Mechanism of Elevation of Serum Gastrin Level in Diabetes Mellitus
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Gastrin levels in the sera of patients with diabetes mellitus, in one group up to 49 years of age and another group over 50 years of age, were higher than the corresponding healthy age controls.<BR>The occurence of hypoacidity in both basal and tetragastrin-stimulated maximal acid output (MAO), showed a higher rate of incidence in diabetics than in tie age matched controls, and a significant negative correlation between MAO and serum gastrin level was seen in diabetic patients. The mechanism of hypergastrinemia in hypacidics can be explained by the lowering of the negative feedback mechanism between acidity and gastrin secretion.<BR>Diabetic patients were divided into a normoacid and hypoacid group, and these were subdivided by the presence or absence of diabetic nephropathy. No hypergastrinemia was seen in normoacid cases without nephropathy, and higher gastrin levels than the normal control were seen in normoacid cases combined with nephropathy. The hypoacid group without regard to the presence or absence of nephropathy revealed high gastrin levels, however, the highest gastrin levels with mean values were observed in hypoacid cases with nephropathy. It was concluded from these facts that hypacidity and nephropathy were the main factors involved in the occurrence of hypergastrinemia in diabetics.<BR>In order to clarify the mechanism of hypergastrinemia observed in diabetic nephropathy, the grade of degradation of gastrin by kidneys obtained from genetic diabetic mice (KKAy) in which glomerular lesions were histologically proven was compared with that of renal tissues obtained from normal control mice.<BR>The investigation was made by incubation of <SUP>131</SUP>I-gastrin with each renal tissue, development of the incubation medium with silica-G thin-layer chromatography, and by calculation of the radioactivities in <SUP>131</SUP>I-gastrin and its degradation products.<BR>The degradation products gradually increased in accordance with incubation time when <SUP>131</SUP>I-gastrin was incubated with normal renal tissue, on the other hand, the grade of degradation was clearly decreased when the renal tissue from a KKAy mouse was used.<BR>It was clear that a low metabolic rate of gastrin by the renal lesions would be the cause of hypergastrinemia in patients with diabetic nephropathy.
- 一般社団法人 日本糖尿病学会の論文
一般社団法人 日本糖尿病学会 | 論文
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