60 research outputs found
Effect of insulin on ultrastructure and glycogenesis in primary cultures of adult rat hepatocytes
Insulin in the presence of high concentrations of glucose has a beneficial trophic effect on the development of primary cultures of hepatocytes. Compared to the situation observed in hormone-free control cultures, the flattening of the reaggregated hepatocytes is enhanced, and the reconstituted cell trabeculae are enlarged and tend to form a confluent monolayer after 3 days; the survival time is prolonged from 3 to 5 or 6 days. Ultrastructural modifications are also initiated by insulin; numerous glycogen particles appear after 24 h, in between the cisternae of the proliferated smooth endoplasmic reticulum. After 48 h, large amounts of glycogen are stored, and numerous polysomes are present. A small number of cells showed an increased synthesis of lipid droplets in the lumen of the smooth endoplasmic reticulum and form liposomes at the same time. After 72 h, cytolysomes filled with glycogen develop, simulating glycogenosis type II. Simultaneously, microtubules and microfilaments, closely related to numerous polysomes, appear in cytoplasmic extensions constituting undulating membranes. The biochemical data demonstrate that, in the absence of insulin, a high concentration of glucose stimulates glycogenesis and hinders glycogenolysis. This effect of glucose on polysaccharide synthesis is progressively lost. The addition of insulin to the culture induces after 48 and 72 h, a three- to fivefold increase of the glucose incorporation into glycogen, as compared to the controls. The presence of insulin is required to maintain the hepatocyte's capacity to store glycogen. Glycogen synthetase is converted into its active form under the influence of glucose. Insulin increases the rate of activation
The eck fistula in animals and humans
In all species so far studied, including man, portacaval shunt causes the same changes in liver morphology, including hepatocyte atrophy, fatty infiltration, deglycogenation, depletion and disorganization of the rough endoplasmic reticulum (RER) and its lining polyribosomes and variable but less specific damage to other organelles. Many, perhaps all, biosynthetic processes are quickly depressed, largely secondary to the selective damage to the RER, which is the "factory" of the cell. These structural and metabolic changes in the liver after portal diversion are caused by the diversion around the liver of the hepatotrophic substances in portal venous blood, of which endogenous insulin is the most important. In experimental animals, the injury of Eck's fistula can be prevented by infusing insulin into the tied-off hilar portal vein. The subtle but far-reaching changes in hepatic function after portal diversion have made it possible to use this procedure in palliating three inborn errors of metabolism: glycogen storage disease, familial hypercholesterolemia, and α1-antitrypsin deficiency In these three diseases, the abnormalities caused by portal diversion have counteracted abnormalities in the patients that were caused by the inborn errors. In these diseases, amelioration of the inborn errors depends on the completeness of the portal diversion. In contrast, total portal diversion to treat complications of portal hypertension is undesirable and always will degrade hepatic function if a significant amount of hepatopetal portal venous blood is taken from the liver. When total portal diversion is achieved (and this is to be expected after all conventional shunts), the incidence of hepatic failure and hepatic encephalopathy is increased. If portal diversion must be done for the control of variceal hemorrhage, a selective procedure such as the Warren procedure is theoretically superior to the completely diverting shunt. In practice, better patient survival has not been achieved after selective shunts than after conventional shunts, but the incidence of hepatic encephalopathy has been less. © 1983 Year Book Medical Publishers, Inc
Antibiofilm, Antioxidant, Antimutagenic Activities and Phenolic Compounds of Allium orientale BOISS.
The effect of ischemia and reperfusion on mitochondrial contact sites in isolated rat hearts
Contact sites may be described as energy
channels between the mitochondria and the cytosol,
created by fusion of the inner and the outer
mitochondrial membranes, and their number depends
highly on the energy state of the cell.
The aim of the present study was to examine the
early changes of ischemia and reperfusion on the number
of mitochondrial contact sites. Therefore isolated rat
hearts were subjected to short periods of ischemia
followed by reperfusion. The left ventricular pressure
(LVP), the contractility (dPIdt,, ) and the heart rate
were measured. The number o? contact sites was
morphometrically evaluated.
As the flow was stopped, LVP, dP/dt and HR
declined rapidly and became undetectable a P2 min of
ischemia. The number of contact sites fe11 to a minimum
after 10 min of ischemia after an initial increase (1 min
of ischemia). A 15 min ischemic period resulted in a
high number of contact sites which decreased again after
20 min of ischemia.
Reperfusion after 2 rnin of ischemia caused an
immediate functional recovery and a high presence of
contact sites. After 15 rnin of reperfusion, al1 values
returned to control values. Reperfusion after 10 rnin of
ischemia resulted in a slow recovery of the number of
contact sites and after 15 rnin of ischemia the number of
contact sites remained low upon reperfusion.
We may conclude that mitochondria lose the ability to form contact sites after more than 15 min of ischemia
and this might be a first indication of irreversible injury
- …