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Sci. STKE, 9 January 2001
Vol. 2001, Issue 64, p. tw8
[DOI: 10.1126/stke.2001.64.tw8]

EDITORS' CHOICE

Cell Biology Decreased Insulin Output in S6K1 Deficiency

Insulin regulates blood glucose levels by stimulating glucose uptake into cells. Pende et al. studied S6 kinase 1 (S6K1)-deficient mice and uncovered a role for S6K1 in glucose homeostasis. s6k1-/- mice exhibited a normal time course of induced insulin secretion; however, the amount of insulin released per cell was decreased, leading to decreased concentrations of circulating insulin. After glucose injection, S6K1-deficient mice were unable to clear the glucose dose quickly; however, this was not a result of insulin resistance, because S6K1-deficient mice treated with insulin were able to clear the injected glucose at a normal rate. Although pancreases from s6k1-/- mice were of normal mass and size, the number of insulin-producing β-cells was decreased, suggesting that decreased insulin secretion resulted from having fewer β-cells. S6K1 deficiency, however, did not directly mediate insulin insufficiency, because previous reports have suggested that treatment of islet cells with an S6K1-specific inhibitor has no effect on insulin secretion. Although other organs and cell types in S6K1-deficient mice were of normal size, β-cells were approximately 75% normal size. Thus, the data indicate that hyperglycemia in s6k1-/- mice is most likely due to reduced β-cell size and number.

Pende, M., Kozma, S.C., Jaquet, M., Oorschot, V., Burcelin, R., Le Marchand-Brustel, Y., Klumperman, J., Thorens, B., and Thomas, G. (2000) Hypoinsulinaemia, glucose intolerance and diminished β-cell size in S6K1-deficient mice. Nature 408: 994-997. [Online Journal]

Citation: Decreased Insulin Output in S6K1 Deficiency. Sci. STKE 2001, tw8 (2001).


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