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J Biol Chem. 2001 Apr 13;276(15):12162-8. Epub 2001 Jan 11.
Glucose and insulin stimulate heparin-releasable lipoprotein lipase activity in mouse islets and INS-1 cells. A potential link between insulin resistance and beta-cell dysfunction.

Cruz WS, Kwon G, Marshall CA, McDaniel ML, Semenkovich CF.

Departments of Medicine, Pathology and Immunology, and Cell Biology and Physiology and the Center for Cardiovascular Research, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

Lipoprotein lipase (LpL) provides tissues with triglyceride-derived fatty acids. Fatty acids affect beta-cell function, and LpL overexpression decreases insulin secretion in cell lines, but whether LpL is regulated in beta-cells is unknown. To test the hypothesis that glucose and insulin regulate LpL activity in beta-cells, we studied pancreatic islets and INS-1 cells. Acute exposure of beta-cells to physiological concentrations of glucose stimulated both total cellular LpL activity and heparin-releasable LpL activity. Glucose had no effect on total LpL protein mass but instead promoted the appearance of LpL protein in a heparin-releasable fraction, suggesting that glucose stimulates the translocation of LpL from intracellular to extracellular sites in beta-cells. The induction of heparin-releasable LpL activity was unaffected by treatment with diazoxide, an inhibitor of insulin exocytosis that does not alter glucose metabolism but was blocked by conditions that inhibit glucose metabolism. In vitro hyperinsulinemia had no effect on LpL activity in the presence of low concentrations of glucose but increased LpL activity in the presence of 20 mm glucose. Using dual-laser confocal microscopy, we detected intracellular LpL in vesicles distinct from those containing insulin. LpL was also detected at the cell surface and was displaced from this site by heparin in dispersed islets and INS-1 cells. These results show that glucose metabolism controls the trafficking of LpL activity in beta-cells independent of insulin secretion. They suggest that hyperglycemia and hyperinsulinemia associated with insulin resistance may contribute to progressive beta-cell dysfunction by increasing LpL-mediated delivery of lipid to islets.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11154699&dopt=Abstract

Int J Syst Evol Microbiol. 2000 Nov;50 Pt 6:2135-9.
Pseudomonas antimicrobica Attafuah and Bradbury 1990 is a junior synonym of Burkholderia gladioli (Severini 1913) Yabuuchi et al. 1993.

Coenye T, Gillis M, Vandamme P.

Laboratory of Microbiology, Universiteit Gent, Ghent, Belgium. tom.coenyug.ac.be

Comparison of the 16S rDNA sequence of Pseudomonas antimicrobica LMG 18920T with published 16S rDNA sequences from other pseudomonads indicated that Pseudomonas antimicrobica belongs to the genus Burkholderia, with Burkholderia gladioli, Burkholderia glumae and Burkholderia plantarii as its closest neighbours. DNA-DNA hybridizations confirmed that Pseudomonas antimicrobica and Burkholderia gladioli represent the same species. Strain LMG 18920T and other Burkholderia gladioli strains were also indistinguishable by SDS-PAGE of whole-cell proteins and had similar biochemical characteristics. The whole-cell fatty acid composition, however, was different from that of other Burkholderia gladioli strains. It is concluded that Pseudomonas antimicrobica is a later synonym of Burkholderia gladioli. As Burkholderia gladioli is known to cause infections in patients with cystic fibrosis and chronic granulomatous disease, the eventual use of strain LMG 18920T as a biological control agent should be approached with caution.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11155989&dopt=Abstract

Int J Syst Evol Microbiol. 2000 Nov;50 Pt 6:2173-80.
Rhodococcus pyridinivorans sp. nov., a pyridine-degrading bacterium.

Yoon JH, Kang SS, Cho YG, Lee ST, Kho YH, Kim CJ, Park YH.

Korea Research Institute of Bioscience and Biotechnology, Yusong, Taejon.

The taxonomic position of a bacterial strain (PDB9T) that is capable of degrading pyridine was clarified by a polyphasic taxonomic approach using phenotypic, chemotaxonomic and genetic methods. The cells, which are rods and branched filaments during the early growth phase, fragment into short rods or cocci, thereby completing the growth cycle. Strain PDB9T was found to have a cell wall of chemotype IV, MK-8(H2) as the predominant menaquinone, mycolic acids with 36-46 carbon atoms and C16:0' C18:1 cis9, 10-methyl-C18:0 (TBSA) as the major fatty acids. The G+C content of the DNA was 66 mol%. The phylogenetic tree showed that strain PDB9T falls within an evolutionary radiation comprising Rhodococcus species and is most closely related to the type strain of Rhodococcus rhodochrous, sharing 99% 16S rDNA similarity. The differences in some phenotypic characteristics and the genetic distinctiveness distinguish strain PDB9T from the Rhodococcus species described previously. Therefore, strain PDB9T should be placed in the genus Rhodococcus as a new species, for which the new name Rhodococcus pyridinivorans sp. nov. is proposed. The type strain of the new species is strain PDB9T (= KCTC 0647BPT = KCCM 80005T).

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11155994&dopt=Abstract

Int J Syst Evol Microbiol. 2000 Nov;50 Pt 6:2189-95.
Dysgonomonas gen. nov. to accommodate Dysgonomonas gadei sp. nov., an organism isolated from a human gall bladder, and Dysgonomonas capnocytophagoides (formerly CDC group DF-3).

Hofstad T, Olsen I, Eribe ER, Falsen E, Collins MD, Lawson PA.

Department of Microbiology and Immunology, University of Bergen, The Gade Institute, Norway.

Results of a polyphasic taxonomic study on an unknown Gram-negative, facultatively anaerobic, coccobacillus-shaped organism isolated from an infected human gall bladder are presented. Phenotypic and molecular taxonomic studies revealed the organism to be close to, but distinct from, organisms designated CDC (Centers for Disease Control and Prevention) group DF-3. The unknown bacterium was readily distinguished from reference strains of Bacteroides, Prevotella, Porphyromonas and related taxa by 16S rRNA gene sequencing, biochemical tests, analysis of cellular long-chain fatty acids and electrophoretic analysis of whole-cell proteins. Based on the results of the present study, it is proposed that the unknown bacterium be classified in a new genus, Dysgonomonas, as Dysgonomonas gadei sp. nov. (type strain CCUG 42882T = CIP 106420T). In addition, a new species, Dysgonomonas capnocytophagoides sp. nov., is proposed to accommodate strains previously belonging to CDC group DF-3. The type species of the genus Dysgonomonas is Dysgonomonas gadei.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11155996&dopt=Abstract

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