Yasufumi Okabe

Administration of D-glucosamine into the third cerebroventricle induced feeding accompanied by hyperglycemia in rats.

D-glucosamine, 2-amino-2-deoxy-D-glucose, is known to be an endogenous glucose analogue and to antagonize glucose uptake and metabolism. The present experiments were aimed to clarify effects of glucosamine and related chemical substances on ingestive behavior, as well as its direct effects on hypothalamic neurons. Infusion of 24 mumole glucosamine into the third cerebroventricle induced feeding within 30 min in 5 rats out of 7 tested, accompanied by increased ambulatory activity. No periprandial drinking was observed. Plasma glucose level increased, peaking at 30 min after the injection. Plasma insulin level tended to increase, but not significantly. Electrophoretic application of glucosamine activated glucose-sensitive neurons in the lateral hypothalamus and suppressed glucoreceptors in the ventromedial hypothalamus. These facts, together with other reported results, suggest that glucosamine can modulate physiological feeding and that carbon 2 of the glucose molecule is important in feeding modulation by glucose analogues.

MR imaging of pituitary hypertrophy due to juvenile primary hypothyroidism: A case report

We present a case of pituitary hypertrophy due to juvenile primary hypothyroidism with subsequent return to normal size after therapy. This clinical entity is well known, but there are few reports on its magnetic resonance (MR) findings. We stress the usefulness of Gadolinium-DTPA-enhanced (Gd-DTPA-enhanced) MRI in the differential diagnosis of pituitary hypertrophy and pituitary adenoma.

Differential Mechanisms of Feeding Modulation Induced by Amino Sugars in Rats

Abstract The present study examined and compared the effects of N-acetylglucosamine and 1-deoxy-N-acetylglucosamine on feeding behavior with those of glucosamine and 1-deoxyglu-cosamine. Infusion of 12 μmole N-acetylglucosamine and 24 μmole 1-deoxy-N-acetylglucosamine into the rat third cerebroventricle did not affect the feeding behavior. However, oral administration of 1200 μmole N-acetylglucosamine elicited feeding and 2400 μmole 1-deoxy-N-acetylglucosamine markedly suppressed feeding. These effects were abolished by truncal vagotomy. Both glucosamine and 1-deoxyglucosamine affected feeding by intra-third cerebroventricular and oral administration. These findings indicate that N-acetyl amino sugars modulate feeding behavior peripherally through the vagal afferent nerve.

Effect of an amino group at carbon 2 of 1-deoxyglucose analogues on anorexia in the rat

A steric hindering group at carbon 2 of 1-deoxyglucose analogues was introduced by epimerization, deoxidation and substitution of a hydroxyl group with either an acetamido or a fluoro group. Injection of this analogue into the rat third cerebroventricle attenuated the feeding suppression produced by 1-deoxyglucose. In contrast, the replacement of a hydroxyl group at carbon 2 with an amino group produced anorexia of the same magnitude as that produced by 1-deoxyglucose. Amination at carbon 2 was more potent than that at carbon 3, 4 or 6. These results indicate that an amino group at carbon 2 of the glucose molecule is important to reinforce the feeding suppression caused by 1-deoxyglucose analogues.

Anorexia induced by toxohormone-l isolated from ascites fluid of patients with hepatoma

To ascertain anorexigenic effect of toxohormone-L, a polypeptide extracted and purified from ascites of patients with hepatoma were infused into the rat third cerebroventricle. Food intake decreased on the first day after infusion of an optimum dose of 10.0 micrograms (p less than 0.05). The suppressive effect on feeding was linearly dose dependent (p less than 0.05). Meal size and latency to the first meal decreased in the 12-h dark period, and the first and the second 4-h cumulative blocks after infusion of a 10.0 micrograms dose (p less than 0.01 for each). The suppressive effects on total food intake and meal size were completely recovered within 24 h after infusion. Neither postprandial intermeal interval nor eating speed was affected. Periprandial drinking, a ratio of water intake to food intake, was not affected after infusion of 5.0 and 10.0 micrograms toxohormone-L. Infusion of a 10.0 micrograms dose showed no effect on ambulation. These findings suggest that anorexia and cachexia produced in cancer patients may essentially be due to the suppressive effect of toxohormone-L on food intake.

Growth retardation in childhood leukemia and lymphoma : special reference to patients with CNS relapse

We studied the growth of 89 patients who were long-term survivors of childhood leukemia and lymphoma. Eight patients with CNS relapse had a greater decrease in height standard deviation score (SDS) after the relapse than 81 patients without CNS relapse (p < 0.0001). Two patients who received cranial irradiation when they were younger than 2 years of age demonstrated a marked decrease in height SDS more than 3.0 SD. Five patients appeared to have a decline in height SDS before their CNS relapse. There were no apparent changes in the weight of patients with or without CNS relapse. In endocrine studies, all eight patients with CNS relapse failed to show the normal growth hormone (GH) response to argi-nine, GH-releasing factor, and glucagon-propranolol tests, while spontaneous GH secretion during sleep was normal. Magnetic resonance imaging (MRI) revealed small pituitary glands in seven patients with CNS relapse. These findings suggest that in leukemia and lymphoma patients with CNS relapse, GH secretion is impaired at the hypothalamic level, resulting in a secondary atrophy of the pituitary gland. The MRI together with selected endocrinologic tests may help to clarify the mechanism of growth impairment in such patients. A decline in height SDS in each patient may be a useful marker for predicting a CNS relapse in a child with leukemia or lymphoma.