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  • 1
    ISSN: 1432-0428
    Keywords: Keywords Insulin secretion, protein kinase, insulin secreting cells, human CaMK II, cloning of new subtypes.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. The Ca2+/calmodulin-dependent protein kinase II (CaMK II) is highly expressed in pancreatic islets and associated with insulin secretion vesicles. The suppression of CaMK II disturbs insulin secretion and insulin gene expression. There are four isoforms of CaMK II, α to δ, that are expressed from different genes in mammals. Our aim was to identify the isoforms of CaMK II expressed in human beta cells by molecular cloning from a human insulinoma cDNA library and to assess its distribution in humans.¶Methods. The previously unknown complete coding sequences of human CaMK II β and the kinase domain of CaMK II δ were cloned from a human insulinoma cDNA library. Quantitative determination of CaMK II isoform mRNA was carried out in several tissues and beta cells purified by fluorescence activated cell sorting and compared to the housekeeping enzyme pyruvate dehydrogenase.¶Results. We found CaMK IIβ occurred in three splice variants and was highly expressed in endocrine tissues such as adrenals, pituitary and beta cells. Liver showed moderate expression but adipose tissue or lymphocytes had very low levels of CaMK II β-mRNA. In human beta cells CaMK II β and δ were expressed equally with pyruvate dehydrogenase whereas tenfold lower expression of CaMK II γ and no expression of CaMK IIα were found.¶Conclusion/interpretation. Although CaMK II δ is ubiquitously expressed, CaMK II β shows preferential expression in neuroendocrine tissues. In comparison with the expression of a key regulatory enzyme in glucose oxidation, pyruvate dehydrogenase, two of the four CaM kinases investigated are expressed at equally high levels, which supports an important role in beta-cell physiology. These results provide the basis for exploring the pathophysiological relevance of CaMK IIβ in human diabetes. [Diabetologia (2000) 43: 465–473]
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 70 (1992), S. 1057-1060 
    ISSN: 1432-1440
    Keywords: Atrial natriuretic peptides ; Artificial pacemaker stimulation ; Left heart catheterization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Brain natriuretic peptide (BNP) is synthesized and released predominantly in the ventricular myocardium whereas atrial natriuretic peptide (ANP) is produced mainly in the atria. This study evaluated whether artificial pacemaker stimulation or left heart catheterization results in specific changes in BNP and ANP plasma levels. Both BNP and ANP responded sensitively to changes in pacemaker stimulation (single-chamber pacemakers; pacing rates of 72 and 92/min) and during the left heart catheterization procedure. However, whereas higher pacing resulted in a more pronounced increase in plasma BNP levels, a stronger ANP release followed catheterization. This incongruous rise in ANP and BNP plasma concentrations points to at least partly independent mechanisms govering the release of BNP and ANP.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1440
    Keywords: Phospholipase A2 ; Pancreatic pseudocysts ; HPLC
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Phospholipase A (PLA) is able to attack membrane phospholipids and thereby plays a putative role in the pathogenesis of pancreatic pseudocysts. We looked for PLA2-like activity in aspirates from human pancreatic pseudocysts. In material originating from one cyst which occurred shortly after an acute pancreatitis attack, hydrolyzing enzymatic activity measured by a sensitive bioassay system for PLA2 activity was found without prior trypsin activation (67×103 U/min/100 µl). A biochemical characterization of this hydrolyzing enzymatic activity was provided after resolution of the respective proteins contained in the cyst fluid by HPLC. High hydrolyzing activities were found in correspondence to one specific, early eluting peak. The purified enzyme had pH optima at 3.5 and 6. Addition of EDTA (5 mM) to the test system abolished the enzymatic activity which mirrored the requirement for calcium ions. The activity was optimal at calcium concentrations ranging from 1–2 mM. Higher calcium concentrations reduced the enzymatic activity. The enzyme showed high heat stability. SDS-gel analysis of the peak showed one single band with a molecular weight of about 20,000 Daltons. Our findings demonstrate the possibility of activated, PLA-like activity in human pancreatic pseudocyst fluid. We speculate that an inappropriate activation of this enzyme in peri- or intrapancreatic “fluid collections” could account for pseudocyst formation after an acute pancreatitis attack.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1433-8580
    Keywords: Camostate (FOY 305) ; Degradation ; Rat liver ; HPLC
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The elimination of the low molecular weight proteinase inhibitor camostate (FOY 305) was studied in rats after oral administration and in the the situ perfused rat liver. After feeding of camostate (400 mg/kg b. w.) only the metabolites (FOY 251, GBA) were detected in blood samples withdrawn from the portal and hepatic vein. This indicated a rapid degradation of FOY 305 after absorption from the gut lumen. The hepatic extraction of the anti-proteolytic active metabolite FOY 251 during a single liver passage was 23%. It remained almost constant over the period of 120 min. In the perfused rat liver, FOY 305 was given in concentrations comparable to the in vivo studies. It was eliminated by 20%. In these experiments, the compound was metabolized to FOY 251 and in minor amounts to guanidino-benzoate (GBA), the latter being an anti-proteolytic ineffective degradation product. In conclusion, a low hepatic extraction of FOY 305 led to pharmacologically effective concentrations of the active metabolite FOY 251 in the circulation after oral ingestion of the proteinase inhibitor.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Research in experimental medicine 189 (1989), S. 257-264 
    ISSN: 1433-8580
    Keywords: Peptide-1(7–36) ; Physiologic incretin ; RINm5F cells ; GLP-1-receptor complex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Glucagon-like peptide-1(7–36)amide [GLP-1(7–36)amide] is supposed to be an important physiologic incretin. Recently, high affinity receptors for GLP-1(7–36)amide have been demonstrated on rat insulinomaderived RINm5F cells. The present study examined the internalization and degradation of the GLP-1-receptor complex. Internalization of the peptide was time- and temperature-dependent. At 37°C binding and internalization was rapid. At 60 min 35% of125I-labeled GLP-1(7–36)amide was internalized. Incubation in the presence of increasing concentrations of nonlabeled GLP-1(7–36)amide resulted in a decrease of internalization of125I-labeled peptide indicating that this process is saturable. Incubation in the presence of 0.2 mM chloroquine, an inhibitor of intracellular hormone degradation, resulted in intracellular accumulation of125I-GLP-1(7–36)amide. HPLC-supported analysis of cell content after internalization of125I-GLP-1(7–36)amide during a 60-min incubation period at 37°C revealed an elution profile showing two maxima of radioactivity: one represented intact labeled GLP-1(7–36)amide, the other an intracellular degradation product of the peptide. Chloroquine caused a 5-fold increase of the peak representing intact125I-GLP-1(7–36)amide thus demonstrating inhibition of degradation of labelled peptide. Furthermore, a 4-fold increase of the other peak occurred possibly mirroring a delay of release of degradation products by chloroquine. It was excluded that chloroquine is able to interfere with GLP-1(7–36)amidebinding to its receptor.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Research in experimental medicine 189 (1989), S. 281-287 
    ISSN: 1433-8580
    Keywords: Serotonin ; Tryptophan ; Small intestine ; Rat ; Pargyline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate the release of serotonin from intestinal enterochromaffin cells, we used an in vitro technique which allows studies excluding overlapping influences from outside the gut. The entire small intestine of rats fed a standard or tryptophan-enriched (3% of total) diet was totally isolated by ligatures with the exception of the superior mesentric artery and portal vein that supply and drain the intestine. Simultaneously to the vascular perfusion (Krebs-Ringer bicarbonate buffer, 0,4% human albumin, 5 mM glucose, 0.6 mM glutamine) the gut lumen was infused (buffer or 0.1 N HCL). Acidification of the gut lumen resulted in an increment of venously released tryptophan and serotonin. After feeding tryptophan-enriched food the release of tryptophan was increased. However, the total amount of released serotonin after tryptophan diet did not differ as compared to that after standard diet. Addition of a monoamino-oxidase inhibitor (pargyline) to the arterial perfusate enhanced the released amount of serotonin 3-fold in the portal venous effluent (at a concentration of 1 mM but not 0.1 mM). Recovery studies done by arterial infusions of serotonin (1 µM, 10µM) and evaluation of the amounts venously released revealed a high loss of infused serotonin (40%–70%). Our data suggest gut-born serotonin to more likely play a paracrine role than a role as a classical hormone.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Research in experimental medicine 185 (1985), S. 503-507 
    ISSN: 1433-8580
    Keywords: Camostate ; Adipocyte ; Lipolysis ; Adrenaline ; Theophylline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of the ε-guanidino acid derivate camostate (FOY 305) on lipolysis of isolated adipocytes was evaluated to test its supposed influence on the reactions of lipid metabolism in experimental shock. Isoprenaline (10−6 M) and theophylline (10−3 M) significantly stimulated lipolysis in vitro. The basal submaximal (isoprenaline 10−6–10−9 M) and maximal (isoprenaline 10−6 M) catecholamine-stimulated lipolysis were not affected by camostate (10−6 M). Furthermore, camostate (0.1–100 × 10−6 M) did not influence half-maximal theophylline-induced lipolysis of the adipocytes. Our findings do not support the suggestion that ε-guanidino acid derivates diminish in shock the increase of free fatty acids in blood via an influence on lipolysis in the peripheral adipose tissue.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-2277
    Keywords: Key words Pancreas-specific protein ; pancreas transplantation ; Neopterin ; pancreas transplantation ; Serum amyloid A ; pancreas transplantation ; Pancreas transplantation ; rejection parameters ; Rejection ; pancreas transplantation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A reliable, noninvasive indicator of pancreatic allograft rejection is urgently needed. In this study, serum (S), plasma (P), and urine (U) levels of pancreas-specific protein (P-PASP, U-PASP), neopterin (S-NEOP, U-NEOP), amylase (U-AMYL), and amyloid A (SAA) were measured daily in ten type I diabetic patients following simultaneous pancreas and kidney transplantation (SPK). Rejection episodes occurred in three isolated pancreas, nine isolated kidney, and five simultaneous pancreas and kidney transplants. In the case of the eight pancreas rejections, SAA was the rejection marker with the highest diagnostic accuracy (94 %). Using P-PASP and U-PASP, an accuracy of 81 % and 79 %, respectively, was achieved. During viral infections, U-NEOP levels increased to a maximum level of 1904 μmol/mol creatinine, whereas during bacterial infections, SAA levels increased to a maximum value of 43 mg/dl. SAA, measured for the first time in SPK, appears to be a valuable rejection parameter. In combination with U-NEOP and U-AMYL, a differential diagnosis between rejection, bacterial infection, and viral infection was possible. Neither U-PASP nor P-PASP monitoring led to a significant improvement in the results.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-5233
    Keywords: Key words Leptin ; Insulin secretion ; Endocrine pancreas ; β-cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Leptin is a hormone produced and secreted from the adipose tissue. Its physiological actions include the regulation of satiety, food intake and energy balance. The production of leptin is increased by high insulin levels. Here, we demonstrate that leptin acts as an inhibitor of glucose-induced (20 mM) insulin secretion from isolated human islets. No effect was observed in the presence of lower glucose levels (2.8 and 10 mM glucose). The pancreatic β-cell might represent a target of a direct physiological action of leptin. We suggest the presence of an “adipo-insular axis” in which leptin mediates negative feedback from the adipose tissue to the endocrine pancreas.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-5233
    Keywords: Glucagon-like-peptide-1 ; Prediabetes ; NOD mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of the insulinotropic gut hormone glucagon-like-peptide-1 (GLP-1) was studied on the residual insulin capacity of prediabetic nonobese diabetic (NOD) mice, a model of insulin-dependent diabetes mellitus (type 1). This was done using isolated pancreas perfusion and dynamic islet perifusion. Prediabetes was defined by insulitis and fasting normoglycemia. Insultis occurred in 100% of NOD mice beyond the age of 12 weeks. K values in the intravenous glucose tolerance test were reduced in 20-week-old NOD mice compared with agematched non-diabetes-prone NOR (nonobese resistant) mice (2.4±1.1 vs 3.8±1.5% min−1,P〈0.05). Prediabetic NOD pancreases were characterized by a complete loss of the glucose-induced first-phase insulin release. In perifused NOD islets GLP-1, at concentrations already effective in normal islets, left the insulin release unaltered. However, a significant rise of glucose-dependent insulin secretion occurred for GLP-1 concentrations〉0.1 nM. This was obtained with both techniques, dynamic islet perifusion and isolated pancreas perfusion, indicating a direct effect of GLP-1 on the beta-cell. Analysis of glucose-insulin dose-response curves revealed a marked improvement of glucose sensitivity of the NOD endocrine pancreas in the presence of GLP-1 (half-maximal insulin output without GLP-1 15.2 mM and with GLP-1 9.4 mM,P〈0.002). We conclude that GLP-1 can successfully reverse the glucose sensing defect of islets affected by insulitis.
    Type of Medium: Electronic Resource
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