Year: 2013
Type: article
Abstract: A new report in this issue of Diabetes providesevidence that at least some metabolic actions ofglucagon may be mediated by fibroblast growthfactor 21 (FGF21). Habegger et al. (1) report that native glucagon raises plasma FGF21 levels in human subjects, confirming the report by Arafat et al. (2). They also find that a synthetic glucagon receptor agonist (IUB288) upregulates FGF21 expression in isolated pri-mary hepatocytes from wild-type, but not glucagon receptor–null, mice. Moreover, the new report shows that IUB288-induced effects to curb diet-induced obesity are absent in mice lacking FGF21. The authors conclude that glucagon controls glucose levels, energy, and lipid me-tabolism, at least in part, via FGF21-dependent pathways. This may constitute an important step forward in our un-derstanding of both glucagon and FGF21 biology. As the authors recognize, many unanswered questions remain. First and foremost is whether the long-acting
Source: Diabetes
DOI: 10.2337/db12-1840
Authors: Eric D. Berglund, Roger H. Unger
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: hybrid
OpenAlex ID: W2102017665