The involvement of the neuronal Golgi apparatus and trans-Golgi network in the human olivary hypertrophy.

We studied the Golgi apparatus (GA) and trans-Golgi network (TGN) in the human olivary hypertrophy by immunohistological methods with organelle specific antibodies against the medial cisternae of the organelle (MG160) and the trans-Golgi network (TGN46). The GA and TGN of enlarged neurons in the inferior olivary nuclei in the early stages after central tract lesions lost the normal network-like configuration, and they were reduced to numerous small disconnected granules (fragmentation). In chronic stages after lesions, the GA and TGN of vacuolated or enlarged neurons showed a variety of morphological profiles, such as normal-looking patterns, fragmentation, reduction in number, and aggregation around nuclei or at a distance in the cytoplasm. In patients with multiple system atrophy, the GA and TGN of the neurons in the inferior olivary nuclei showed almost similar findings to those seen in the chronic stages after brainstem lesions. These results suggest that the GA and TGN are affected in degenerating neurons by anterograde transneuronal mechanisms.

Effects of exercise on plasma and liver lipids of rats. IV. Effects of exercise on hepatic cholesterogenesis and fecal steroid excretion in rats.

The effects of treadmill exercise on hepatic cholesterogenesis and fecal steroid excretion were studied using male Wistar rats fed a commercial pellet ration. Exercise, in comparison with ad libitum or pair-feeding sedentary groups, caused the following significant changes: (i) a reduction in the concentration of plasma triglyceride, phospholipid and cholesterol; (ii) a reduction in liver weight; (iii) increases in hepatic 3-hydroxy-3-methylglutaryl-CoA reductase activity and incorporation of mevalonate into digitonin precipitable sterol; (iv) increases in excretion of neutral and acidic steroids into the feces; (v) the increase in lipoprotein lipase activity in the cardiac muscle, and (vi) the decrease in the concentration of carcass triglyceride but not of cholesterol. These data suggest that the mechanism responsible for the plasma cholesterol-lowering effect of exercise is attributable to an increase in exretion of fecal neutral and acidic steroids accompanied by an acceleration of cholesterol turnover in the body.