Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies with hepatocyte cultures have defined four hepatocyte mitogens which can transmit a complete mitogenic signal in cultures kept in completely defined conditions. These four mitogens are epidermal growth factor (EGF), acidic fibroblast growth factor (aFGF), hepatopoietin A/hepatocyte growth factor (HPTA/HGF) and hepatopoietin B (HPTB). In this study, we investigated the effect of aFGF, HGF and the mito-inhibitor transforming growth factor beta (TGF-beta) on cultured hepatocytes isolated from livers of rats treated with the xenobiotic hepatic tumor promoters phenobarbital (PB) and alpha-hexachlorocyclohexane (alpha-HCH). Male F344 rats were treated with each of these two xenobiotics to stimulate hepatic DNA synthesis and augmentative hepatomegaly. At different times on the regimens with tumor promoters, hepatocytes were isolated and placed in primary culture. DNA synthesis of hepatocytes in culture stimulated by these two growth factors and the suppression of DNA synthesis affected by TGF-beta were examined as a function of time of treatment in vivo with these two promoters. Following day 10, hepatocytes from both promoter regimens became unresponsive to these two growth factors for the rest of the duration of the treatment (day 90). TGF-beta suppressed DNA synthesis stimulated by growth factors but did not affect the high background DNA synthesis stimulated by xenobiotics themselves.
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PMID:Long-term treatment with hepatic tumor promoters inhibits mitogenic responses of hepatocytes to acidic fibroblast growth factor and hepatocyte growth factor. 171 12

A 17-year-old boy presented with growth retardation, marked hepatomegaly, and sexual infantilism. Elevated fasting serum insulin levels and a blunted hypoglycemic response to exogenous insulin (up to 0.35 unit/kg) demonstrated severe insulin resistance. Neither anti-insulin nor anti-insulin receptor antibodies were present. The molecular size of his circulating insulin and its binding to IM-9 lymphocytes was normal. Despite high circulating insulin values, both erythrocytes and cultured skin fibroblasts showed normal insulin binding capacity and affinity. Tissue responsiveness was examined by measuring the insulin-induced increase in 2-deoxyglucose uptake into fibroblasts. Although the basal glucose transport rate was slightly lower than that of controls, the insulin-induced increase was normal. However, the normal increase in thymidine incorporation in response to insulin was blunted, as were the thymidine incorporation responses to epidermal growth factor and fibroblast growth factor. These studies demonstrate the possible existence of a new form of post-insulin receptor defect as a cause of insulin resistance, but underscore the difficulty that exists in defining the exact nature of the defect in these disorders.
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PMID:A new form of insulin resistance with growth retardation, fatty liver, and hypogonadotropic hypogonadism. 638 36