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Biomedical subjects

H Greten

Publications and source records attributed to H Greten.

268 records · Page 15Linked to original sources
PubMed1969

Evidence for separate monoglyceride hydrolase and triglyceride lipase in post-heparin human plasma.

Post-heparin plasma contains an enzyme or enzymes with both triglyceride lipase (TGL) and monoglyceride hydrolase (MGH) activities. A simple and reproducible radioactive assay for measurement of MGH activity was developed and used, with a previously reported assay for TGL, to study lipolysis in plasma. After the injection of heparin, enzymatic activity against both tri- and monoglycerides appeared and disappeared from plasma at approximately the same rates. However, in contrast to TGL activity, MGH activity was: (a) much greater, (b) considerably less heat-sensitive, (c) unaffected by three inhibitors (NaCl, protamine, and pyrophosphate), (d) not influenced by radical changes in fat and carbohydrate content of the diet, and (e) normal in familial Type I hyperlipoproteinemia. The dichotomy between MGH and TGL activities in patients with genetic deficiency of TGL constitutes strong evidence that these are two different enzymes. The findings further indicate that when post-heparin lipolytic activity is measured for the purpose of detecting TGL deficiency, it may be necessary to perform the assay with a substrate free from partial glycerides.

Diet↗
PubMedDate not supplied

A comparative study of human tissue and post-heparin plasma triglyceride lipases.

Human post-heparin plasma contains at least two different triglyceride lipases (TGL). The plasma lipolytic activity has been attributed to extra-hepatic and hepatic origin. Both post-heparin triglyceride lipases were partially purified and characterized. With heparin-Sepharose 4 B affinity chromatography it was possible to partially purify human adipose tissue lipoprotein lipase (LPL) as well as a lipase from human liver. The effects of NaCl, pre-heparin plasma, pH and temperature on these two tissue lipases and plasma lipases were studied in parallel. Antibodies were produced against plasma hepatic triglyceride lipase (plasma H-TGL) that did not cross react with LPL. TGL activity of human liver was completely inhibited by antibodies against plasma H-TGL. From these results it appears that human post-heparin plasma contains two triglyceride lipase activities which originate from liver and extra-hepatic tissues such as adipose tissue.

Adipose Tissue↗
PubMedDate not supplied

N alpha-carboxyacyl analogues of CCK with a substituted Gly: interaction with pancreatic and gallbladder CCK receptors.

It has been reported that certain N alpha-carboxyacyl analogues of CCK-8 and of CCK-7 with a substituted Gly in position 3 or 4 of the peptide possess higher potencies at stimulating pancreatic enzyme secretion than at stimulating gallbladder contraction, suggesting that these analogues are able to differentiate subtypes of CCKA receptors. However, no studies examined directly the interaction of these peptides with the CCK receptors in both tissues. In the present study, CCK-8 and various N alpha-carboxyacyl analogues of CCK-7 and of CCK-8 were prepared by solid phase synthesis using Fmoc chemistry and were purified by HPLC; molecular weight and sufficient sulfation were determined by mass spectrometry. [125I]Bolton-Hunter(BH)-CCK-8 binding to sections of the guinea pig pancreas and gallbladder was determined under identical conditions; amylase release from pancreatic acini and contraction of gallbladder muscle strips were measured in vitro. Each peptide stimulated amylase release (EC50): CCK-8 (0.09 nM) > Suc[Sar3]CCK-7 (0.23 nM) > des(SO3)CCK-8 (28 nM) > Suc[D-Trp4]CCK-8 (32 nM) > Suc[D-Trp3]CCK-7 (53 nM) > Pht[D-Trp3]CCK-7 (180 nM) > Glt[D-Trp3]CCK-7 (220 nM). The same relative potencies were found for stimulation of gallbladder contraction, and for the inhibition of [125I]BH-CCK-8 binding to pancreas and gallbladder sections. These data demonstrate that the CCKA receptors in the pancreas and on gallbladder smooth muscle possess similar affinities for the various N alpha-carboxyacyl analogues of CCK-7 and CCK-8 with a substituted Gly and provide further evidence that the CCKA receptors in gallbladder and pancreas cannot be distinguished pharmacologically.

Amylases↗
PubMedDate not supplied

Effects of adrenergic antihypertensive drugs on sterol synthesis in freshly isolated human mononuclear leukocytes.

The effects of the adrenergic antihypertensive drugs propranolol, clonidine, alpha-methyldopa, urapidil, indoramin, and prazosin on the relative rate of sterol synthesis were studied in freshly isolated human mononuclear leukocytes. Incubation of cells for 6 h in a medium containing lipid-depleted serum led to a threefold increase in the incorporation of [14C]acetate or tritiated water into sterols. (-)-Epinephrine added at zero time to the incubation medium inhibited the relative rate of sterol synthesis by 32% at a concentration of 1 mumol/L. The non-specific beta-blocker propranolol, added at equimolar concentrations, almost abolished the epinephrine-induced suppression. The beta-blocker per se had no effect on the incorporation of [14C]acetate into sterols up to a concentration of 1 mumol/l. The alpha 2-agonist clonidine and alpha-methyldopa, added in increasing concentrations at zero time, inhibited the relative rate of sterol synthesis, yielding a sigmoidal log dose-effect curve. The suppression was 43 and 24%, respectively, at a concentration of 0.1 mmol/L. The alpha 1-antagonists indoramin, prazosin, and urapidil, up to a concentration of 10 mumol/L, had no effect per se, or on the epinephrine-induced suppression of the relative synthesis rate of sterols. The results give evidence that various antihypertensive adrenergic drugs, depending on their action on beta- or alpha-adrenergic receptors, have different effects on cholesterol biosynthesis and therefore may affect cellular cholesterol homeostasis.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

Disseminated cryptococcosis in a patient with AIDS.

We report the case of a 31-year-old AIDS patient who had generalized cryptococcal disease with involvement of the lungs, bone marrow, gastrointestinal tract and skin as well as chorioretinitis which may have been due also to Cryptococcus neoformans infection. Initially there was no involvement of the central nervous system. The patient recovered after 43 days' treatment with fluconazole and amphotericin B and flucytosine initially. Four months later he presented with a cryptococcal splenic abscess despite secondary prevention with fluconazole and twice-weekly liposomal amphotericin B. After splenectomy the patient was discharged in good health. One year later he died of cryptococcal meningitis.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

Apo E-containing lipoproteins in low or high density lipoprotein deficiency.

Apolipoprotein (apo) E-containing subfractions of very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), and high density lipoprotein (HDL) have been described in normolipidemic and hyperlipidemic subjects. These lipoproteins exist, however, in the presence of large amounts of apo A-I- and apo B-containing lipoproteins so that it has been difficult to assess the independence of these apo E-containing subclasses from the major lipoprotein classes. The present study has approached this question by taking advantage of three hypolipidemic states in which one or more of the major apolipoproteins is deficient or absent. After separating lipoproteins from whole plasma by molecular sieve chromatography followed by radioimmunoassay of column fractions, we found that two subjects with abetalipoproteinemia had no apo E-containing lipoproteins the size of VLDL or IDL and all the plasma apo E was in a fraction of large HDL. Two subjects with Tangier disease and two with familial apo A-I/C-III deficiency had extremely low levels of HDL cholesterol and of apo A-I-containing lipoproteins. In spite of the absence of classical HDL, a major fraction of apo E-containing lipoproteins was reproducibly observed at the elution volume characteristic of large HDL and was identical to that found in normal subjects. These data thus suggest the existence of apo E-containing lipoproteins that are the size of HDL and are not dependent upon the presence of either apo B or apo A-I. While studies in normal subjects indicate that apo E is associated with other apolipoproteins in HDL, further investigations will be needed to determine the full composition of these apo E-containing lipoproteins in the lipoprotein-deficient patients described in this report.

Abetalipoproteinemia↗
PubMedDate not supplied

Inhibition of the apolipoprotein B mRNA editing enzyme-complex by hnRNP C1 protein and 40S hnRNP complexes.

The apolipoprotein (apo) B mRNA can be modified by a posttranscriptional base change from cytidine to uridine at nucleotide position 6666. This editing of apo B mRNA is mediated by a specific enzyme-complex of which only the catalytic subunit APOBEC-1 (apo B mRNA editing enzyme component 1) has been cloned and extensively characterized. In this study, two-hybrid selection in yeast identified hnRNP C1 protein to interact with APOBEC-1. Recombinant hnRNP C1 protein inhibited partially purified apo B mRNA editing activity from rat small intestine and bound specifically to apo B sense RNA around the editing site. The inhibition of apo B mRNA editing by hnRNP C1 protein was not due to masking of the RNA substrate as the mutant protein M104 spanning the RNA-binding domain of hnRNP C1 protein bound strongly to the apo B RNA, but did not inhibit the editing reaction. The apo B mRNA editing enzyme-complex of rat liver nuclear extracts sedimented in sucrose density gradients around 22-27S, but did not contain hnRNP C1 protein that was found exclusively within 40S hnRNP complexes. The removal of 40S hnRNP complexes increased the activity of the 22-27S editing enzyme-complex. Adding back 40S hnRNP complexes with hnRNP C1 protein resulted in an inhibition of the 22-27S apo B mRNA editing enzyme-complex, while addition of 18S fractions had no effect. In conclusion, hnRNP C1 protein identified by two-hybrid selection in yeast is a potent inhibitor of the apo B mRNA editing enzyme-complex. The abundant hnRNP C1 protein, which is contiguously deposited on nascent pre-mRNA during transcription and is involved in spliceosome assembly and mRNA splicing, is a likely regulator of the editing of apo B mRNA which restricts the activity of APOBEC-1 to limited and specific editing events.

APOBEC-1 Deaminase↗
PubMedDate not supplied

Human pancreatic cancer cell lines express the CCKB receptor.

BACKGROUND/AIMS: The gastrointestinal peptide gastrin might be a stimulatory effector of the growth of human pancreatic cancer cell lines. Several authors suggest that this effect is mediated by CCKB receptors. However, no studies have examined human pancreatic cells for CCKB receptor expression. The study was designed to evaluate cell lines from human pancreatic cancer (n = 6), or normal pancreatic ducts (n = 2), pancreatic tumor and control tissues (n = 9) for CCKB receptor expression. METHODOLOGY: RNA from cell lines and tissues was subject to DNAse digestion, reverse transcription and amplification using CCKB receptor cDNA sequence specific oligonucleotides via polymerase chain reaction (PCR). After confirmation of CCKB receptor sequence, the products were examined using southern blot analysis. The relative expression was determined by photodensitometrical quantification and normalization to the housekeeping gene beta-actin. RESULTS: Six pancreatic tumor cell lines expressed the CCKB receptor. Amplification of CCKB receptor cDNA from 2 cell lines derived from non-malignant human pancreatic duct cell lines resulted in products with a significantly lower copy number. Tissues like stomach and brain served as positive controls. CONCLUSIONS: These results provide evidence that most human pancreatic cancer cell lines of ductal origin express CCKB receptor mRNA. Malignant pancreatic tissue may overexpress these receptors in comparison with normal tissue.

Adenocarcinoma↗