Db/db Mice
Db/db Mice - Related Videos
06:17
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Cited by 287 •
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Deficits in muscular strength occur in many clinical conditions such as motor neuron disease. The inverted screen and weight lifting tests described here measure strength in mice almost exclusively, with minimal influence of factors such as coordination.
36:30
Small Bowel Transplantation In Mice
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Cited by 2 •
2007
The mouse small bowel transplantation model has been recognized as an important tool to study mechanismes of immune rejection and screen new immunosuppressive drugs. However, this model is limited to use because the techniques involved is an extremely technically challenge. Now we introduce the modified technique.
07:02
Trace Fear Conditioning in Mice
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Cited by 32 •
2014
In the following experiment we describe a protocol for trace fear conditioning in mice. This type of associative memory includes a trace period that separates the neutral stimulus and the unconditioned stimulus.
07:56
Parabiosis in Mice: A Detailed Protocol
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Cited by 175 •
2013
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09:43
Video-oculography in Mice
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Cited by 24 •
2012
Video-oculography is a very quantitative method to investigate ocular motor performance as well as motor learning. Here, we describe how to measure video-oculography in mice. Applying this technique on normal, pharmacologically-treated or genetically modified mice is a powerful research tool to explore the underlying physiology of motor behaviors.
FAQs
The homozygous Lepr mutation disrupts the long-form leptin receptor, so leptin cannot effectively signal through its normal hypothalamic pathway. This weakens central regulation of energy balance and contributes to increased food intake and abnormal metabolic control. The model therefore connects a defined signaling defect with the emergence of obesity, insulin resistance, and worsening glucose dysregulation.
Their phenotype reflects interacting metabolic disturbances rather than weight gain alone. Impaired leptin signaling promotes hyperphagia and severe obesity, while insulin resistance reduces effective glucose regulation. Over time, these abnormalities are associated with progressive hyperglycemia, making Db/db mice useful for examining how disrupted energy-balance signaling relates to broader metabolic disease.
The defining biological disturbance in Db/db mice is leptin-receptor dysfunction, specifically loss of effective signaling through the long-form Lepr receptor. This distinguishes them from models in which obesity may arise through another genetic mechanism. Comparing such models helps investigators determine which findings reflect receptor-level leptin signaling defects and which represent more general consequences of genetic obesity.
The model supports investigation of glucose regulation, adipose tissue biology, and diabetic complications alongside obesity and insulin resistance. These connected outcomes allow researchers to examine metabolic disease as a progressive process rather than as an isolated change in body mass. The same system can also help relate altered energy-balance signaling to downstream tissue and disease responses.
Researchers use the reproducible phenotype to investigate whether candidate treatments influence metabolic abnormalities associated with the model. Studies can focus on glucose regulation, insulin resistance, adipose tissue biology, or disease progression, depending on the therapeutic question. Because the animals show defined leptin-receptor dysfunction and progressive hyperglycemia, treatment responses can be interpreted within a consistent metabolic context.
Findings may clarify how impaired leptin signaling contributes to metabolic disease and may identify effects of interventions on glucose control, adipose tissue, or diabetic complications. The model is especially relevant when researchers need a consistent system for connecting an energy-balance defect with disease progression. Results also help frame how leptin-receptor dysfunction relates to other obesity mechanisms.