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  • 1
    Publication Date: 2011-08-24
    Description: Representatives of the family Methanosarcinaceae were analyzed phylogenetically by comparing partial sequences of their methyl-coenzyme M reductase (mcrI) genes. A 490-bp fragment from the A subunit of the gene was selected, amplified by the PCR, cloned, and sequenced for each of 25 strains belonging to the Methanosarcinaceae. The sequences obtained were aligned with the corresponding portions of five previously published sequences, and all of the sequences were compared to determine phylogenetic distances by Fitch distance matrix methods. We prepared analogous trees based on 16S rRNA sequences; these trees corresponded closely to the mcrI trees, although the mcrI sequences of pairs of organisms had 3.01 +/- 0.541 times more changes than the respective pairs of 16S rRNA sequences, suggesting that the mcrI fragment evolved about three times more rapidly than the 16S rRNA gene. The qualitative similarity of the mcrI and 16S rRNA trees suggests that transfer of genetic information between dissimilar organisms has not significantly affected these sequences, although we found inconsistencies between some mcrI distances that we measured and and previously published DNA reassociation data. It is unlikely that multiple mcrI isogenes were present in the organisms that we examined, because we found no major discrepancies in multiple determinations of mcrI sequences from the same organism. Our primers for the PCR also match analogous sites in the previously published mcrII sequences, but all of the sequences that we obtained from members of the Methanosarcinaceae were more closely related to mcrI sequences than to mcrII sequences, suggesting that members of the Methanosarcinaceae do not have distinct mcrII genes.
    Keywords: Exobiology
    Type: International journal of systematic bacteriology (ISSN 0020-7713); Volume 45; 3; 554-9
    Format: text
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European journal of nutrition 23 (1984), S. 181-205 
    ISSN: 1436-6215
    Keywords: Coffein ; Glukoneogenese ; Lipolyse ; Diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Medicine
    Description / Table of Contents: Summary The metabolic actions of coffeine were investigated in the rat (90 mg/kg bw coffeine intravenously during 3 hours) and in human volunteers (35 mg/kg bw coffeine orally) in the fasting state. Additionally, the effects of coffeine were measured during simultaneous intravenous glucose infusion (0.25 mg/kg bw/h during 6 hours in humans and 1.8 mg/kg bw/h during 3 hours in the rat). In the fasting rat, intravenous coffeine caused an increase in the serum concentrations of glucose, urea, insulin, and free fatty acids, whereas a decrease in glucoplastic amino acids was found. As the liver glycogen concentration was not altered, the increase in blood glucose should be due to an increase in glyconeogenesis. During simultaneous application of carbohydrates and coffeine, the increases in the concentration of blood glucose and serum insulin were intensified, whereas the serum concentrations of lactate and urea as well as hepatic glycogen were not altered. In fasting male volunteers coffeine caused an increase in the concentrations of blood glucose, cortisol, insulin, free fatty acids, free glycerol and ketone bodies. During intravenous glucose infusion, coffeine intensified the decrease in serum phosphate induced by carbohydrates. Neither in volunteers nor in the experimental animal, an alteration in the concentrations of cholesterol or serum triglycerides or serum uric acid was effected by coffeine. It is concluded that high dosed coffeine causes peripheral insulin resistance in the human being as well as in the experimental animal. This peripheral insulin resistance is shown by the simultaneous large increases in concentrations of serum insulin, blood glucose and concentration of free fatty acids. In this situation insulin obviously is not able to inhibit lipolysis or gluconeogenesis nor to increase peripheral glucose utilisation. These metabolic effects of coffeine show some similarities to the metabolic situation in diabetes mellitus type 2 (Non Insulin Dependent Diabetes mellitus).
    Notes: Zusammenfassung Die Stoffwechselwirkungen von Coffein wurden an Ratten (ca. 90 mg/kg Körpergewicht/h Coffein i.v. über 3 h) und an stoffwechselgesunden Versuchspersonen (ca. 25 mg/kg KG oral) im nüchternen Zustand untersucht. Außerdem wurden die Coffeinwirkungen während gleichzeitiger intravenöser Glukoseapplikation (0,25 g/ kg KG/h über 6 h beim Menschen bzw. ca. 1,8 g/kg KG/h über 3 h bei Ratten) beobachtet. Bei nüchternen Ratten wurde nach intravenöser Coffeinapplikation ein Anstieg der Konzentration von Glukose, Harnstoff, Insulin und von Freien Fettsäuren im Serum ermittelt. Gleichzeitig sanken die Konzentrationen der meisten glukoplastischen Aminosäuren im Serum ab. Der Leberglykogengehalt zeigte keine Veränderungen, daher muß die Glukoneogenese als Ursache des Blutzuckeranstieges angesehen werden. Bei gleichzeitiger Applikation von Kohlenhydraten und Coffein kam es bei Ratten zu einem verstärkten Ansteigen der Konzentrationen von Blutzucker und von Seruminsulin, während die Serumspiegel des Laktats und des Harnstoffes sowie die Leberglykogenkonzentration keine Veränderungen aufwiesen. Bei nüchternen Versuchspersonen wurde nach Coffeinverabreichung ein signifikanter Anstieg der Konzentrationen von Glukose, Cortisol, Freien Fettsäuren, Freiem Glycerin und von Ketonkörpern im Serum bzw. Blut beobachtet. Während der Glukoseinfusion konnte beim Menschen nach Coffeingabe ein verstärkter Anstieg der Konzentration des Blutzuckers und des Seruminsulins ermittelt werden. Durch Coffein wurde außerdem das kohlenhydratinduzierte Absinken des anorganischen Phosphats im Serum bei Mensch und Ratte verstärkt. Weder bei freiwilligen Versuchspersonen noch bei Ratten konnte ein Einfluß des Coffeins auf die Serumtriglyceride, das Serumcholesterin oder die Serumharnsäure festgestellt werden. Es wird gefolgert, daß Coffein in hoher Dosierung bei Versuchspersonen und bei Versuchstieren eine periphere Insulinresistenz bewirkt. Diese periphere Insulinresistenz durch Coffein drückt sich darin aus, daß trotz erheblichen Anstieges der Seruminsulinkonzentration gleichzeitig auch die Konzentration von Glukose und von Freien Fettsäuren erhöht ist. Insulin ist in dieser Situation nicht imstande, die Lipolyse und die Glukoneogenese zu hemmen oder die periphere Glukoseverwertung zu steigern. Diese Coffeineffekte ähneln formal der Stoffwechselsituation beim Erwachsenendiabetes (Typ II).
    Type of Medium: Electronic Resource
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