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Biomedical subjects

D Perrin

Publications and source records attributed to D Perrin.

At least 91 records · Page 5Linked to original sources
PubMed1983

Effect of dynorphin on insulin and somatostatin secretion, calcium uptake, and c-AMP levels in isolated rat islets of Langerhans.

Dynorphin-[1-13], at concentrations of 5.8 X 10(-12) to 5.8 X 10(-9) M, stimulated insulin secretion from isolated islets of Langerhans of the rat, in medium containing 6 mM glucose. Higher concentrations of dynorphin had no significant effect on secretion. Dynorphin (5.8 X 10(-9) M) was unable to initiate insulin release from islets in the presence of 2 mM glucose, or to increase insulin secretion further in the presence of 20 mM glucose or 6 and 12 mM glyceraldehyde. Dynorphin-induced insulin secretion from islets was blocked by verapamil (5 microM) or by chlorpropamide (72 microM), but not by a mu opiate receptor antagonist, naloxone (0.11 microM), or by ICI 154129, a specific antagonist for the delta receptor (0.25 microM). Dynorphin had no effect on islet somatostatin secretion, under conditions in which insulin secretion was greatly stimulated. Glucose (20 mM) and glyceraldehyde (6 and 12 mM) significantly increased both insulin and somatostatin secretion. Dynorphin (5.8 X 10(-9) M) increased 45Ca2+ uptake into islets, and also increased intracellular islet c-AMP levels. These changes persisted when higher concentrations of dynorphin were used. These results suggest that (1) dynorphin is a very potent stimulus for insulin secretion; (2) dynorphin does not affect somatostatin secretion in static incubations of islets, in the same way as does glucose and glyceraldehyde; (3) dynorphin's effects may involve increased calcium ion movement and can be blocked by verapamil; (4) dynorphin can also increase islet c-AMP, and could thereby modulate the responsiveness of other secretagogues; (5) the actions of dynorphin on insulin secretion are not mediated by delta or mu opiate receptors in islets.

Animals↗
PubMed1982

Analysis of lambda receptor and beta-lactamase synthesis and export using cloned genes in a minicell system.

We have cloned lamB, the gene for lambda receptor (an outer membrane protein), on a small plasmid which also carries the gene for beta-lactamase (a periplasmic protein). We have identified a promoter in the region of malK, the gene immediately preceding lamB, which is active in minicells but relatively inactive in vitro. Using a minicell system, we have found that both lambda receptor and beta-lactamase are made as full length precursors which are subsequently processed. We also show that the lambda receptor precursor can be exported to the outer membrane before it is processed. Mature beta-lactamase is found only in the periplasm, suggesting that processing may be a requirement for export to the periplasm.

Bacteriophage lambda↗
PubMed1982

A system for genetic analysis in gene lamB: first results with lambda-resistant tight mutants.

We describe a system for genetic analysis in gene lamb. It consists of a phage which allows mapping, complementation and sequencing studies of lamB mutations and of the sequence of gene lamB. We present results obtained with this system for a set of mutations conferring tight resistant to phage lambda. This leads to a first identification of three residues in the LamB protein which are important for adsorption of phage lambda h+. Residues 151 and 382 are important for reversible adsorption while residues 401 is important for irreversible adsorption. We briefly review other tight mutations affecting gene lamB and discuss some implications of the results on phage receptor interactions, LamB-protein structure and membrane insertion.

Adsorption↗
PubMed1982

Alport's syndrome: experience at Hôpital Necker.

We review the characteristic morphologic features identifiable by electron microscopy that have been described in patients presenting with Alport's syndrome. They are diffuse thickening and splitting of the glomerular basement membrane (GBM), which are either isolated or associated with thinning. In occasional cases, only diffuse thinning can be seen. Our study of 100 families followed in Necker's hospital, of which 60 patients have had electron microscopic examination of their renal parenchyma, demonstrates that these GBM changes are highly suggestive of Alport's syndrome. All the patients included in the study fulfilled the following clinical criteria: familial incidence, nerve deafness in the propositus or in another member of the family, renal disease with progression to renal failure in the proband or in another member of the kindred. Although a failure in the proband or in another member of the kindred. Although a normal GBM was found in five patients, the GBM changes should be one of the criteria for the definition of the syndrome. Results dealing with a few other problems raised by this syndrome are reported. They concern the antigenicity and the biochemical composition of the GBM, the incidence of macular and perimacular changes, and the genetic transmission of the disease. It is concluded that Alport's syndrome is genetically heterogeneous and that the GBM ultrastructural changes are observed in most patients whatever the type of genetic transmission.

Adolescent↗
PubMed1981

Secretion into the bacterial periplasmic space of chicken ovalbumin synthesized in Escherichia coli.

Ovalbumin is secreted by the tubular gland cells without cleavage of a signal sequence at the N-terminus. In Escherichia coli strains which produce a chicken ovalbumin-like protein (OLP) from a plasmid-cloned gene, the OLP is synthesized on membrane-bound polysomes and secreted without cleavage into the periplasmic space. In contrast, a deleted protein, which lacks 126 amino acids in the N-terminal half, is not secreted and is synthesized from free polysomes. Our results are compatible with the presence, in the N-terminal half of the molecule, of a signal sequence necessary for the transport across the membrane.

Animals↗
PubMed1981

Cell replication in the islets of langerhans of adult rats: effects of pregnancy, ovariectomy and treatment with steroid hormones.

It was possible to vary the replication rate of cells in the islets of Langerhans of adult rats. The rate of incorporation of [3H]thymidine into islet DNA was increased at 12 days of pregnancy to 2.3-fold and at 19 days of pregnancy to 1.3-fold that in control rats. Ovariectomy, which leads to lowered plasma levels of ovarian steroids, induced a significant and unexpected increase in the rate of thymidine incorporation into islets; treatment of ovariectomized rats with 2 micrograms oestradiol/rat per day for 3 days reversed this upward trend. When islets from normal rats were cultured with certain combinations of steroid hormones including progesterone and oestradiol or with insulin secretagogues, with the exception of glucose, a decreased rate of DNA synthesis was usually found compared with that in control rats. Since treatment with steroid hormones inhibited incorporation of [3H]thymidine into islets from ovariectomized rats and directly reduced incorporation into tissue-cultured islets from normal rats in vitro, it was concluded that increased levels of steroid hormones were not responsible for the higher rate of regeneration of islet cells in pregnant rats. However, a striking correlation between levels of blood glucose in vivo and DNA synthesis in islets in vitro has been observed.

Animals↗
PubMed1981

Insulin release and steroid-hormone binding in isolated islets of langerhans in the rat: effects of ovariectomy.

Ovariectomized rats showed a 30% increase in body weight and food intake over a 9 day period after operation. When pair-fed with normal controls, they had comparatively higher fasting serum levels of glucose and lower levels of insulin and progesterone than the normal rats. Treatment with oestradiol reversed these results. Insulin release from islets isolated from ovariectomized rats was significantly lower than from those of normal controls; the secretory responses were improved after administration of oestradiol to ovariectomized rats. Cytosol receptors for progesterone and oestradiol were measured in a 105 000 g supernatant fraction of islets from normal, ovariectomized and oestrogen-treated ovariectomized rats. Progesterone-receptor binding was dramatically reduced after ovariectomy but was restored to normal levels by oestradiol treatment of the rats. Oestradiol-receptor binding was not significantly affected by ovariectomy but was increased several fold by oestrogen treatment of ovariectomized rats. These results suggest that islets of Langerhans contain receptors for both progesterone and oestradiol, and that this receptor population is subject to change. Progesterone--but not oestradiol--receptor measurements could be correlated with alterations in the rates of secretion of insulin from islets. Oestrogen administration in vivo had profound effects on subsequent insulin release from islets, though this may have been mediated by way of an increase in the quantity of the progesterone receptor.

Animals↗
PubMed1980

Effect of enkephalins and morphine on insulin secretion from isolated rat islets.

The direct effects of an enkephalin analogue, (D-Ala2/MePhe4/Met/(O)-o1) enkephalin (DAMME), on insulin release from isolated islets of Langerhans of the rat have been investigated. DAMME had a dose-dependent effect on insulin secretion: low concentrations (10(-10) to 10(-8) mol/l) were stimulatory while high concentrations (10(-5) mol/l) were inhibitory in the presence of 8 mmol/l glucose. Similar effects were found with met-enkephalin, and with the longer acting alanine substituted met-enkephalin. Morphine sulphate (5 X 10(-7) mol/l) also stimulated insulin release. The effects of enkephalin and morphine were blocked by the specific opiate antagonist naloxone hydrochloride (1.2 X 10(-6) mol/l). The insulin secretory response of perifused islets to enkephalins and morphine was rapid, corresponding to the first phase of glucose induced insulin release. These observations suggest that there may be opiate receptors in islets, and that opioid peptides could modulate insulin release.

Animals↗
PubMed1980

Synthesis and maturation of lambda receptor in Escherichia coli K-12: in vivo and in vitro expression of gene lamB under lac promoter control.

The lambda receptor is an outer membrane protein from Escherichia coli K-12 lamB, its structural gene, is part of the maltose regulon. We have cloned this gene in a phage so that it is under the control of the lac promoter. The phage was devised in such a way that it can infect lamB mutants and that chromosomal lamB mutations can be transferred to it. In vivo, the lambda receptor is expressed under lac promoter control and is exported normally to the outer membrane, independently of the expression of the other genes of the maltose regulon. In vitro, DNA of the phage allows efficient synthesis of the lamB product. The protein--or pre-lambda-receptor--made in vitro contains an NH2-terminal sequence of about 25 amino acids not found in the lambda receptor. We have detected no inactivation of phage lambda by the pre-lambda-receptor. Conversion of the pre-lambda-receptor to a form that has the apparent molecular weight of the mature lambda receptor was achieved. A lamB mutation that blocks export in vivo also blocks conversion in vitro.

Bacterial Proteins↗
PubMed1980

DNA sequence encoding the NH2-terminal peptide involved in transport of lambda receptor, an Escherichia coli secretory protein.

lamB encodes the lambda receptor of Escherichia coli, an outer membrane protein. We have identified the beginning of the lamB gene by correlating DNA nucleotide sequence with a partial sequence of the primary translation product of lamB. We show that lambda receptor is synthesized as a precursor containing an extra 25 amino acids at its NH2 terminus. These amino acids are predominately hydrophobic and probably comprise a structure required for initiation of transport of lambda receptor from the cytoplasm to the outer membrane.

Amino Acid Sequence↗
PubMed1980

Perimacular changes in Alport's syndrome.

From 1962 to 1977, 79 patients with Alport's syndrome underwent serial fundoscopic examination. In 29 patients (24 males, 5 females), symmetric bilateral perimacular changes were found, consisting of bright, whitish or yellowish dense granulations, surrounding the foveal area. Fluorescein angiography was normal in 8/8 studied cases. All 29 patients had bilateral lenticonus and neural hearing loss; ultrastructural lesion of glomerular basement membrane was present in 11/11 studied patients. Chronic renal failure developed in 26 patients, with 20 treated by maintenance hemodialysis. In contrast, perimacular lesions were absent in the other 50 patients (27 males, 23 females). Anterior lenticonus was detected in none; perceptive deafness was demonstrated in only 20; kidney ultrastructural lesions in 16 of 30 studied cases. Patients with perimacular changes had significantly earlier renal failure (P less than 0.001) than patients without. In conclusion, perimacular changes appear as a simple and reliable indicator of Alport's syndrome, often associated with early renal failure.

Adolescent↗