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We have previously reported that a decrease in hepatocyte growth factor (HGF), which has many protective functions against endothelial damage by high d-glucose, might be a trigger of endothelial injury. However, the regulation of vascular HGF in diabetes mellitus (DM) has not been clarified in vivo, although vascular disease is frequently observed in DM patients. In addition, our previous report revealed that a prostaglandin I(2) (PGI(2)) analogue prevented endothelial cell death through the induction of vascular HGF production in cultured human epithelial cells. Thus, in this study, we examined the effects of a PGI(2) analogue in the regulation of the local HGF system using DM rats. A PGI(2) analogue (beraprost sodium; 300 and 600 micro g/kg per day) or vehicle was administered to 16-week-old DM rats induced by administration of streptozotocin for 28 days. Endothelial function was evaluated by the vasodilator response to acetylcholine, and the expression of vascular HGF mRNA was measured by Northern blotting. Of importance, expression of HGF mRNA was significantly decreased in the blood vessels of DM rats as compared with non-DM (P<0.01). In addition, the in vitro vasodilator response of the abdominal aorta to acetylcholine was markedly impaired in DM rats. Importantly, the vasodilator response was restored by PGI(2) treatment in a dose-dependent manner (P<0.01), whereas N(omega)-nitro-l-arginine methyl ester inhibited the restoration of endothelial function. Of particular interest, vascular HGF mRNA and protein were significantly increased in the blood vessels of DM rats treated with PGI(2) as compared with vehicle. Similarly, an increase in HGF protein was also confirmed by immunohistochemical analysis. In addition, the specific HGF receptor, c-met, was also increased by PGI(2) treatment. Overall, this study demonstrated that treatment with a PGI(2) analogue restored endothelial dysfunction in DM rats, accompanied by the induction of vascular HGF and c-met expression. Increased local vascular HGF production by a PGI(2) analogue may prevent endothelial injury, potentially resulting in the improvement of endothelial dysfunction.
School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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School of Arts, Sciences & Humanities, University of Sao Paulo, Sao Paulo, Brazil
Department of Biosciences, Mackenzie Presbyterian University, Sao Paulo, Brazil
Departments of Pharmaceutical Chemistry & Cellular and Molecular Pharmacology, University of California, San Francisco, California, USA
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of Sao Paulo, SP, Brazil
Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
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It is well known that thyroid hormone affects body composition; however, the effect of the thyroid hormone receptor β (TRβ)-selective thyromimetic GC-1 on this biological feature had not been demonstrated. In the current study, we compared the effects of a 6-week treatment with triiodothyronine (T3; daily injections of 3 or 6 μg/100 g body weight) or GC-1 (equimolar doses) on different metabolic parameters in adult female rats. Whereas all animals gained weight (17–25 g) in a way not basically affected by T3 or GC-1 treatment, only T3 treatment selectively increased food intake (50–70%). Oxygen consumption was significantly and equally increased (50–70%) by T3 and GC-1. Analysis of body composition by dual-energy X-ray absorptiometry (DEXA) revealed that, whereas control animals gained about 80% of fat mass, T3- or GC-1-treated animals lost 70–90 and ~20% respectively. Direct analysis of the carcass showed that T3 treatment promoted a 14–74% decrease in fat content but GC-1 treatment promoted only a 15–23% reduction. The gain in lean mass by DEXA and the carcass protein content were not affected by T3 or GC-1 treatment. However, the mass of individual skeletal muscles was negatively affected by T3 but only barely by GC-1. These findings highlight the potential use of GC-1 for the treatment of obesity and the metabolic syndrome.