subject: BCKDH
involved in the metabolism of leucine. Insulin release is stimulated by Glucose
in high levels. Leucine and Alanine also work on Increasing Insulin release by
Increasing activity of BCKDH in the presence of GLUTAMINE. Glutamine is
metabolized to Glutamate (not a secretagogue) via its DEAMINATION Glutamate
Dehydrgenase. Glucose diminishes the leucine activity by diminshing the BCKDH
enzymes' production(dec. the mRNA)
object_opposite: BCKDH = Branched Chain Dehydrogenase. Hyperinsulinemia, which potentially could result from the combined glucose and leucine/glutamine insulin release. Malate is not a secretagouge. Alanine is
misc: bit.ly/1AF2yIr University of Wisconsin
author_year: Micheal MacDonald/91 Deborah McKenie
journal_volume_page: Journal of Biologic Chemistry(266)/1335-40
object_opposite: BCKDH = Branched Chain Dehydrogenase. Hyperinsulinemia, which potentially could result from the combined glucose and leucine/glutamine insulin release. Malate is not a secretagouge. Alanine is
misc: bit.ly/1AF2yIr University of Wisconsin
author_year: Micheal MacDonald/91 Deborah McKenie
journal_volume_page: Journal of Biologic Chemistry(266)/1335-40
Search mTOR
subject: Trained immunity is secondary
to Histone modification.The biochemical characterizations of the β-glucan–trained
monocytes revealed elevated aerobic glycolysis with increased glucose
consumption and lactate production, and higher intracellular ratio of
nicotinamide adenine dinucleotide (NAD+) to its reduced form (NADH). The
dectin-1–Akt–mTOR–HIF-1α pathway (mTOR, mammalian target of rapamycin; HIF-1α,
hypoxia-inducible factor–1α) was responsible for the metabolic shift induced by
β-glucan
object_opposite: reduced basal respiration rate, increased glucose consumption and lactate production, and higher intracellular ratio of nicotinamide adenine dinucleotide (NAD+) to its reduced form (NADH). Note that blockage of the pathway blocked the trained memory
misc: Trained memory. The dectin-1–Akt–mTOR–HIF-1α pathway (mTOR, mammalian target of rapamycin; HIF-1α, hypoxia-inducible factor–1α) was responsible for the metabolic shift induced by β-glucan
author_year: http://bit.ly/1CE0Rcj
journal_volume_page: http://bit.ly/1CE0Rcj
object_opposite: reduced basal respiration rate, increased glucose consumption and lactate production, and higher intracellular ratio of nicotinamide adenine dinucleotide (NAD+) to its reduced form (NADH). Note that blockage of the pathway blocked the trained memory
misc: Trained memory. The dectin-1–Akt–mTOR–HIF-1α pathway (mTOR, mammalian target of rapamycin; HIF-1α, hypoxia-inducible factor–1α) was responsible for the metabolic shift induced by β-glucan
author_year: http://bit.ly/1CE0Rcj
journal_volume_page: http://bit.ly/1CE0Rcj
Search : regulation of T-cell differentiation
subject: Mammalian target of rapamycin
(mTOR), article mTOR, metabolism, and the regulation of T-cell differentiation
and function
object_opposite:
misc: Involved in TH1 / TH2 differentiation
author_year: Adam T. Waickman and Jonathan D. Powell*/12
journal_volume_page: Immunological Reviews Metabolism and Autophagy in the Immune System Volume 249, Issue 1, pages 43–58, September 20TH1 TH2 differentiatin
object_opposite:
misc: Involved in TH1 / TH2 differentiation
author_year: Adam T. Waickman and Jonathan D. Powell*/12
journal_volume_page: Immunological Reviews Metabolism and Autophagy in the Immune System Volume 249, Issue 1, pages 43–58, September 20


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