An Electron Microscopic Study of Lipoprotein Production and Release by the Isolated Perfused Rat Liver.

Abstract

above the normal limit, was obtained. The Aminolevulinic acid, porphobilinogen, and other patient, a 54-year-old male with Hgb SC disease and infected leg ulcer, showed 9 total porphyrin values from 4 to 149 pg/24 hr and only one value, 208 pg/24 hr above the normal limit of 180 pg/24 hr.Discussion. Our findings reveal a rather consistent moderate, occasionally marked increase of urinary copro-, total, and uroporphyrins-in this order-and to a slight extent of porphyrin precursors ALA, PBG, and AA during painful and febrile sickle cell crises. Although the number of cases is small, it is our impression that total urinary porphyrin excretion generally parallels the severity of clinical symptomatology and is normal during recovery and the steady state.Of considerable interest is the close resemblance of prominent clinical features in sickle cell crisis and acute porphyria, particularly evident in cases with episodes of excruciating abdominal pain which in both conditions has led to unnecessary laparotomies (9,10,11) . Besides increase of urinary porphyrins there is evidence of vasoconstriction in both diseases(9,10,12,13).Summary. Porphyrin excretion in urine was studied in 18 patients with sickle cell disease, including multiple observations in 6 patients during 7 typical painful and febrile crises. With few exceptions there was moderate to marked elevation of copro-, total, and uroporphyrins at time of pain and fever. aminoacetone during crises were within range of normal variation or only slightly increased. Following subsidence of pain and fever, total porphyrin values returned toward normal. Similarities between clinical features of painful sickle cell crisis and acute porphyria are pointed out.

Immunohistochemical localization of low density lipoprotein receptors in adrenal gland, liver, and intestine.

“…It is further worthwhile noting that lipoprotein formation proceeds whether there is exogenous lipid or not (44), and the synthesis of apoB continues, although at a somewhat reduced rate, even after bile diversion (45). The presence of receptors in villus cells raises the interesting possibility that endogenous cholesterol from LDL contributes, along with exogenous cholesterol and newly synthesized sterol, to the formation of lipoproteins.…”

Effects of chronic ethanol feeding on serum lipoprotein metabolism in the rat

“…Furthermore, whereas normally oxygen is utilized in the liver primarily for lipid oxidation (40), when ethanol is given, it becomes the main fuel for the liver (41); its oxidation thus supplants that of lipids. Moreover, the endoplasmic reticulum is the site of lipid esterification and lipoprotein production (42,43). It is possible that the proliferation of the smooth endoplasmic reticulum induced by ethanol (44)(45)(46) plays a role in the increased capacity of the alcoholic fatty liver to produce serum lipoproteins.…”

Pathogenesis of Postprandial Hyperlipemia in Rats Fed Ethanol-Containing Diets

“…This The mechanism of what appears to be an increased capacity to produce lipoproteins after prolonged ethanolfeeding is unknown, but could be linked to the proliferation (23) and increased activity (24) of the hepatic smooth endoplasmic reticulum. Indeed, this structure is the main site of fatty acid esterification (25) and lipoprotein production (26). Furthermore, Joly, Feinman, Ishii, and Lieber (27) have recently shown that chronic ethanol-feeding is associated with increased activity of hepatic L-a-glycerophosphate acyltransferase, a microsomal enzyme involved in fatty acid esterification.…”