The stuctural and functional unit in the human liver (liver acinus)

Revelation of simple and complex liver acini after portal transplantation of pancreatic islets or thyroid follicles in rats

“…Complex liver acini were already depicted by Rappaport in his dye injection studies. [6][7][8] Our study corroborates his results. Small portal tracts represent the corresponding structure of the liver vasculature that supply complex acini.…”

“…[6][7][8] Thus, the correctness of his model could not be proven. In the following years several attempts have been made to visualize this smallest anatomical unit of the liver, often in a critical approach.…”

“…Rappaport suggested 3 metabolic zones (I-III) that envelope the central axis like layers of the bulb. [6][7][8] He also claimed that zone III of both acinus halves of the idealized section plane communicate at the terminal end of the TPV (Fig. 1A).…”

“…While the former is based on a structural point of view derived from the microanatomy of the liver of the pig, which is subdivided into hexagonal lobules by fibrous septa, the latter is described as a hierarchal model of microcirculatory units (simple and complex liver acini) developed by Rappaport after having studied the staining patterns following dye microinjections and the microanatomy of hepatic lesions. [6][7][8] Rappaport proposed the existence of an irregularly shaped simple liver acinus, made up by hepatocytes that drain the blood from a terminal portal vessel, the so-called terminal portal venule (TPV), which forms the central axis of the acinus, and from which a glomus of sinusoids branches off centrifugally. The venous blood is collected by draining hepatic venules (HV) in the periphery of these acini.…”

“…This is something even Rappaport himself was not able to do when using his dye injection models. [6][7] Here, we report on our observations made by examining morphologically altered liver acini in animal models that were originally designed to study hormonally induced hepatocarcinogenesis. [14][15][16][17][18][19][20][21][22][23] The altered morphology of the liver acini was induced by local action of hormones [such as insulin and tri-iodothyronine (T3)] on the hepatocellular metabolism after transplantation of endocrine tissues into the rat liver, resulting in considerable changes of the hepatocellular phenotype of the downstream liver acini, such as an excess in glycogen and/or fat storage in the insulin model [14][15][16][17][18][21][22][23] or increased basophilia and loss of glycogen in the T3 model.…”