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[Changes of insulin secretion in obese children on 2 different diets].

In this work, we studied a group of obese children submitted to two different types of diet (ketogenic and hypocaloric) for 8 weeks and the relationship with liberation of insulin by beta cells of Langerhans islands. It was shown that in children under ketogenic diet, the drop in weight, together with the liberation of insulin, was significantly greater than in those given hypocaloric diet. The possible role of gastrointestinal hormones and opther factors related with the diet are evaluated. It is concluded that the greater reduction in body weight in patients given ketogenic diet is an important factor in the normalization of plasmatic insulin levels.

Adolescent↗

Motilin.

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Action Potentials↗

Cephalic phase, reflex insulin secretion. Neuroanatomical and physiological characterization.

Using chronically catheterized, freely moving male Wistar rats, we have shown that the sweet taste of a saccharin solution reliably triggers a rapid cephalic phase insulin response (CPIR), in the absence of any significant change of glycemia. To establish the neural mediation of this reflex response we used rats that were cured from streptozotocin diabetes by intrahepatic islet-transplantation as a denervated B-cell preparation. The complete lack of any saccharin-induced CPIR in these rats suggests that it is indeed mediated by the peripheral autonomic nervous system, and that the insulin-stimulating gastrointestinal hormones are not involved in this response. It was further found that this reflex insulin secretion is not easily extinguishable and thus might have an unconditioned component. To investigate the central neural pathways involved in this reflex response we used both electrophysiological methods in anesthetized and semi-micro CNS manipulations in freely moving rats. On the basis of our preliminary results, and several reports, using the decerebrate rat preparation for measuring behavioral or saliva secretory oral taste reactivity, it appears that the CPIR might be organized at the brain stem/midbrain level, receiving strong modulatory influences from the diencephalon. But much further work has to be done to establish the central nervous circuitry. Finally, in two experiments, aiming at the question of how important and physiologically relevant the CPIR might be, we found that, on one hand, its lack can result in pathological oral glucose tolerance and on the other hand its exaggeration might contribute to the behavioral reaction to highly palatable sweet food and the resulting development of dietary obesity.

Animals↗

Collagenous colitis: an abnormal collagen table? Two new cases and review of the literature.

Two patients with "collagenous colitis" characterized by abdominal pain and chronic watery diarrhea are described. Colorectal biopsies showed a marked, band-like collagenous deposit under the surface epithelium. Transmission electron microscopy showed an abnormally thickened collagen table under a thickened basal lamina. Immunofluorescence showed no specific lesions. Radioimmunoassay of several gastrointestinal hormones revealed no abnormality. Examination of colorectal biopsies of a large control series (564 patients) did not show a comparable diffuse thickening of the collagen table in various types of inflammatory bowel diseases. Furthermore, no obvious age-related change of the collagen layer was found. The clinical history of our two patients is compared with three analogous cases, previously described. From our findings and those of others it can be concluded that collagenous colitis is a separate entity.

Aged↗

Mechanism of the excitatory action of motilin on isolated rabbit intestine.

Synthetic motilin caused a dose-dependent contraction on isolated rabbit intestinal segments, including the duodenum, ileum, and rectum. The contraction of duodenum was significantly greater than that in the ileum or rectum. In the duodenum, motilin was approximately 100 times as potent as acetylcholine on molar basis. The motilin-induced contractions were not influenced by atropine, chlorpheniramine, cimetidine, phentolamine, propranolol, cinanserin, 1-sar-8-ala-angiotensin II, or aspirin. Motilin did not affect the contraction induced by transmural electrical stimulation or acetylcholine. The response to motilin was unaffected by acetylcholine. Removal of Ca++ from bathing media or verapamil suppressed the motilin-induced contractions to a significantly greater extent than the contractions induced by acetylcholine. Thus, it may be concluded that motilin produces intestinal contractions by acting directly on smooth muscles, but not by acting on pharmacologically known drug receptors nor by releasing neurotransmitters such as endogenous acetylcholine. Motilin does not appear to modify autonomic nerve functions.

Acetylcholine↗

[Studies on the total synthesis of cholecystokinin-pancreozymin. Synthesis of the suitably protected fragment corresponding to the sequence 24--33 (author's transl)].

The synthesis is described of a suitably protected decapeptide derivative corresponding to the C-terminal tyrosin-O-sulfate-containing sequence 24--33 of cholecystokinin-pancreozymin as key fragment for the total synthesis of this gastrointestinal hormone or its 39-variant. This peptide derivative has been prepared according to our newly developed procedure based on the direct use of N-acyltyrosine-O-sulfate barium salt. Additionally, removal of the protecting groups followed by purification via chromatographic methods produced the decapeptide amide in good yields and with a high degree of purity as a fully active cholecystokinin-pancreozymin related peptide.

Cholecystokinin↗

Gastric function in hypopituitarism: a biochemical study.

The specific trophic effects of gastrointestinal hormones on gastric function are now recognized. In addition, pituitary, thyroid and adrenal hormones play an important role in maintaining over all gastric function. The majority of studies regarding hormonal effects on the stomach, however, have been carried out only in experimental animals. This paper reports a patient with gastric atrophy and hypopituitarism. Following therapy of the hypopituitarism with cortisone acetate, sodium levothyroxine and testosterone, the following observations were made: serum gastrin increased 137%; mucosal DNA synthesis and content and gastric acid secretion all increased. These data indicate in this one patient the role of these hormones in gastric function.

Cortisone↗