Research & Development

Ongoing Internal Research

Longitudinal Disease Development

NASH model disease development and progression has been studied by Woodland in our male and female NASH/fibrosis models. Rather than just focusing on end-point biology, we have collected samples "on the way" to the NASH fibrosis endpoint.

In the schematic below we took animals every two weeks throughout the model starting just before the start of the high fat diet and out to 12 weeks. We have liver samples including FFPE and flash frozen as well as blood fractions archived for your target ID and validation. In addition, we have looked at over 300 genes by microarray to evaluate gene expression in fibrosis, fatty liver and inflammation pathways. Data may be accessed for your project.
















In the second schematic and data we show that hyperglycemia can accelerate and exacerbate fibrosis in our modeling.

In ongoing research projects we will explore additional physiological insults likely to be comorbidity factors in human patients including "leaky-gut syndrome" and alcoholic insults to the fibrotic liver. These are experimental new programs we are developing at the request of clients interested in the role of the gut microbiome in liver diseases and alcohol on top of NASH. These are real-world insults that patients experience that can have profound effects on the development and progression (rate) of NASH.

And lastly, combination models with either carbon tetrachloride (CCl4) or thioacetamide (TAA) on top of the metabolic perturbations can again exacerbate fibrosis and provide a slightly more robust endpoint against which to measure your drug’s efficacy.

There are no truly predictive animal models of human disease that take decades to develop, including NASH. However, by attention to the physiological drivers of disease, we are able to assess drug activity to affect the component drivers of steatosis, inflammation and fibrosis and in so doing, we have shown that some of the more worrisome sequelae such as precancerous lesions in the liver can be reduced (2017 and 2018 poster data).

accelerated fibrosis.png

Metabolically-induced liver cancer

Liver cancer in a NASH mouse

At Woodland Biosciences, we have begun to look at the sequelae of our NASH and fibrosis disease modeling. While it is a goal of most preclinical research programs to halt or reverse fibrotic disease in the liver, this is not the cause of morbidity. NASH and Cirrhosis patients progress to liver failure, die from cardiovascular disease or progress to Hepatocellular Carcinoma (HCC).

We have started to model this progression and have found that drugs that are effective in slowing fibrosis or other metabolic parameters of NASH are effective in reducing lesion number and size in livers of treated animals compared to controls.


Woodland presented a poster on this work at 2018 AACR meeting in Chicago (Poster #4088). The poster is available under "News".



Extending DIO Modeling into NASH

Adding insult to injury

Woodland asked the question, "What are the pathological consequences of extending the DIO model" with both increasing time and adding chemical insult to the obesity in the model.

While the studies are currently ongoing, we know that we can exacerbate hyperglycemia and expect to affect fibrosis in the model. Data available in 4th quarter 2019.

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