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Biomedical subjects

A Futenma

Publications and source records attributed to A Futenma.

25 records · Page 2Linked to original sources
PubMed1992

[Glomerulonephritis and superoxide dismutase].

To study the role of reactive oxygen species (ROS) in chronic renal disease, we studied the localization of Cu, Zn-superoxide dismutase (SOD) in glomeruli of patients with IgA nephropathy by immunohistochemistry on 37 kidney specimens consisting of 32 IgA nephropathy and normal parts of the 5 resected kidneys with renal tumors serving as controls. To evaluate the change in renal function, creatinine clearance (Ccr) was assessed at the time of biopsy and 1 year after the biopsy. In the normal kidney, Cu, Zn-SOD was localized in the tubular cells, and not in the glomeruli. In the kidney with IgA nephropathy, Cu, Zn-SOD was detected on the epithelial side of the glomerular capillary wall in addition to the tubular cells. The extent of localization of this enzyme was compared with the clinical findings at the time of biopsy. When Cu, Zn-SOD was stained strongly in the glomeruli, the histological change of the glomeruli was milder, and the renal function appeared to be more preserved; the decrease in Ccr one year after the renal biopsy was inhibited. These findings suggest that Cu, Zn-SOD has beneficial actions for renal function as anti-oxidative factors.

Adolescent↗
PubMed1989

Vagally mediated insulin secretion by stimulation of brain cholinergic neurons with neostigmine in bilateral adrenalectomized rats.

This study investigated the relationship between central cholinergic neurons and insulin secretion in bilateral adrenalectomized fed rats. Neostigmine (a cholinesterase inhibitor, 5 x 10(-8) mol) administered into the third cerebral ventricle produced significant increases in hepatic venous plasma insulin and glucose concentrations, whereas i.v. injection of the same dose of neostigmine did not. Prior acute subdiaphragmatic vagotomy or i.p. pre-injection with methylatropine (10(-8) mol) completely prevented the neostigmine-induced rise in plasma insulin concentration. Intraperitoneal pretreatment with hexamethonium (5 x 10(-8) mol) also significantly reduced the plasma insulin response. These peripheral pretreatments did not change the plasma glucose response to neostigmine. Intraventricular co-administration of 10(-9) mol methylatropine, a dose that was ineffective when pre-injected i.p., eliminated the plasma insulin and glucose responses to neostigmine, whereas hexamethonium (5 x 10(-8) mol) had no influence on either response to neostigmine. These observations suggest that stimulation of central cholinergic-muscarinic neurons with third cerebral ventricular injection of neostigmine results in vagally mediated insulin secretion in bilateral adrenalectomized fed rats.

Adrenalectomy↗
PubMed1988

The roles of glucagon and adrenal epinephrine in mediating hyperglycemia induced by third cerebroventricular injection of bombesin.

The roles of glucagon and adrenal epinephrine in mediating bombesin-induced central hyperglycemia were further studied in anesthetized rats. Bombesin (10(-9) mol) injected into the third cerebral ventricle produced an increase in plasma concentrations of glucose, glucagon, and epinephrine. Prior bilateral adrenalectomy completely prevented the hyperglucagonemic and hyperglycemic responses to third cerebral ventricle injection of bombesin. These results support the view that bombesin-induced increases in plasma glucose and glucagon are fully dependent on adrenal epinephrine secretion. Furthermore, during constant intravenous infusion of somatostatin, the hyperglycemic response to third cerebral ventricle injection of bombesin was not significantly influenced despite complete inhibition of the increase in plasma glucagon. Therefore, it is suggested that bombesin-induced central hyperglycemia is mainly mediated by epinephrine itself rather than via epinephrine-stimulated glucagon secretion.

Animals↗
PubMed1985

[Clinical study on glucose intolerance and insulin response in obstructive jaundice].

Insulin responses to oral glucose loads were studied in patients with obstructive jaundice and compared with those of other liver diseases (fatty liver, chronic hepatitis and liver cirrhosis), pancreatic diseases, and definite diabetes mellitus. Compared with their corresponding glucose intolerance, high insulin responses were characteristic in fatty liver, chronic hepatitis and liver cirrhosis, and insulin responses and insulinogenic index decreased in chronic hepatitis and liver cirrhosis as glucose intolerance progressed. In obstructive jaundice with the pancreatic ducts stenotic or obstructed, insulin responses were suppressed in comparison with their corresponding glucose intolerance, and also insulinogenic index were below 0.5 in most of the cases. However, in obstructive jaundice with the pancreatic ducts intact, high insulin responses were observed in almost half of the cases with insulinogenic index above 0.5, and insulin response and insulinogenic index decreased as glucose intolerance progressed. While most cases of fatty liver, chronic hepatitis and liver cirrhosis with insulinogenic index above 0.5 were distributed in non-diabetes zone in sigma BS-sigma IRI plane (Kosaka's), those with insulinogenic index below 0.5 were distributed in intermediate zone. Most cases with obstructive jaundice with pancreatic ducts stenotic or obstructed, had insulinogenic index below 0.5 and were distributed in diabetes zone. However, half of cases with obstructive jaundice with pancreatic ducts intact, had insulinogenic index above 0.5 and their distribution in non-diabetes zone, while the other half had insulinogenic index below 0.5 and their distribution in diabetes zone. Therefore, it may be concluded that insulin responses increase at the early stage of obstructive jaundice mainly under influence of liver dysfunction itself, but that insulin response is suppressed at later stage of obstructive jaundice as pancreatic islets are affected.

Blood Glucose↗