Transgenic mice expressing human fibroblast growth factor-19 display increased metabolic rate and decreased adiposity

Endocrinology. 2002 May;143(5):1741-7. doi: 10.1210/endo.143.5.8850.

Abstract

The fibroblast growth factors (FGFs), and the corresponding receptors, are implicated in more than just the regulation of epithelial cell proliferation and differentiation. Specifically, FGF23 is a regulator of serum inorganic phosphate levels, and mice deficient in FGF receptor-4 have altered cholesterol metabolism. The recently described FGF19 is unusual in that it is nonmitogenic and appears to interact only with FGF receptor-4. Here, we report that FGF19 transgenic mice had a significant and specific reduction in fat mass that resulted from an increase in energy expenditure. Further, the FGF19 transgenic mice did not become obese or diabetic on a high fat diet. The FGF19 transgenic mice had increased brown adipose tissue mass and decreased liver expression of acetyl coenzyme A carboxylase 2, providing two mechanisms by which FGF19 may increase energy expenditure. Consistent with the reduction in expression of acetyl CoA carboxylase 2, liver triglyceride levels were reduced.

MeSH terms

  • Adipose Tissue / drug effects
  • Adipose Tissue / physiology*
  • Adipose Tissue, Brown / metabolism
  • Animals
  • Body Temperature / genetics
  • Body Temperature / physiology
  • Body Weight / genetics
  • Body Weight / physiology
  • Calorimetry, Indirect
  • Diabetes Mellitus / metabolism
  • Diet
  • Dietary Fats / pharmacology
  • Energy Metabolism / drug effects
  • Energy Metabolism / genetics*
  • Fibroblast Growth Factors / biosynthesis*
  • Fibroblast Growth Factors / genetics*
  • Glucose / metabolism
  • Glucose Tolerance Test
  • Humans
  • Liver / metabolism
  • Mice
  • Mice, Transgenic
  • Phenotype

Substances

  • Dietary Fats
  • FGF19 protein, human
  • Fibroblast Growth Factors
  • Glucose