Table 1.
Pathophysiological activity of endocrine FGFs.
| Up-Regulation | Down-Regulation | Increase | Decrease | |
|---|---|---|---|---|
| FGF19 | ||||
| Glycogen synthesis | Bile acid synthesis | Extrahepatic cholestasis | IBD | |
| Gluconeogenesis | Chronic hemodialysis | NAFLD | ||
| Primary bile acid malabsorption | ||||
| Obesity | ||||
| FGF21 | ||||
| Hepatic fatty acid oxidation | Ovulation | Type 2 diabetes | Anorexia | |
| Ketogenesis | Growth hormone signaling | Metabolic syndrome | Nervosa | |
| Glucogenesis | NAFLD | |||
| Thermogenesis | Coronary heart disease | |||
| WAT browing | ||||
| Growth hormone resistance | ||||
| Weight loss | ||||
| Ovulation | ||||
| FGF23 | ||||
| Calcium secretion | Renal phosphate absorption | ADHR | Hemodialysis | |
| Life span | Bone and renal calcium reabsorption | XLH rickets | Familial tumoral calcinosis | |
| Vitamin D synthesis | TIO | |||
| PTH secretion | Cardiac hypertrophy |
ADHR, autosomal dominant hypophosphataemic rickets; FGF, fibroblast growth factor; IBD, irritable bowel disease; NAFLD, non-alcoholic fatty liver disease; PTH, parathyroid hormone; TIO, tumor-induced osteomalacia; WAT, white adipose tissue; and XLH, X-linked hypophosphataemic.