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. 2014 Apr 1;9(4):e93207. doi: 10.1371/journal.pone.0093207

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© 2014 Hohmann et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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(A) Sketch of hypothesized mechanisms of liver size regulation after partial hepatectomy. Liver size regulation is modulated by hepatocyte (HC) proliferation and apoptosis. A partial hepatectomy (pHx) alters liver size and therefore the relation between the organ and the organism. As a consequence, changes in the portal blood flow are observed. HCs respond to portal blood flow changes. The two hypothesized triggers for proliferation or apoptosis that relate to the portal blood flow are the altered metabolic load (ML) per HC and the altered hemodynamics (HD). (B) Feedback mechanism for the HD hypothesis. The main assumption is marked in green. The partial hepatectomy results in a change of the shear stress level which triggers proliferation and therefore affects the hepatocyte (HC) number . (C) Feedback mechanism for the ML hypothesis. The main assumption is marked in green. The partial hepatectomy alters the metabolic load per hepatocyte (HC) and hence the intracellular buffer level . The functional relation between the buffer rate and is illustrated in Figure S3B. The intracellular buffer affects the HC number . The according growth rate per hepatocyte is given by , see Figure S3D. At the same time, HCs degrade metabolites from the intracellular buffer at the rate which depends on , see Figure S3C.

Inline graphic — (A) Sketch of hypothesized mechanisms of liver size regulation after partial hepatectomy. Liver size regulation is modulated by hepatocyte (HC) proliferation and apoptosis. A partial hepatectomy (pHx) alters liver size and therefore the relation between the organ and the organism. As a consequence, changes in the portal blood flow are observed. HCs respond to portal blood flow changes. The two hypothesized triggers for proliferation or apoptosis that relate to the portal blood flow are the altered metabolic load (ML) per HC and the altered hemodynamics (HD). (B) Feedback mechanism for the HD hypothesis. The main assumption is marked in green. The partial hepatectomy results in a change of the shear stress level which triggers proliferation and therefore affects the hepatocyte (HC) number . (C) Feedback mechanism for the ML hypothesis. The main assumption is marked in green. The partial hepatectomy alters the metabolic load per hepatocyte (HC) and hence the intracellular buffer level . The functional relation between the buffer rate and is illustrated in Figure S3B. The intracellular buffer affects the HC number . The according growth rate per hepatocyte is given by , see Figure S3D. At the same time, HCs degrade metabolites from the intracellular buffer at the rate which depends on , see Figure S3C.