Search PubMed⌕ Search

Biomedical subjects

B Otto

Publications and source records attributed to B Otto.

At least 37 records · Page 2Linked to original sources

Gastric emptying of solid and liquid meals in healthy controls compared with long-term type-1 diabetes mellitus under optimal glucose control.

BACKGROUND: Neuropathy of the enteric nervous system and hyperglycaemia are regarded as the main causes of diabetic gastroparesis. PATIENTS AND METHODS: In ten patients with Type-1 diabetes mellitus and sensomotoric neuropathy gastric emptying half times were compared with ten healthy controls by employing the 13C-octanoic acid and the 13C-sodiumacetate breath test, resp., following the intake of equally composed and isocaloric liquid and solid meals. Plasma glucose concentrations were controlled by permanent intravenous administration of insulin. RESULTS: In diabetes mellitus gastric emptying half times after the intake of the liquid meal (p < 0.05) but not after ingestion of the solid meal were slightly prolonged. Gastric emptying half times in patients and controls were not different when liquid and solid meals were compared. CONCLUSIONS: Acute hyperglycaemia appears to be more important than the neuropathy of the enteric nervous system in the pathophysiology of diabetic gastroparesis. The rate of gastric emptying is obviously not dependent on the phase of a meal, but rather on the composition and the caloric content.

Adult↗

Euglycemic hyperinsulinemia, but not lipid infusion, decreases circulating ghrelin levels in humans.

The orexigenic and anabolic gastric hormone ghrelin is secreted in response to acute and chronic energy requirements. While pre-prandial increases and post-prandial decreases of plasma ghrelin levels in rodents and humans seem to indicate a role for the novel peptide hormone as an afferent meal initiator or "hunger hormone", the precise mechanisms which are suppressing ghrelin secretion in response to caloric intake remain largely unknown. We show here that human ghrelin levels decrease by almost 50% under hyperinsulinemic euglycemic clamp conditions (no.=4, p=0.001), revealing physiologically relevant increases of insulin levels as an independent determinant of circulating ghrelin levels. In a second study, 3-4-fold increased plasma free fatty acid levels, as another metabolic candidate for the modulation of circulating ghrelin concentrations, were generated by constant lipid infusion, but failed to change plasma ghrelin. Simultaneous elevation of free fatty acids and insulin again markedly decreased ghrelin concentration (no.=4, p=0.01). Insulin induced suppression of circulating ghrelin levels (or the lack thereof) could be a mechanism with relevance for the understanding of the (patho-) physiology of meal initiation and termination, the pathogenesis of the metabolic syndrome and for the development of respective therapeutic perspectives.

Adult↗

Effects of duodenal fat, protein or mixed-nutrient infusions on epigastric sensations during sustained gastric distension in healthy humans.

Duodenal fat modulates sensory and motor responses to gastric distension and raises plasma cholecystokinin compared with glucose. The effects of protein (also releasing cholecystokinin), or mixed nutrients (with a balanced macronutrient composition), on gastrointestinal sensations in relation to gastric relaxation and plasma cholecystokinin concentrations are not known. The aim of this study was therefore to compare the effects of duodenal infusion of fat, protein or mixed nutrients during sustained gastric distension (mimicking the intragastric presence of food) on these parameters. In 10 healthy subjects, gastric distension to fullness was maintained for 90 min, while gastric volume, sensations and plasma cholecystokinin were monitored during duodenal infusion of isotonic saline or nutrients (2 kcal min-1). During saline infusion, all parameters remained unchanged for 90 min. Initially, only lipid increased plasma cholecystokinin, gastric volume and scores for sensations. Cholecystokinin and gastric volume responses to protein and mixed nutrients were delayed and not associated with significant changes in sensations. In conclusion, the intensity of gastrointestinal sensations is related to, but not entirely explained by, the magnitude in intragastric volume and plasma cholecystokinin changes. Our results offer new insights into the role of dietary nutrient composition in gastrointestinal sensations, and may have implications for the dietary management of digestive symptoms.

Adult↗

[Arterial aneurysm within a tumor in a pediatric patient].

A middle cerebral artery aneurysm, completely enclosed in a large frontotemporal anaplastic astrocytoma, is demonstrated in a 11-month-old girl admitted for intracranial hypertension. Clipping of the aneurysm along with radical resection was successfully performed. Five years later, follow-up neurological examination is normal, aneurysm occlusion and no evidence of tumor recurrence are demonstrated by angiogram and MRI. The association of brain tumor and aneurysm is discussed, and documented with the only two cases of a neoplasm surrounding on aneurysm reported in the literature.

Astrocytoma↗

Fat digestion modulates gastrointestinal sensations induced by gastric distention and duodenal lipid in humans.

BACKGROUND AND AIMS: It is unclear whether fat digestion is required for the induction of gastrointestinal sensations and whether different fats have different effects. We investigated the effect of fat digestion and of medium-chain triglycerides (MCTs; C < 12) and long-chain triglycerides (LCTs; C > 16) on gastrointestinal sensations. METHODS: In a double-blind study, 15 healthy subjects were studied on 5 occasions during which LCT or MCT emulsions (2 kcal/min), with or without 120 mg tetrahydrolipstatin (THL, lipase inhibitor), or sucrose polyester (SPE, nondigestible fat) were infused intraduodenally in randomized order. After 30 minutes, the proximal stomach was distended in 1 mm Hg steps/min. Intensity of gastrointestinal sensations (on a 0-10 visual analog scale), plasma cholecystokinin (CCK) levels, and gastric volumes were assessed throughout. RESULTS: LCT and MCT increased gastric volume at baseline pressure compared with SPE, and LCT more than MCT. THL entirely abolished this effect (volumes [mL]: LCT, 213 +/- 19; LCT-THL, 39 +/- 3; MCT, 155 +/- 12; MCT-THL, 43 +/- 5; SPE, 44 +/- 5). Only LCT increased plasma CCK levels (pmol/L per 30 minutes: LCT, 21 +/- 2; LCT-THL, 9 +/- 1; MCT, 9 +/- 1; MCT-THL, 11 +/- 1; SPE, 9 +/- 1). During distentions, intragastric volumes were greater during infusion of LCT and MCT than during the respective THL conditions or SPE, but plasma CCK levels did not change. The intensity of sensations increased (hunger decreased) more with LCT than with MCT. During infusion of THL or SPE, the effects were smaller than during LCT or MCT. CONCLUSIONS: Fat digestion is required for the modulation of gastrointestinal sensations during gastric distention. The effects of fat depend on the fatty acid chain length and are not entirely explained by release of CCK.

Adult↗

The tobacco plasma membrane aquaporin NtAQP1.

This paper gives a summary of a project to characterize a tobacco aquaporin. The cDNA and gene, including the 5' upstream region, for the tobacco aquaporin NtAQP1 has been isolated and the encoded protein characterized. The significance of promoter regions for an abscisic acid- and gibberellic acid-induced gene expression could be restricted to a region between -1450 and -1112 upstream of the transcription start point by transient transformation of a bicistronic vector into tobacco protoplasts. NtAQP1 expression in tobacco plants was found to be elevated in flowers, stems and roots. In roots, the protein was detected close to xylem vessels in pitch-like structures. Studies with a NtAQP1-GFP fusion indicated a plasma membrane location. For a functional analysis, the cDNA was expressed in Xenopus oocytes. NtAQP1 was found to be a heavy metal-insensitive aquaporin with additional permeability for glycerol. Mutation of a threonine at position 233 to a cysteine transformed NtAQP1 into a heavy metal-sensitive aquaporin.

Adaptation, Physiological↗

Role of duodenal lipid and cholecystokinin A receptors in the pathophysiology of functional dyspepsia.

BACKGROUND/AIMS: We aimed to evaluate the role of fat and cholecystokinin (CCK) in the pathophysiology of functional dyspepsia (FD) by investigating symptoms and plasma CCK levels following increasing doses of duodenal lipid during gastric distension, and the effect of CCK-A receptor blockade. SUBJECTS/METHODS: In study A, six FD patients were studied on three occasions during duodenal infusion of saline or lipid (1.1 (L-1) or 2 kcal/min (L-2)) and proximal gastric distensions. Six healthy subjects were also studied as controls during L-2 only. In study B, the effect of the CCK-A antagonist dexloxiglumide (5 mg/kg/h) on L-2 induced symptoms was studied in 12 FD patients. Changes in gastric volume at minimal distending pressure and plasma CCK (study A) were assessed, gastric distensions were performed using a barostat, and dyspeptic symptoms were monitored. RESULTS: Lipid increased gastric volume compared with saline (DeltaV (ml): saline 15 (20), L-1 122 (42), L-2 114 (28)) in patients and even more so in controls (221 (37); p<0.05). During distensions, symptoms were greater during L-2 than during saline or L-1, and greater in patients than in controls, while gastric compliance was smaller in patients than in controls (p<0.05). Lipid increased plasma CCK levels in patients and controls (p>0.05). Dexloxiglumide abolished the increase in gastric volume (DeltaV (ml): dexloxiglumide 17 (9), placebo 186 (49)) and dyspeptic symptoms (sum of scores: dexloxiglumide 24 (7), placebo 44 (19)) during duodenal lipid infusion. Dexloxiglumide also reduced gastric compliance (ml/mm Hg: dexloxiglumide 51 (7), placebo 72 (11)) and symptoms (sum of scores: dexloxiglumide 101 (17), placebo 154 (21)) during gastric distension. CONCLUSION: CCK-A receptors are involved in the generation of dyspeptic symptoms by duodenal lipid during gastric distension.

Adult↗

Weight gain decreases elevated plasma ghrelin concentrations of patients with anorexia nervosa.

OBJECTIVE: Ghrelin is a new gastric hormone that has been identified as an endogenous ligand for the growth hormone (GH) secretagogue receptor subtype 1a (GHS-R1a). Ghrelin administration however not only stimulates GH secretion but also induces adiposity in rodents by increasing food intake and decreasing fat utilization. We hypothesized that impaired ghrelin secretion in anorexia nervosa may be involved in the pathogenesis of this eating disorder. To examine this hypothesis and to further investigate the role for ghrelin in regulating energy homeostasis, we analyzed circulating ghrelin levels in patients with anorexia nervosa and examined possible correlations with clinical parameters before and after weight gain. METHODS: Plasma ghrelin levels were measured in overnight fasting plasma samples from 36 female patients with anorexia nervosa (age: 25.0+/-1.2 years, BMI: 15.2+/-0.2 kg/m(2)) before and after weight gain following psychotherapeutic treatment intervention in a psychosomatic institution. Plasma ghrelin levels were also measured in fasting plasma samples from 24 age-matched female controls (31+/-1.4 years, BMI: 22.9+/-0.45 kg/m(2)). For quantification of ghrelin levels a commercially available radioimmunoassay (Phoenix Pharmaceuticals, USA) was used. RESULTS: Fasting plasma ghrelin levels in anorectic patients were significantly higher (1057+/-95 pg/ml) than in normal age-matched female controls (514+/-63 pg/ml n=24, P=0.02). Therapeutic intervention in a psychosomatic institution caused an BMI increase of 14% (P<0.001) leading to a significant decrease in circulating ghrelin levels of 25%, (P=0.001). A significant negative correlation between Deltaghrelin and DeltaBMI was observed (correlation coefficient: -0.47, P=0.005, n=36). CONCLUSION: We show for the first time that fasting plasma levels of the novel appetite-modulating hormone ghrelin are elevated in anorexia nervosa and return to normal levels after partial weight recovery. These observations suggest the possible existence of ghrelin resistance in cachectic states such as caused by eating disorders. Future studies are necessary to investigate putative mechanisms of ghrelin resistance such as a possible impairment of intracellular ghrelin receptor signaling in pathophysiological states presenting with cachexia.

Adolescent↗

Engineered acid-stabile human interferon gamma.

Loss of anti-viral potency upon pH2-treatment is an inherent feature of interferon (IFN)-gamma. The phenomenon seems to be caused by dissociation of IFN-gamma homodimer into subunits upon acidification and subsequent self-association of monomers into aggregates with reduced activity after neutralization. We demonstrated that acid-stability could be engineered into human IFN-gamma without affecting its specific activity. An artificial intra-monomer disulphide bond E7C/S69C stabilizes the dimeric form of the cytokine, which retained its full bioactivity after exposure to pH2. Acidification did not modify the antigenic structure of IFN-gamma as proved by a panel of mouse anti-human IFNgamma antibodies.

Amino Acid Substitution↗

Cell-specific expression of the mercury-insensitive plasma-membrane aquaporin NtAQP1 from Nicotiana tabacum.

The aquaporin NtAQP1 from Nicotiana tabacum L. is insensitive to heavy-metal ions. In addition to water, the transport of urea or glycerol is facilitated by this plasma-membrane-located water channel. Northern hybridization and whole-mount in situ hybridization revealed a high steady-state level of NtAQP1-RNA in roots, a decreased content in shoots and a low content in leaves. By immunolocalization with an antibody targeted to the N-terminus of the aquaporin, the localization of NtAQP1-protein at sites of expected high water transport rates from and to the apoplast or symplast could be demonstrated. The specific pattern of NtAQP1 distribution in petioles strongly indicates a transcellular movement of water.

Aquaporin 1↗

Accuracy of 13C-urea breath test in clinical use for diagnosis of Helicobacter pylori infection.

UNLABELLED: The 13C-urea breath test (UBT) is a noninvasive test for diagnosis of Helicobacter pylori infection of gastric mucosa. The aim of this prospective study was to assess the accuracy of a simple UBT in clinical routine use. METHODS: The study population comprised of 100 patients (49 f, 51 m) requiring diagnostic upper GI endoscopy. One biopsy specimen was taken from the gastric antrum, body and fundus, respectively, for standard histological examination and one additional specimen from each location was transformed into transport medium for cultivation of H. pylori. After vaccination of the culture plates the biopsies were tested for urease activity (UAT). After recovery from endoscopy the patients had to pass an one liter endexspiratory breath sample before and 15 min after drinking 200 ml orange juice, pH 3.6, containing 75 mg of 13C-urea. 13CO2 was measured in the breath samples using isotope-selective nondispersive infrared spectrometry. RESULTS: Defining gold standard groups with all biopsy tests (from antrum and corpus) positive or negative the 13CO2 delta over baseline (DOB) cut-off level of UBT was set at 6.5/1000 in order to best discriminate positive from negative patients (ROC analysis). UBT was positive in 37% of all subjects. Taken UAT and histological examination together (positive when both tests were positive) UBT displayed a sensitivity of 92%, a specificity of 94%, a positive predictive value of 89%, and a negative predictive value of 94%. When including the results of culture sensitivity and negative predictive value reached almost 100%. The mean of the 13CO2-DOB values from H. pylori-positive duodenal or gastric ulcer patients did not differ from controls (H. pylori-positive patients without lesions). The 13CO2-DOB values of the ulcer group were correlated significantly with the active inflammatory component of gastritis in antrum, corpus, and fundus. CONCLUSION: UBT with this setup detects H. pylori infection in clinical routine use with high accuracy. The increase of exhaled 13CO2 does not predict ulcer disease but reflects the degree of active inflammation of gastric mucosa.

Biopsy↗

Relationship between increasing duodenal lipid doses, gastric perception, and plasma hormone levels in humans.

Duodenal lipid causes gastric relaxation, CCK secretion, and nausea. Vasopressin has been implicated in motion sickness-related nausea. We hypothesized that increasing doses of lipid enhance gastric relaxation and CCK-vasopressin secretion, resulting in a dose-related exacerbation of nausea. Nine healthy subjects received isotonic saline or lipid (1, 2, or 3 kcal/min, L1, L2, L3) duodenally. Changes in gastric volume, sensations, and plasma hormone levels were assessed during infusions and isobaric gastric distensions. Lipid infusions increased gastric volume, plasma CCK (but not vasopressin) levels, and gastric compliance during distensions, compared with saline. Plasma CCK levels were related to the dose of lipid administered [CCK levels at 30 min (pmol/l), saline: 1.1 +/- 0.2, L1: 1.8 +/- 0.2, L2: 3.0 +/- 0.2, L3: 4.3 +/- 0.6]. During distensions, nausea increased in intensity with increasing doses of lipid [score (where 0 is no sensation and 100 is strongest sensation), saline: 7 +/- 4, L1: 19 +/- 7, L2: 44 +/- 7, L3: 66 +/- 8]; however, no further rise in plasma CCK occurred. Because neither lipid nor distension alone induced significant nausea, we conclude that the interaction between these stimuli together with a modulation by CCK is responsible for the effects observed. Vasopressin is not involved in lipid- and distension-induced nausea.

Adult↗

[Mycoses in fish].

Over 4 years 1.241 fish were examined mycologically. In 182 (14.7%) of them positive results were obtained. Most of the isolates belonged to the following genera: Cladosporium, Saprolegnia, Candida and Penicillium. Fungal infections were correlated with findings of Saprolegnia, Branchiomyces, Pythium, Ichtyophonus and sometimes Cladosporium. Most fungal isolates were etiologically irrelevant for diseases or death.

Animals↗