The formation of arachidonic acid metabolites [prostaglandin (PG)D2, PGE2, PGF2 alpha, 6oxo-PGF1 alpha and thromboxane (TX)B2] has been examined in the frontal, temporal, and parieto-occipital regions of the cortex in the postmortem brains from five patients with a pathologically verified Alzheimer-type dementia (ATD) and in eight, age-matched controls. The study disclosed that the amount of PGD2 and TXB2 found in the ATD brains was greater than in controls, and that the formation of PGD2 was significantly increased in the frontal cortex of the ATD brains. Other PG metabolites, however, showed no significant changes in the ATD group. Since it is known that PGD2 is synthesized mainly in neurons, our results seem to suggest that the preserved cortical neurons in the ATD brain have an accelerated PGD2 production.

To investigate the mechanism of insulin insensitivity during fasting and hyperresponsiveness to insulin after refeeding, insulin binding, 2-deoxyglucose uptake and glucose oxidation were measured in adipocytes from three groups of rats: control, 48 h fasted, and 48 h refed after 48 h fasting. In 48 h fasted rats, fat cell diameters were decreased to five-sixths of that of the controls and plasma insulin levels were decrease to less than half of the controls; however, after 48 h refeeding, these parameters were restored to normal. In adipocytes from fasted rats, insulin binding was increased but insulin-stimulated 2-deoxyglucose uptake glucose oxidation were significantly decreased as compared to that of the controls. In adipocytes of refed rats, insulin bindings was slightly increased as compared to the controls, accompanied by a slightly decreased 2-deoxyglucose uptake and completely restored glucose oxidation. Conclusions from these studies are that both disorders in coupling of insulin-receptor complexes to glucose transport systems and intracellular glucose metabolism play major roles in the insulin insensitivity of adipocytes from fasted rats, whereas, in adipocytes from refed rats, intracellular glucose metabolism, rather than glucose transport, is mainly involved in restoring insulin sensitivity.

Effects of insulin and glucagon on lipoprotein lipase activity in rat adipose tissue were studied in vitro. Adipose tissue from normal or streptozotocin-diabetic rats was incubated in Krebs-Ringer bicarbonate buffer for 60 min at 38 degrees C in the presence of heparin and lipoprotein lipase released from the tissue into the incubation medium was measured. Diabetic rats showed markedly low activities of adipose tissue lipoprotein lipase. Insulin (500 microU/ml) increased lipoprotein lipase activity in adipose tissue from diabetic rats. Glucagon (500 pg/ml), on the other hand, decreased the enzyme activity in normal rat adipose tissue. The results indicate that insulin and glucagon cause reciprocal changes of lipoprotein lipase activity in rat adipose tissue.

Neuraminidase treatment of triton-solubilized insulin receptors from rat fat cell membranes caused release of sialic acid and changed the isoelectric point (pI) of the insulin receptor from 4.7 to 5.6. Neuraminidase had no effect on the number or affinity of insulin receptors. These results indicate that the insulin receptor contains sialic acid, but that this sialic acid is not involved in the binding reaction.

Changea in components in kallikrein-kinin system have been studied in 15 cases with disseminated Intravascular coagulation (DIC). Nine out of the total cases had infection and six cases had malignancy as primary diseases. Plasma prekallikrein (FKK) was determined by a radiochemical assay using 3H-TAME according to Imanari et al.(1974). High and low molecular weight kininogens (HMWK and LMWK) were bioassayed according to Uchida and Katori (in press). If plasma factor XII, measured in each case, was less than 50 % of normal, values of PKK and HMWK in examined plasma were caliculated from those in 1:1 mixture of examined plasma and normal plasma. All of PKK, HMWK and LMWK Showed moderate to marked decrease in every case with DIC. The values for PKK, HMWK and LMWK were 0.23 0.07 TAME unit/ml (normally 0.620.13), 0,20 0.07 ug(bradykinin equiv.)/ml (normally 0.66 0.14) and 1.24 0.44 ug/ml (normally 2.57 0.41), respectively. There was a significant correlation between PKK and antithrombin III levels (r=0.66, P 0.001) in those cases with DIC. PKK was also directly correlated with HMWK and factor XII. Decrease in PKK and HMWK may be chiefly due to consumption. The mechanism for reduction In LMWK, however, remains to be determined. It may be concluded that plasma prekallikrein, high and low molecular weight kininogens decrease in DIC.