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Updated: Jun 4, 2026
Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)
Published on: January 7, 2018
Wound healing in mice with high-fat diet- or ob gene-induced diabetes-obesity syndromes: a comparative study
Oliver Seitz1, Christoph Schürmann, Nadine Hermes
1Pharmazentrum Frankfurt/ZAFES, Institut für Allgemeine Pharmakologie und Toxikologie, Klinikum der Johann Wolfgang Goethe-Universität, Theodor-Stern-Kai 7, 60590 Frankfurt am Main, Germany.
Abstract:
In the past, the genetically diabetic-obese diabetes/diabetes (db/db) and obese/obese (ob/ob) mouse strains were used to investigate mechanisms of diabetes-impaired wound healing. Here we determined patterns of skin repair in genetically normal C57Bl/6J mice that were fed using a high fat diet (HFD) to induce a diabetes-obesity syndrome. Wound closure was markedly delayed in HFD-fed mice compared to mice which had received a standard chow diet (CD). Impaired wound tissue of HFD mice showed a marked prolongation of wound inflammation. Expression of vascular endothelial growth factor (VEGF) was delayed and associated with the disturbed formation of wound margin epithelia and an impaired angiogenesis in the reduced granulation tissue. Normal wound contraction was retarded and disordered. Wound disorders in obese C57Bl/6J mice were paralleled by a prominent degradation of the inhibitor of NFκB (IκB-α) in the absence of an Akt activation. By contrast to impaired wound conditions in ob/ob mice, late wounds of HFD mice did not develop a chronic inflammatory state and were epithelialized after 11 days of repair. Thus, only genetically obese and diabetic ob/ob mice finally developed chronic wounds and therefore represent a better suited experimental model to investigate diabetes-induced wound healing disorders.
Insights
High-fat diets impair wound healing in mice by prolonging inflammation and disrupting blood vessel formation. Genetically diabetic mice (ob/ob) are better models for chronic diabetes-related wound issues.
Area of Science:
- Wound healing research
- Metabolic disease models
Background:
- Diabetes and obesity significantly impair wound healing.
- Previous studies utilized genetically diabetic-obese mouse models (db/db, ob/ob).
Purpose of the Study:
- To investigate skin repair mechanisms in diet-induced obesity and diabetes.
- To compare wound healing in high-fat diet (HFD)-fed mice versus genetically diabetic mice.
Main Methods:
- Induction of diabetes-obesity syndrome in C57Bl/6J mice using a high-fat diet (HFD).
- Comparison of wound closure and tissue repair between HFD-fed mice and standard chow diet (CD)-fed mice.
- Analysis of inflammatory markers, vascular endothelial growth factor (VEGF), and cellular signaling pathways (NFκB, Akt).
Main Results:
- HFD-fed mice exhibited delayed wound closure and prolonged inflammation compared to CD-fed mice.
- Impaired wound healing in HFD mice was associated with delayed VEGF expression, disturbed epithelialization, and reduced angiogenesis.
- Obese C57Bl/6J mice showed degradation of IκB-α without Akt activation, unlike ob/ob mice.
- HFD-induced wounds did not become chronic, resolving within 11 days, unlike ob/ob mouse wounds.
Conclusions:
- Diet-induced obesity and diabetes in C57Bl/6J mice cause delayed wound healing but do not lead to chronic wounds.
- Genetically obese and diabetic ob/ob mice are more suitable models for studying chronic, diabetes-induced wound healing disorders.
