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Maternal protein deficiency affects mesenchymal stem cell activity in the developing offspring.
Richard O C Oreffo1, Benjamin Lashbrooke, Helmtrud I Roach
1University Orthopaedics, Bone and Joint Research Group, University of Southampton, General Hospital, SO16 6YD Southampton, UK. roco@soton.ac.uk
Bone
|August 16, 2003
Summary
Maternal protein restriction in rats delays bone development by altering mesenchymal stem cell function, potentially programming later-life osteoporosis. Offspring showed reduced colony formation and delayed differentiation, with later catch-up growth.
Area of Science:
- Bone Biology
- Developmental Programming
- Stem Cell Research
Background:
- Environmental factors, including maternal nutrition, influence skeletal growth trajectories.
- The precise cellular mechanisms underlying skeletal growth programming by early life nutrition remain unclear.
Purpose of the Study:
- To investigate the impact of maternal protein insufficiency on bone marrow stromal cell (mesenchymal stem cell) function in rat offspring.
- To determine if offspring's bone cell colony formation, proliferation, and differentiation are altered by maternal diet.
- To assess the response of these cells to growth hormone (GH), 1,25(OH)2D3, and IGF-1.
Main Methods:
- A rat model using dams fed either a normal (18% casein) or low (9% casein) protein diet during gestation.
- Offspring were fed a normal protein diet postnatally and harvested at 8, 12, and 16 weeks.
- Analysis of colony-forming unit-fibroblastic (CFU-F) numbers, alkaline phosphatase activity, and osteoblast proliferation/differentiation.
Main Results:
- At 8 weeks, offspring of protein-restricted dams showed significantly reduced CFU-F and alkaline phosphatase-positive CFU-F.
- Osteoblast proliferation and differentiation responses to IGF-1 and GH were modulated differently between control and low-protein groups at specific time points.
- Alkaline phosphatase specific activity was decreased at 8 weeks but increased at 12 and 16 weeks in the low-protein group, indicating delayed development and subsequent catch-up.
Conclusions:
- Maternal protein restriction during pregnancy delays the normal proliferation and differentiation of mesenchymal stem cells in offspring.
- These early-life alterations in stem cell function may represent a mechanism for programming osteoporosis and related skeletal issues later in life.
- A 'catch-up' growth or physiological shift in bone cell activity occurs with skeletal maturity in offspring exposed to maternal protein deficiency.