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Stephan Herzig

Researcher at Heidelberg University

Publications -  176
Citations -  10185

Stephan Herzig is an academic researcher from Heidelberg University. The author has contributed to research in topics: Adipose tissue & Insulin resistance. The author has an hindex of 44, co-authored 155 publications receiving 8461 citations. Previous affiliations of Stephan Herzig include Technische Universität München & Salk Institute for Biological Studies.

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CREB regulates hepatic gluconeogenesis through the coactivator PGC-1

TL;DR: Fasting hyperglycaemia* is strongly correlated with type II diabetes, so the results suggest that the activation of PGC-1 by CREB in liver contributes importantly to the pathogenesis of this disease.
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TRB3: A tribbles Homolog That Inhibits Akt/PKB Activation by Insulin in Liver

TL;DR: It is shown that TRB3, a mammalian homolog of Drosophila tribbles, functions as a negative modulator of Akt, which contributes to insulin resistance in individuals with susceptibility to type II diabetes.
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PGC-1 promotes insulin resistance in liver through PPAR-α-dependent induction of TRB-3

TL;DR: It is shown that, in the liver, TRB-3 is a target for PPAR-α, a fasting-inducible inhibitor of the serine-threonine kinase Akt/PKB, which indicates a link between nuclear hormone receptor and insulin signaling pathways, and suggest a potential role for TRb-3 inhibitors in the treatment of type 2 diabetes.
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Glucocorticoids, metabolism and metabolic diseases

TL;DR: This review focuses on the role of the GC-GR axis for metabolic homeostasis and dysregulation, emphasizing tissue-specific functions of GCs in the control of energy metabolism.
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Cyclooxygenase-2 Controls Energy Homeostasis in Mice by de Novo Recruitment of Brown Adipocytes

TL;DR: Studying mouse models, it is shown that cyclooxygenase (COX)–2, a rate-limiting enzyme in prostaglandin (PG) synthesis, is a downstream effector of β-adrenergic signaling in WAT and is required for the induction of BAT in Wat depots, which suggests that the PG pathway regulates systemic energy homeostasis.