Hepatectomy impairs hepatic processing of somatostatin-14
Identifieur interne : 002D97 ( Main/Exploration ); précédent : 002D96; suivant : 002D98Hepatectomy impairs hepatic processing of somatostatin-14
Auteurs : Steven E. Raper [États-Unis] ; Piyush C. Kothary [États-Unis] ; Norihiro Kokudo [États-Unis] ; John Del Valle [États-Unis]Source :
- The American Journal of Surgery [ 0002-9610 ] ; 1993.
English descriptors
- Teeft :
- Actual counts, Aliquot, American journal, Bile, Bile duct, Biliary, Biliary radioactivity, Biliary secretion, Chloroquine, Colchicine, Duct, Error bars, Gamma counter, Growth factor, Hepatectomized, Hepatectomy, Hepatic, Hepatic processing, Hepatic radioactivity, Hepatic regeneration, Hepatic uptake, Hepatocyte, Hplc, Injection figure, Intact tracer, Intraperitoneal, Intraperitoneal saline, Intraportal, Intraportal injection, Intraportally, Leupeptin, Liver plasma membranes, Liver regeneration, Lysosomal, Methods section, Microtubule, Microtubule inhibitors, Molecular form, Pathway, Pharmacologic, Pharmacologic manipulation, Pretreated, Pretreatment, Radioactivity, Radiolabeled, Radiolabeled somatostatin, Raper, Receptor, Regeneration, Sham, Sham hepatectomy, Somatostatin, Time course, Tracer, Various times, Vinblastine.
Abstract
Somatostatin-14 (SS-14) inhibits the hepatotrophic effect of a variety of growth factors in cultured hepatocytes. We hypothesized that hepatic somatostatin processing might be altered during regeneration. Male Sprague-Dawley rats underwent the intraportal injection of radiolabeled SS-14 after sham or 70% hepatectomy. To study the mechanisms of hepatic SS-14 transport in the rat, the lysosomal enzyme inhibitors, chloroquine and leupeptin, and the microtubule inhibitors, vinblastine and colchicine, were administered 1 to 2 hours prior to the intraportal injection of SS-14. Bile was collected, organs were weighed, and radioactivity was quantitated. The analysis of serial timed collections of bile revealed that, for saline, chloroquine, and leupeptin, peak biliary radioactivity appeared at 20 minutes. Pretreatment with vinblastine and colchicine abolished the 20-minute peak of radioactivity. The appearance of biliary and hepatic iodine 125-SS-14 (125I-[tyr11]-SS-14) at various times after 70% hepatectomy showed a significant decrease starting at 2 hours, which persisted for up to 24 hours. In regenerating liver, both vinblastine and chloroquine decreased 125I-[tyr11]-SS-14 in bile and the liver. In summary, after sham or 70% hepatectomy, vinblastine and colchicine inhibit biliary and increase hepatic 125I-[tyr11]-SS-14 accumulation. After 70% hepatectomy was performed, chloroquine also inhibited 125I-[tyr11]-SS-14 accumulation. We concluded that an important mechanism for hepatic regeneration is decreased responsiveness to SS-14, by decreased SS-14 uptake and increased SS-14 degradation.
Url:
DOI: 10.1016/S0002-9610(05)80409-X
Affiliations:
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Le document en format XML
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<term>Bile duct</term>
<term>Biliary</term>
<term>Biliary radioactivity</term>
<term>Biliary secretion</term>
<term>Chloroquine</term>
<term>Colchicine</term>
<term>Duct</term>
<term>Error bars</term>
<term>Gamma counter</term>
<term>Growth factor</term>
<term>Hepatectomized</term>
<term>Hepatectomy</term>
<term>Hepatic</term>
<term>Hepatic processing</term>
<term>Hepatic radioactivity</term>
<term>Hepatic regeneration</term>
<term>Hepatic uptake</term>
<term>Hepatocyte</term>
<term>Hplc</term>
<term>Injection figure</term>
<term>Intact tracer</term>
<term>Intraperitoneal</term>
<term>Intraperitoneal saline</term>
<term>Intraportal</term>
<term>Intraportal injection</term>
<term>Intraportally</term>
<term>Leupeptin</term>
<term>Liver plasma membranes</term>
<term>Liver regeneration</term>
<term>Lysosomal</term>
<term>Methods section</term>
<term>Microtubule</term>
<term>Microtubule inhibitors</term>
<term>Molecular form</term>
<term>Pathway</term>
<term>Pharmacologic</term>
<term>Pharmacologic manipulation</term>
<term>Pretreated</term>
<term>Pretreatment</term>
<term>Radioactivity</term>
<term>Radiolabeled</term>
<term>Radiolabeled somatostatin</term>
<term>Raper</term>
<term>Receptor</term>
<term>Regeneration</term>
<term>Sham</term>
<term>Sham hepatectomy</term>
<term>Somatostatin</term>
<term>Time course</term>
<term>Tracer</term>
<term>Various times</term>
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<front><div type="abstract" xml:lang="en">Somatostatin-14 (SS-14) inhibits the hepatotrophic effect of a variety of growth factors in cultured hepatocytes. We hypothesized that hepatic somatostatin processing might be altered during regeneration. Male Sprague-Dawley rats underwent the intraportal injection of radiolabeled SS-14 after sham or 70% hepatectomy. To study the mechanisms of hepatic SS-14 transport in the rat, the lysosomal enzyme inhibitors, chloroquine and leupeptin, and the microtubule inhibitors, vinblastine and colchicine, were administered 1 to 2 hours prior to the intraportal injection of SS-14. Bile was collected, organs were weighed, and radioactivity was quantitated. The analysis of serial timed collections of bile revealed that, for saline, chloroquine, and leupeptin, peak biliary radioactivity appeared at 20 minutes. Pretreatment with vinblastine and colchicine abolished the 20-minute peak of radioactivity. The appearance of biliary and hepatic iodine 125-SS-14 (125I-[tyr11]-SS-14) at various times after 70% hepatectomy showed a significant decrease starting at 2 hours, which persisted for up to 24 hours. In regenerating liver, both vinblastine and chloroquine decreased 125I-[tyr11]-SS-14 in bile and the liver. In summary, after sham or 70% hepatectomy, vinblastine and colchicine inhibit biliary and increase hepatic 125I-[tyr11]-SS-14 accumulation. After 70% hepatectomy was performed, chloroquine also inhibited 125I-[tyr11]-SS-14 accumulation. We concluded that an important mechanism for hepatic regeneration is decreased responsiveness to SS-14, by decreased SS-14 uptake and increased SS-14 degradation.</div>
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