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Transgenic mouse models resistant to diet-induced metabolic disease: is energy balance the key?
Laura A A Gilliam1, P Darrell Neufer
1Department of Physiology, East Carolina University, Greenville, NC, USA.
Abstract:
The prevalence and economic burden of obesity and type 2 diabetes is a driving force for the discovery of molecular targets to improve insulin sensitivity and glycemic control. Here, we review several transgenic mouse models that identify promising targets, ranging from proteins involved in the insulin signaling pathway, alterations of genes affecting energy metabolism, and transcriptional metabolic regulators. Despite the diverse endpoints in each model, a common thread that emerges is the necessity for maintenance of energy balance, suggesting pharmacotherapy must target the development of drugs that decrease energy intake, accelerate energy expenditure in a well controlled manner, or augment natural compensatory responses to positive energy balance.
Insights
Discovering new molecular targets for obesity and type 2 diabetes is crucial. Research highlights the importance of maintaining energy balance for improving insulin sensitivity and glycemic control through various therapeutic strategies.
Area of Science:
- Metabolic research
- Molecular biology
- Pharmacology
Background:
- Rising prevalence and economic impact of obesity and type 2 diabetes.
- Urgent need for novel molecular targets to enhance insulin sensitivity and glycemic control.
Purpose of the Study:
- To review transgenic mouse models identifying promising molecular targets for metabolic diseases.
- To synthesize findings regarding energy balance in the context of therapeutic interventions.
Main Methods:
- Review of transgenic mouse models.
- Analysis of molecular targets within insulin signaling, energy metabolism, and transcriptional regulation.
- Identification of common themes across diverse models.
Main Results:
- Identified targets include proteins in insulin signaling, genes affecting energy metabolism, and transcriptional regulators.
- Maintenance of energy balance emerged as a critical factor across different models.
- Diverse therapeutic strategies are suggested, focusing on energy intake, expenditure, and compensatory responses.
Conclusions:
- Transgenic mouse models offer valuable insights into molecular targets for obesity and type 2 diabetes.
- Pharmacotherapy should aim to restore energy balance by modulating energy intake, expenditure, or compensatory mechanisms.
- Future drug development must consider the complex interplay of energy homeostasis in metabolic disease treatment.
