Sung Hee Um

TL;DR: It is reported that S6K1-deficient mice are protected against obesity owing to enhanced β-oxidation, however on a high fat diet, levels of glucose and free fatty acids still rise in S6k1- deficient mice, resulting in insulin receptor desensitization.

TL;DR: In this article, S6K1-deficient mice are protected against obesity owing to enhanced β-oxidation, but on a high fat diet, levels of glucose and free fatty acids still rise in S6k1-dependent mice, resulting in insulin receptor desensitization.

TL;DR: It is shown that mice deficient for S 6K1 or S6K2 are born at the expected Mendelian ratio, and analysis of S6 phosphorylation in the cytoplasm and nucleoli of cells derived from the distinct S7K genotypes suggests that both kinases are required for full S6osphorylation but that S6k2 may be more prevalent in contributing to this response.

TL;DR: Filtration of amino acids into humans leads to S6K1 activation, inhibition of insulin-induced class 1 PI3K activation, and insulin resistance, and S 6K1 may mediate deleterious effects, like insulin resistance and potentially type 2 diabetes in the face of nutrient excess.

TL;DR: The mTOR gene is disrupted and embryonic development of homozygous mTOR − / − mice appears to be arrested at E5.5; such embryos are severely runted and display an aberrant developmental phenotype, consistent with the inability to establish embryonic stem cells from mTOR +/ − embryos.