{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:39:06Z","timestamp":1791297546025,"version":"4.1.0"},"reference-count":43,"publisher":"National Academy of Sciences","issue":"24","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2003,11,25]]},"abstract":"<jats:p>\n                    Peroxisome proliferator-activated receptor \u03b3 (PPAR\u03b3) is a nuclear receptor, which controls adipocyte differentiation. We targeted with homologous recombination the PPAR\u03b32-specific exon B, resulting in a white adipose tissue knockdown of PPAR\u03b3. Although homozygous (\n                    <jats:italic>PPAR<\/jats:italic>\n                    \u03b3\n                    <jats:sup>\n                      <jats:italic>hyp\/hyp<\/jats:italic>\n                    <\/jats:sup>\n                    ) mice are born with similar weight as the WT mice, the\n                    <jats:italic>PPAR<\/jats:italic>\n                    \u03b3\n                    <jats:sup>\n                      <jats:italic>hyp\/hyp<\/jats:italic>\n                    <\/jats:sup>\n                    animals become growth retarded and develop severe lipodystrophy and hyperlipidemia. Almost half of these\n                    <jats:italic>PPAR<\/jats:italic>\n                    \u03b3\n                    <jats:sup>\n                      <jats:italic>hyp\/hyp<\/jats:italic>\n                    <\/jats:sup>\n                    mice die before adulthood, whereas the surviving\n                    <jats:italic>PPAR<\/jats:italic>\n                    \u03b3\n                    <jats:sup>\n                      <jats:italic>hyp\/hyp<\/jats:italic>\n                    <\/jats:sup>\n                    animals overcome the growth retardation, yet remain lipodystrophic. In contrast to most lipodystrophic models, the adult\n                    <jats:italic>PPAR<\/jats:italic>\n                    \u03b3\n                    <jats:sup>\n                      <jats:italic>hyp\/hyp<\/jats:italic>\n                    <\/jats:sup>\n                    mice only have mild glucose intolerance and do not have a fatty liver. These metabolic consequences of the lipodystrophy are relatively benign because of the induction of a compensatory gene expression program in the muscle that enables efficient oxidation of excess lipids. The\n                    <jats:italic>PPAR<\/jats:italic>\n                    \u03b3\n                    <jats:sup>\n                      <jats:italic>hyp\/hyp<\/jats:italic>\n                    <\/jats:sup>\n                    mice unequivocally demonstrate that PPAR\u03b3 is the master regulator of adipogenesis\n                    <jats:italic>in vivo<\/jats:italic>\n                    and establish that lipid and glucose homeostasis can be relatively well maintained in the absence of white adipose tissue.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2336090100","type":"journal-article","created":{"date-parts":[[2003,11,25]],"date-time":"2003-11-25T15:59:06Z","timestamp":1069775946000},"page":"14457-14462","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":172,"title":["Compensation by the muscle limits the metabolic consequences of lipodystrophy in PPAR\u03b3 hypomorphic mice"],"prefix":"10.1073","volume":"100","author":[{"given":"Hana","family":"Koutnikova","sequence":"first","affiliation":[{"name":"Institut de G\u00e9n\u00e9tique et de Biologie Mol\u00e9culaire et Cellulaire, Centre National de la Recherche Scientifique\/Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale\/Universit\u00e9 Louis Pasteur, 67404 Illkirch, France; and Institut Clinique de la Souris, G\u00e9nopole Strasbourg, 67404 Illkirch, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Terrie-Anne","family":"Cock","sequence":"additional","affiliation":[{"name":"Institut de G\u00e9n\u00e9tique et de Biologie Mol\u00e9culaire et Cellulaire, Centre National de la Recherche Scientifique\/Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale\/Universit\u00e9 Louis Pasteur, 67404 Illkirch, France; and Institut Clinique de la Souris, G\u00e9nopole Strasbourg, 67404 Illkirch, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mitsuhiro","family":"Watanabe","sequence":"additional","affiliation":[{"name":"Institut de G\u00e9n\u00e9tique et de Biologie Mol\u00e9culaire et Cellulaire, Centre National de la Recherche Scientifique\/Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale\/Universit\u00e9 Louis Pasteur, 67404 Illkirch, France; and Institut Clinique de la Souris, G\u00e9nopole Strasbourg, 67404 Illkirch, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sander M.","family":"Houten","sequence":"additional","affiliation":[{"name":"Institut de G\u00e9n\u00e9tique et de Biologie Mol\u00e9culaire et Cellulaire, Centre National de la Recherche Scientifique\/Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale\/Universit\u00e9 Louis Pasteur, 67404 Illkirch, France; 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