Type 2 Diabetes Mellitus Reversed through White Adipose Tissue Targeting - EMG

Type 2 Diabetes Mellitus Reversed through White Adipose Tissue Targeting

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A team of researchers from University of British Columbia, Vancouver, Canada, and the Karolinska Institute, Solna, Sweden, have produced findings showing that targeting of white adipose tissue, both in vitro and in vivo, positively improves type 2 diabetic characteristics in the form of symptom reversal and prevention. Their results were recently published in the EBioMedicine journal.

Overconsumption of calories leads to expansion of white adipose tissue (WAT) to store the excess energy as fat, an occurrence that when uncontrolled (i.e., through the accumulation of fat and desensitisation to insulin) represents as one of, if not the primary, causes of type 2 diabetes mellitus (T2DM). In this study, researchers were interested in determining whether a cell surface marker called CD248 influences WAT and progression of diabetic disease.

Tissue-specific gene expression analysis was conducted for thin, obese, T2DM-negative, and T2DM-possitive patients, revealing that for those who were insulin-resistant or obese the CD248 gene was upregulated, leading to increased surface expression on WAT cells. This finding preliminarily identified CD248 as biomarker for insulin resistance, however through further in vitro assays the team were able to show that the protein is involved in other cellular processes that mediate insulin resistance, including but not limited to hypoxia response.

Using a WAT-specific, CD248 knockdown mouse model, the researchers highlighted that even following a high-fat diet and onset of obesity these animals did not develop T2DM. Reduced expression of CD248 in the adipose tissue did not lead to any adverse effects, meaning that this molecule represents a potentially novel target in the ongoing search for a T2DM cure. The investigators also noted an additional interesting finding: “the insulin sensitivity of mice that already have diabetes can be improved by reducing CD248 levels in the fat cells, even while they remain obese,” commented co-senor author Dr Edward Conway.

Whilst further research is needed to delineate the precise functions of CD248 in T2DM manifestation, and the fact that the road from laboratory discoveries to clinical utility is long, such promising findings have researchers in the diabetic field understandably optimistic for the future.

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