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by Marijana Domazet, Wednesday, February 13, 2013 | Categories: Obesity

Although the relationship between obesity and diabetes is unlikely to be a surprise to most individuals today, the exact underlying processes for this link are still largely unknown. Now, a study has come out to suggest that two specific proteins (called TBK1 and IKKE) may play an important role in the inflammatory response that is common in obesity and insulin resistance as well as maintaining metabolic balance. In addition to that, the findings of the study indicate that the medication Amlexanox may be useful to inhibit these responses in mice. Here we briefly consider the implications of this research.

The research, which was recently published in Nature Medicine, was an animal study where mice were either given a high calorie diet or a calorie restricted diet. Within the former group, where the mice became obese over time, some mice were given a pharmacological treatment called Amlexanox whereas others were given alternative treatments (which did not produce remarkable results). The key findings indicated that mice given Amlexanox exhibited reversible weight loss, improved insulin sensitivity and attenuated hepatic steatosis (i.e. fatty degeneration). These findings were found both in mice that were obese due to dietary obesity and mice that had genetically induced obesity. This led the researchers to suggest that there is a need for future studies with humans to establish whether Amlexanox would be a suitable treatment for obesity or diabetes.

We were not surprised to read about these findings, as we are aware of substantial evidence that supports the idea of a potential association between diabetes and obesity being inflammatory in nature. But, as previously mentioned, it is not clear to date where this inflammatory response would occur. Nevertheless, when inflammatory pathways have been disrupted via pharmacological means in past studies, the results have indicated that the link between obesity and insulin resistance has also been disrupted. Therefore it is fair to say that although the findings may not be novel, they do appear to have a sound theoretical basis grounded in findings from past studies.

What makes the findings from this study interesting is the suggestion that inhibiting two specific proteins (TBK1 and IKKE) leads to improving metabolic dysfunctions in mice. This opens up several areas worth investigating. Intuitively, the first area may be to consider whether Amlexanox is an effective treatment for humans to use in this area and if there is a suitable dosage. On a more cynical note, it is worth questioning whether it would be realistic to maintain the effects in the long term without adverse side effects in humans. Another area appears on a deeper scale, where the role the aforementioned proteins in an inflammatory response (i.e. primary or secondary, mediating or moderating) is investigated in depth. Lastly, it is worth asking whether the role of these proteins play in processes among mice is equal to the role these proteins may play in human processes.

If these findings are shown to be true, it is likely that it will be a while before Amlexanox is recommended as a treatment for obesity or diabetes. However, given that Amlexanox is an off-patent medication used to treat asthma in humans (though not in the UK), the cost-benefit of researching and marketing it for further use may work as an incentive to hasten future research.

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