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Updated: Feb 25, 2026
Body Composition and Metabolic Caging Analysis in High Fat Fed Mice
Published on: May 24, 2018
FGF21 improves glucose homeostasis in an obese diabetes-prone mouse model independent of body fat changes
Thomas Laeger1,2, Christian Baumeier1,2, Ilka Wilhelmi1,2
1Department of Experimental Diabetology (DIAB), German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Arthur-Scheunert-Allee 114-116, 14558, Nuthetal, Germany.
Aims/Hypothesis:
Fibroblast growth factor 21 (FGF21) is considered to be a promising therapeutic candidate for the treatment of type 2 diabetes. However, as FGF21 levels are elevated in obese and diabetic conditions we aimed to test if exogenous FGF21 is sufficient to prevent diabetes and beta cell loss in New Zealand obese (NZO) mice, a model for polygenetic obesity and type 2 diabetes.
Methods:
Male NZO mice were treated with a specific dietary regimen that leads to the onset of diabetes within 1 week. Mice were treated subcutaneously with PBS or FGF21 to assess changes in glucose homeostasis, energy expenditure, food intake and other metabolic endpoints.
Results:
FGF21 treatment prevented islet destruction and the onset of hyperglycaemia, and improved glucose clearance. FGF21 increased energy expenditure by inducing browning in subcutaneous white adipose tissue. However, as a result of a compensatory increased food intake, body fat did not decrease in response to FGF21 treatment, but exhibited elevated Glut4 expression.
Conclusions/Interpretation:
FGF21 prevents the onset of diet-induced diabetes, without changing body fat mass. Beneficial effects are mediated via white adipose tissue browning and elevated thermogenesis. Furthermore, these data indicate that obesity does not induce FGF21 resistance in NZO mice.
Insights
Fibroblast growth factor 21 (FGF21) prevents diet-induced type 2 diabetes in mice by increasing energy expenditure and promoting white adipose tissue browning. This therapeutic approach shows promise for managing diabetes without altering body fat mass.
Area of Science:
- Metabolic research
- Endocrinology
- Obesity and diabetes studies
Background:
- Fibroblast growth factor 21 (FGF21) is a potential therapeutic for type 2 diabetes.
- Elevated FGF21 levels in obesity and diabetes raise questions about exogenous FGF21 efficacy.
- New Zealand obese (NZO) mice serve as a model for polygenic obesity and type 2 diabetes.
Purpose of the Study:
- To determine if exogenous FGF21 can prevent diabetes and beta cell loss in NZO mice.
- To investigate the metabolic effects of FGF21 treatment in a diet-induced obesity model.
Main Methods:
- Male NZO mice were subjected to a diabetes-inducing diet.
- Mice received subcutaneous injections of either phosphate-buffered saline (PBS) or FGF21.
- Metabolic endpoints including glucose homeostasis, energy expenditure, and food intake were assessed.
Main Results:
- FGF21 treatment prevented hyperglycemia and islet destruction, improving glucose clearance.
- FGF21 increased energy expenditure through browning of white adipose tissue.
- Despite increased food intake, body fat mass remained unchanged; Glut4 expression was elevated.
Conclusions:
- FGF21 effectively prevents diet-induced diabetes onset and beta cell loss in NZO mice.
- The therapeutic benefits of FGF21 are linked to enhanced thermogenesis and white adipose tissue browning.
- Obesity does not appear to induce FGF21 resistance in this mouse model.
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