Title

Reflecting On Macos: Why It Failed And What We Can Learn From Its Demise

Keywords

Autophagy; Brown adipose tissue; Epinephrine; Fasting; Metabolism; Steatosis

Abstract

Epinephrine is one of the major hormones involved in glucose counter-regulation and gluconeogenesis. However, little is known about its importance in energy homeostasis during fasting. Our objective is to study the specific role of epinephrine in glucose and lipid metabolism during starvation. In our experiment, we subject regular mice and epinephrine-deficient mice to a 48-h fast then we evaluate the different metabolic responses to fasting. Our results show that epinephrine is not required for glucose counter-regulation: epinephrine-deficient mice maintain their blood glucose at normal fasting levels via glycogenolysis and gluconeogenesis, with normal fasting-induced changes in the peroxisomal activators: peroxisome proliferator activated receptor γ coactivator α (PGC-1α), fibroblast growth factor 21 (FGF-21), peroxisome proliferator activated receptor α (PPAR-α), and sterol regulatory element binding protein (SREBP-1c). However, fasted epinephrine-deficient mice develop severe ketosis and hepatic steatosis, with evidence for inhibition of hepatic autophagy, a process that normally provides essential energy via degradation of hepatic triglycerides during starvation. We conclude that, during fasting, epinephrine is not required for glucose homeostasis, lipolysis or ketogenesis. Epinephrine may have an essential role in lipid handling, possibly via an autophagy-dependent mechanism. © 2012 Elsevier Ltd.

Publication Date

6-1-2012

Publication Title

Paedagogica Historica

Volume

48

Issue

6

Number of Pages

469-484

Document Type

Article

Personal Identifier

scopus

DOI Link

https://doi.org/10.1080/00309230.2011.554423

Socpus ID

84863470231 (Scopus)

Source API URL

https://api.elsevier.com/content/abstract/scopus_id/84863470231

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