utah 84112, ** Program in Cardiovascular Gene Therapy, Cardiovascular
Research Center, Massachusetts General Hospital-East, Charlestown,
Massachusetts 02129, and §§ Research Division,
Joslin Diabetes Center and Department of Medicine, Harvard Medical
School, Boston, Massachusetts 02215
*
This work was supported by National Institutes of Health
Grants HL66957, HL50692, AR40197, AG15052, and AG17241 (to K. W.), HL62886 and DK58073 (to E. D. A.), and HL59521 and HL61557 (to A. R.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Established investigator of the American Heart Association.
¶¶
To whom correspondence should be addressed: Molecular
Cardiology/CVI, Boston University School of Medicine, 715 Albany St., Boston, MA 02118. Tel.: 617-414-2392; Fax: 617-414-2391; E-mail: kxwalsh@bu.edu.
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