Effects of malnutrition on microvillus membrane glucose transport and physical properties.
We examined sodium-dependent glucose transport, membrane lipid composition, and membrane fluidity in microvillus membrane vesicles isolated from the distal intestine of infant rabbits subjected to protein-energy malnutrition and age-matched controls. In vesicles from malnourished animals, sodium-dependent glucose transport was significantly enhanced, as evidenced by a twofold increase in maximal transport capacity, Jmax. Carrier affinity for glucose, as assessed by the Km of the transport process, was unaffected. These alternations were associated with marked changes in microvillus membrane composition. Malnourished animals had an increase in the lipid-to-protein ratio of the microvillus membrane, which suggests that malnutrition might be associated with either a reduction in membrane protein or an increase in membrane lipid. This would be expected to increase the fluidity of the microvillus membrane. However, we observed no differences in either the static or dynamic component of membrane fluidity, using multiple fluorescent probes, between dietary groups. Further analysis of membrane lipids was undertaken to establish whether quantitative differences in lipid subclasses could explain this discrepancy. We found that nutrient deprivation produced numerous alterations in membrane lipids. The major findings were an increase in both the cholesterol-to-phospholipid and phosphatidylethanolamine-to-phosphatidylcholine ratios. Both alterations would be expected to decrease membrane fluidity and presumably represent a compensatory response to the loss of membrane protein. Thus chronic postnatal protein-energy malnutrition initiates several adaptive responses that include major alterations in the chemical composition of the microvillus membrane. The resulting effect preserves efficient glucose transport and maintains the physical properties of the microvillus membrane.
Butzner
J D
JD
Gastrointestinal Research Group, University of Calgary, Alberta, Canada.
Brockway
P D
PD
Meddings
J B
JB
D000818:Animals; D001693:Biological Transport, Active; D005947:Glucose / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism*; D007421:Intestine, Small / Q000378:metabolism; D007700:Kinetics; D008051:Lipid Bilayers / Q000378:metabolism; D008563:Membrane Lipids / Q000378:metabolism; D008871:Microvilli / Q000378:metabolism*; D010743:Phospholipids / Q000378:metabolism; D011502:Protein-Energy Malnutrition / Q000378:metabolism*; D011817:Rabbits; D012016:Reference Values
D008051:Lipid Bilayers; D008563:Membrane Lipids; D010743:Phospholipids; D005947:Glucose