-
Vol 62, August 2022 - current issue
-
Vol 27, September 2019
-
Vol 26, August 2019
-
Vol 25, July 2019
-
Vol 24, June 2019
-
Vol 23, May 2019
-
Vol 22, April 2019
-
Vol 21, March 2019
-
Vol 20, February 2019
-
Vol 19, January 2019
-
Vol 18, December 2018
-
Vol 17, November 2018
-
Vol 16, October 2018
-
Vol 15, September 2018
-
Vol 14, August 2018
-
Vol 13, July 2018
-
Vol 12, June 2018
-
Vol 11, May 2018
-
Vol 10, April 2018
-
Vol 9, March 2018
-
Vol 8, February 2018
-
Vol 7, January 2018
-
Vol 6 No 12, December 2017
-
Vol 6 No 11, November 2017
-
Vol 6 No 10, October 2017
-
Vol 6 No 9, September 2017
-
Vol 6 No 8, August 2017
-
Vol 6 No 7, July 2017
-
Vol 6 No 6, June 2017
-
Vol 6 No 5, May 2017
-
Vol 6 No 4, April 2017
-
Vol 6 No 3, March 2017
-
Vol 6 No 2, February 2017
-
Vol 6 No 1, January 2017
-
Vol 5 No 12, December 2016
-
Vol 5 No 11, November 2016
-
Vol 5 No 10, October 2016
-
Vol 5 No 9, September 2016
-
Vol 5 No 8, August 2016
-
Vol 5 No 7, July 2016
-
Vol 5 No 6, June 2016
-
Vol 5 No 5, May 2016
-
Vol 5 No 4, April 2016
-
Vol 5 No 3, March 2016
-
Vol 5 No 2, February 2016
-
Vol 5 No 1, January 2016
-
Vol 4 No 12, December 2015
-
Vol 4 No 11, November 2015
-
Vol 4 No 10, October 2015
Cover Story Current Issue

Non-alcoholic fatty liver disease (NAFLD) encompasses a set of pathologies associated with ectopic lipid accumulationin hepatocytes. NAFLD can progress to non-alcoholic steatohepatitis (NASH), an inflammatory condition which is increasing in prevalence in parallel with other diseases connected to lipid metabolism, such as type 2 diabetes and cardiovascular disease. NASH is characterized by hepatic necrosis, increased inflammatory signaling, immune cell infiltration, and the potential to progress to fibrosis, cirrhosis, hepatocellular carcinoma, and ultimately liver failure.
David Montefusco, Maryam Jamil, Melissa A. Maczis, William Schroeder, ... L. Ashley Cowart
Current Issue
FGF2 disruption enhances thermogenesis in brown and beige fat to protect against adiposity and hepatic steatosis

Objective
Fibroblast growth factor 2 (FGF2) has been reported to play divergent roles in white adipogenic differentiation, however, whether it regulates thermogenesis of fat tissues remains largely unknown. We therefore aimed to investigate the effect of FGF2 on fat thermogenesis and elucidate the underlying mechanisms.
Methods
FGF2-KO and wild-type (WT) mice were fed with chow diet and high-fat diet (HFD) for 14 weeks. The brown and white fat mass, thermogenic capability, respiratory exchange ratio, and hepatic fat deposition were determined. In vitroexperiments were conducted to compare the thermogenic ability of FGF2-KO- with WT-derived brown and white adipocytes. Exogenous FGF2 was supplemented to in vitro-cultured WT brown and ISO-induced beige adipocytes. The FGFR inhibitor, PPARγ agonist, and PGC-1α expression lentivirus were used with the aid of technologies including Co-IP, ChIP, and luciferase reporter assay to elucidate the mechanisms underlying the FGF2 regulation of thermogenesis.
Results
FGF2 gene disruption results in increased thermogenic capability in both brown and beige fat, supporting by increased UCP1 expression, enhanced respiratory exchange ratio, and elevated thermogenic potential in response to cold exposure. Thus, the deletion of FGF2 protects mice from high fat-induced adiposity and hepatic steatosis. Mechanistically, in vitroinvestigations indicated FGF2 acts in autocrine/paracrine fashions. Exogenous FGF2 supplementation inhibits both PGC-1α and PPARγ expression, leading to suppression of UCP1 expression in brown and beige adipocytes.
Conclusions
These findings demonstrate that FGF2 is a novel thermogenic regulator, suggesting a viable potential strategy for using FGF2-selective inhibitors in combat adiposity and associated hepatic steatosis.
FGF2 disruption enhances thermogenesis in brown and beige fat to protect against adiposity and hepatic steatosis

Objective
Fibroblast growth factor 2 (FGF2) has been reported to play divergent roles in white adipogenic differentiation, however, whether it regulates thermogenesis of fat tissues remains largely unknown. We therefore aimed to investigate the effect of FGF2 on fat thermogenesis and elucidate the underlying mechanisms.
Methods
FGF2-KO and wild-type (WT) mice were fed with chow diet and high-fat diet (HFD) for 14 weeks. The brown and white fat mass, thermogenic capability, respiratory exchange ratio, and hepatic fat deposition were determined. In vitroexperiments were conducted to compare the thermogenic ability of FGF2-KO- with WT-derived brown and white adipocytes. Exogenous FGF2 was supplemented to in vitro-cultured WT brown and ISO-induced beige adipocytes. The FGFR inhibitor, PPARγ agonist, and PGC-1α expression lentivirus were used with the aid of technologies including Co-IP, ChIP, and luciferase reporter assay to elucidate the mechanisms underlying the FGF2 regulation of thermogenesis.
Results
FGF2 gene disruption results in increased thermogenic capability in both brown and beige fat, supporting by increased UCP1 expression, enhanced respiratory exchange ratio, and elevated thermogenic potential in response to cold exposure. Thus, the deletion of FGF2 protects mice from high fat-induced adiposity and hepatic steatosis. Mechanistically, in vitroinvestigations indicated FGF2 acts in autocrine/paracrine fashions. Exogenous FGF2 supplementation inhibits both PGC-1α and PPARγ expression, leading to suppression of UCP1 expression in brown and beige adipocytes.
Conclusions
These findings demonstrate that FGF2 is a novel thermogenic regulator, suggesting a viable potential strategy for using FGF2-selective inhibitors in combat adiposity and associated hepatic steatosis.
2021 impact factor: 8.568
The 60 Second Metabolist
In this section authors briefly report on their work recently published in Molecular Metabolism.
Watch the most recent interviews by clicking the video still.
Here is a video of Vimeo. When the iframes is activated, a connection to Vimeo is established and, if necessary, cookies from Vimeo are also used. For further information on cookies policy click here.