Related Experiment Videos
Insulin alters cell proliferation during the early development of rodent kidney
1Département d'anatomie et de biologie cellulaire, Université de Sherbrooke, Québec, Canada.
Abstract:
The effects of insulin on early differentiated 15-day fetal mouse kidneys were assessed using an organotypic culture system. High concentrations (30 to 125 mU/ml) of the hormone drastically reduced (50%) the incorporation of 3H-thymidine in replicating cells without affecting either differentiation of forming nephrons or epithelio-mesenchymal relationships. When compared to insulin-like growth factor-I or the potent phorbol ester PMA, the action of insulin seemed to specifically deregulate some components of the transductional machinery controlling cell proliferation. This is opposed to the previous demonstration of a positive influence of insulin on cell proliferation in the human fetal kidney. The results suggest that the common definition of insulin as a fetal growth promoter may depend on the developmental stage of each organ, particularly for the mammalian kidney.
Insights
High insulin concentrations inhibit fetal mouse kidney cell proliferation. This suggests insulin
Area of Science:
- Developmental Biology
- Nephrology
- Endocrinology
Background:
- Insulin is generally considered a fetal growth promoter.
- Previous studies indicated insulin positively influences human fetal kidney cell proliferation.
- The specific effects of insulin on early mammalian kidney development require further investigation.
Purpose of the Study:
- To investigate the impact of insulin on early differentiated fetal mouse kidney cells.
- To determine if insulin affects cell proliferation, differentiation, or epithelio-mesenchymal relationships in developing kidneys.
- To compare insulin's effects with insulin-like growth factor-I and phorbol ester PMA.
Main Methods:
- Organotypic culture system used to study 15-day fetal mouse kidneys.
- Assessment of 3H-thymidine incorporation to measure cell proliferation.
- Evaluation of nephron differentiation and epithelio-mesenchymal relationships.
Main Results:
- High insulin concentrations (30-125 mU/ml) significantly reduced 3H-thymidine incorporation by 50% in replicating cells.
- Insulin did not affect nephron differentiation or epithelio-mesenchymal relationships.
- Insulin's action appeared to specifically deregulate components of the cell proliferation transductional machinery, unlike insulin-like growth factor-I or PMA.
Conclusions:
- Insulin can inhibit cell proliferation in the early differentiated fetal mouse kidney.
- The role of insulin as a fetal growth promoter may be organ- and developmental stage-dependent.
- These findings contrast with previous observations in human fetal kidney development.