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Serum fibroblast growth factor‐21 is responsive to a hypocaloric very low carbohydrate ketogenic diet but not a low fat diet
Author(s) -
Kawiecki Diana M,
Freidenreich Daniel J,
Quann Erin E,
Labonte Cherise C,
Puglisi Michael J,
Ballard Kevin D,
Volk Brittanie M,
Forsythe Cassandra E,
Fernandez MariaLuz L,
Kraemer William J,
Volek Jeff S
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1092.2
Subject(s) - endocrinology , medicine , ketogenic diet , fgf21 , lipolysis , ketogenesis , ketosis , carbohydrate , triglyceride , overweight , ketone bodies , carbohydrate metabolism , insulin , fibroblast growth factor , chemistry , metabolism , adipose tissue , cholesterol , obesity , diabetes mellitus , receptor , psychiatry , epilepsy
Ketogenic diets were recently shown to induce hepatic expression and increase circulating levels of fibroblast growth factor 21 (FGF‐21), which coordinates lipid homeostasis by inducing hepatic lipid oxidation, ketogenesis, lipolysis, and triglyceride clearance. Very low carbohydrate ketogenic diets (VLCKD) in humans consistently improve features of metabolic syndrome. We hypothesized a VLCKD would increase FGF‐21 in adults. Fasting serum FGF‐21 concentrations were measured by RIA in 39 overweight men and women who consumed a VLCKD (1504 kcal:%CHO:fat:protein=12:59:28) or a low fat diet (LFD) (1478 kcal:%CHO:fat:protein=56:24:20) for 12 weeks. All subjects had detectable levels of FGF‐21 in serum with no gender differences. FGF‐21 was reduced (p<0.05) by the VLCKD (2.51 ± 0.75 to 2.19 ± 0.56) and unchanged after the LFD (3.02 ± 0.61 to 3.03 ± 0.69). Baseline concentrations and delta changes in FGF‐21 were not correlated with weight loss, body fat, glucose, insulin, lipoproteins, or other metabolic syndrome markers. Contrary to our expectations, these findings indicate that serum FGF‐21 concentrations decrease after a hypocaloric, ketogenic diet in overweight humans. The metabolic significance of this response is unclear, but may represent a down‐regulation in the need for lipolytic signaling as a consequence of the potent stimulatory effects of carbohydrate restriction on hepatic lipid oxidation.