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1 School of Biosciences, Cardiff University, Cardiff, United Kingdom
2 Division of Molecular Neuroendocrinology, National Institute for Medical Research, London, United Kingdom
3 Department of Biomedical Sciences, College of Osteopathic Medicine, Ohio University, Athens, Ohio, United States
4 Department of Child Health, Wales College of Medicine, Cardiff University, Cardiff, United Kingdom
5 Department of Biomedical Sciences, College of Osteopathic Medicine, Ohio University, Athens, Ohio, United States; Edison Biotechnology Institute, Ohio University, Athens, Ohio, United States
* To whom correspondence should be addressed. E-mail: wellst{at}cardiff.ac.uk.
This study describes the previously uncharacterized ontogeny and regulation of truncal adipose reserves in the profoundly growth hormone (GH)-deficient dwarf (dw/dw) rat. We show that, despite normal proportionate food intake, dw/dw rats develop abdominal leanness and hypoleptinemia (circulating leptin halved in dw/dw males; p<0.05) during puberty. This contrasts with the hyperleptinemia seen in moderately GH-deficient transgenic growth retarded (Tgr) rats (circulating leptin doubled at 6 weeks of age; p<0.05) and in GH-receptor/binding protein (GHR/BP)-null mice (circulating leptin doubled; p<0.05). This lean/hypoleptinemic phenotype was not completely normalized by GH treatment, but dw/dw rats developed abdominal obesity in response to neonatal monosodium glutamate (MSG)-treatment or maintenance on a high-fat diet. Unlike Tgr rats, dw/dw rats did not become obese with age; plasma leptin levels and fat pad weights becoming similar to those in Wild-Type rats. In contrast to truncal leanness, tibial marrow adiposity was normal in male and doubled in female dwarves (p<0.01), this increase being attributable to increased adipocyte number (p<0.01). Neonatal MSG-treatment and high-fat feeding elevated marrow adiposity in dw/dw rats by inducing adipocyte enlargement (p<0.05). These results demonstrate that despite the lipolytic influence of GH, severe GH-deficiency in dw/dw rats is accompanied by a paradoxical leanness. This lean/hypoleptinemic phenotype is not solely attributable to reduced GH signalling and does not appear to result from a reduction in nutrient intake or the ability of dw/dw adipocytes to accumulate lipid. Disruption of preadipocyte differentiation or adipocyte proliferation in the dw/dw rat may lead to the development of this unusually lean/hypoleptinemic phenotype.
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