Sidney A Jones | PubMed Health

PubMed2003

Triiodothyronine is a survival factor for developing oligodendrocytes.

Thyroid hormone plays an important role in oligodendrocyte development. The studies presented here suggest that thyroid hormone is required for oligodendrocyte survival during development. Oligodendrocyte precursor cells, astrocytes and microglia were cultured in a defined media. Oligodendrocyte precursor cell differentiation was induced by growth factor removal. Time course studies revealed that oligodendrocytes cultured in the presence or absence of triiodothyronine (T3) develop similarly during the first 3 days of development. Oligodendrocytes cultured in the absence of T3, however, die after developmental day 3. TdT-Mediated dUDP Nick End Labeling assay and Hoechst staining indicate that T3 rescues developing oligodendrocytes from death by apoptosis. Apoptosis is likely induced by the presence of the cytokines TNFalpha and IL-1beta. However, expression of these cytokines is not altered by thyroid hormone administration. Thus, thyroid hormone has been demonstrated to effect proliferation, myelin gene expression and now the survival of developing oligodendrocytes.

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PubMed2002

A fasting-induced decrease in plasma glucose concentration does not affect the insulin response to ingested protein in people with type 2 diabetes.

We previously have reported that protein, on a weight basis, is just as potent as glucose in increasing the insulin concentration in people with type 2 diabetes. In people without diabetes, protein is only approximately 30% as potent as glucose in this regard. In the present study, we tested the hypothesis that the increased insulin responsiveness to protein in people with type 2 diabetes is due to the elevated plasma glucose concentration in these individuals. Seven male subjects with untreated type 2 diabetes were given 50 g protein in the form of very lean beef at 8 AM after an overnight fast. On another occasion, the same individuals were fasted for an additional 24 hours to lower their plasma glucose concentration to near the normal reference range. They were then given 50 g protein. The 8 AM glucose concentration was lower after 24 hours of additional fasting, as expected. After ingestion of the protein meal, there was an unexpected, modest increase in glucose concentration after an additional 24 hours of fasting that was not observed with only an overnight fast. Despite the approximately 15% lower plasma glucose concentration at the time of the protein meal, the insulin responses were nearly identical. Thus, the greater insulin response to ingested protein is not likely to be due merely to a higher initial glucose concentration.

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