Disaccharidasenaktivität und Monosaccharidabsorption bei genetisch adipösen Mäusen

Abstract

Bei genetisch adipösen Mäusen und ihren normalgewichtigen Geschwistern wurden die Galaktoseabsorption in vitro und die Disaccharidasen-Aktivität des Dünndarms untersucht. Während zwischen beiden Gruppen keine Unterschiede in der Galaktose-Absorption bestanden, waren die Disaccharidasen Maltase, Isomaltase und Saccharase bei genetisch adipösen Mäusen signifikant erhöht. Disaccharidase activity and monosaccharide absorption in genetically adipose miceThe absorption of galactose in vitro and the disaccharidase activity of the small intestine were measured in genetically adipose mice and in their siblings of normal weight. There were no differences in galactose absorption between the two groups, but maltase, isomaltase and sucrase were significantly higher in the genetically adipose mice.1949 trat im Jackson Memorial Laboratory in Bar Harbor/USA spontan eine autosomal rezessiv sich vererbende Mutante der Hausmaus auf, die sich durch eine Hyperglykämie und durch eine im Alter von 4-6 Wochen bereits erkennbare, stetig zunehmende Fettsucht auszeichnete (1). Die seither aufgedeckten Stoffwechselabweichungen dieser genetisch adipösen, hyperglykämischen Mäuse sind von MAYER (2, 3) zusammengestellt worden. Als Teilursache für die Progredienz der Adipositas wird die Inaktivität der Tiere angeschuldigt (4). Es ist außerdem über eine gesteigerte GlucoseAbsorption berichtet worden (5). In der vorliegenden Arbeit werden die beiden wichtigsten Schritte der Kohlenhydrataufnahme vom Darm in das Blut -die Spaltung der Disaccharide und die Monosaccharidabsorption -durch Bestimmung der Disaccharidasenaktivität und der Galaktoseabsorption bei genetisch adipösen Mäusen untersucht.

MONOSACCHARIDE TRANSPORT BY THE SMALL INTESTINE OF LEAN AND GENETICALLY OBESE (ob/ob) MICE

“…4) provided little indication of an effect of the (ob/ob) genotype on transport expressed per gram dry weight of tissue, and since the dry weight of tissue per unit DNA is similar in 10-week-old lean and obese mice (Table 1) there would seem to be no effect of genotype on transport per epithelial cell (changes in total mucosal DNA reflect changes in villus epithelial cell population in 10-week-old mice, A. P. Morton, unpublished work). von Grimmel et al (1970) also found no effect of genotype on the influx of a single concentration of galactose (55 mM) across the brush border, and in the severely hyperglycaemic (db/db) mouse the kinetics of monosaccharide influx, expressed per millilitre of tissue water are similar to lean controls (Ramaswamy et al 1979). By contrast, Bihler & Freund (1975) found Vmax expressed per millilitre of tissue water substantially elevated in 8-to 12-week-old obese mice compared with lean controls.…”

“…The aim of this work was to establish the nature of the adaptation of monosaccharide transport and to determine whether transport of monosaccharides exhibited a pattern of adaptation similar to that shown by the size of the intestine. Previous measurements of monosaccharide transport by the obese mouse intestine (Binder, Herskovic, Spiro & Spencer, 1966;von Grimmel, Rakow, Rommel, Lacher & Burkhardt, 1970;Bihler & Freund, 1975) did not examine the effect of the development of the syndrome on monosaccharide transport and produced differing conclusions as to the nature of the adaptation.…”

Sugar transport in the small intestine of obese hyperglycemic, fed and fasted mice

“…They concluded that increased carbohydrate absorption in these animals is an adaptive phenomenon related to hyperphagia but this is not supported by their observation that chronic underfeeding of ob/ob mice did not cause a significant decrease in glucose absorption. More recently, Grimmel et al [29] reported that the activity of several disaccharidases was increased in ob/ob mice but that galactose transport in vitro was not significantly greater than in the lean littermates. The galactose concentration used in their study, 55.5 mM, was so high, however, that any changes in the specific active sugar transport system could have been overshadowed by large diffusional fluxes, osmotic changes, etc.…”

“…It is well established that there is a time lag of several days between the induction of diabetes and the increase in sugar transport. At the same time, a number of other changes in intestinal function become apparent, such as an increase in the transport of amino acids [32], bile acids [33] and sodium [11], as well as in the activity of the brush border disaccharidases, maltase, isomaltase and sucrase [29,[34][35][36][37]. There is also a similar lag between the administration of insulin in vivo and the reversal of this effect.…”