scholarly journals Fibroblast growth factor 21 is independently associated with severe hepatic steatosis in non‐obese HIV‐infected patients

2019 ◽  
Vol 39 (8) ◽  
pp. 1514-1520 ◽  
Author(s):  
Michael Praktiknjo ◽  
Natalie Djayadi ◽  
Raphael Mohr ◽  
Robert Schierwagen ◽  
Jenny Bischoff ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Hepatic Steatosis ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth

SAT-319-Fibroblast growth factor 21 is independently associated with severe hepatic steatosis in non-obese HIV-infected patients

2019 ◽  
Vol 70 (1) ◽  
pp. e780
Author(s):  
Michael Praktiknjo ◽  
Djayadi Natalie ◽  
Bischoff Jenny ◽  
Mohr Raphael ◽  
Robert Schierwagen ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Hepatic Steatosis ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth

scholarly journals Naringenin Prevents Obesity, Hepatic Steatosis, and Glucose Intolerance in Male Mice Independent of Fibroblast Growth Factor 21

Endocrinology ◽  
2015 ◽  
Vol 156 (6) ◽  
pp. 2087-2102 ◽  
Author(s):  
Julia M. Assini ◽  
Erin E. Mulvihill ◽  
Amy C. Burke ◽  
Brian G. Sutherland ◽  
Dawn E. Telford ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Growth Factor ◽  
Glucose Tolerance ◽  
Fibroblast Growth Factor ◽  
Hepatic Steatosis ◽  
Metabolic Adaptation ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Wild Type ◽  
Metabolic Dysregulation

Abstract The molecular mechanisms and metabolic pathways whereby the citrus flavonoid, naringenin, reduces dyslipidemia and improves glucose tolerance were investigated in C57BL6/J wild-type mice and fibroblast growth factor 21 (FGF21) null (Fgf21−/−) mice. FGF21 regulates energy homeostasis and the metabolic adaptation to fasting. One avenue of this regulation is through induction of peroxisome proliferator-activated receptor-γ coactivator-1α (Pgc1a), a regulator of hepatic fatty acid oxidation and ketogenesis. Because naringenin is a potent activator of hepatic FA oxidation, we hypothesized that induction of FGF21 might be an integral part of naringenin's mechanism of action. Furthermore, we predicted that FGF21 deficiency would potentiate high-fat diet (HFD)-induced metabolic dysregulation and compromise metabolic protection by naringenin. The absence of FGF21 exacerbated the response to a HFD. Interestingly, naringenin supplementation to the HFD robustly prevented obesity in both genotypes. Gene expression analysis suggested that naringenin was not primarily targeting fatty acid metabolism in white adipose tissue. Naringenin corrected hepatic triglyceride concentrations and normalized hepatic expression of Pgc1a, Cpt1a, and Srebf1c in both wild-type and Fgf21−/− mice. HFD-fed Fgf21−/− mice displayed greater muscle triglyceride deposition, hyperinsulinemia, and impaired glucose tolerance as compared with wild-type mice, confirming the role of FGF21 in insulin sensitivity; however, naringenin supplementation improved these metabolic parameters in both genotypes. We conclude that FGF21 deficiency exacerbates HFD-induced obesity, hepatic steatosis, and insulin resistance. Furthermore, FGF21 is not required for naringenin to protect mice from HFD-induced metabolic dysregulation. Collectively these studies support the concept that naringenin has potent lipid-lowering effects and may act as an insulin sensitizer in vivo.

Exendin-4 regulates lipid metabolism and fibroblast growth factor 21 in hepatic steatosis

Metabolism ◽  
2014 ◽  
Vol 63 (8) ◽  
pp. 1041-1048 ◽  
Author(s):  
Jinmi Lee ◽  
Seok-Woo Hong ◽  
Se Eun Park ◽  
Eun-Jung Rhee ◽  
Cheol-Young Park ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Hepatic Steatosis ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth
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