In a series of articles, we have addressed the research advances in tackling high levels of insulin in the body. One of the major incentives that drive diabetes research is to discover what causes insulin levels to increase in the body, especially in the case of obesity.
In science it is not enough to just state that obesity is a risk factor for type 2 diabetes. Scientists are curious to know why obesity is a risk factor. What happens in the state of obesity that does not occur in the absence of the obese state.
The question has certainly been tackled in different ways in different research laboratories.
Research has provided us with different candidates, such as ceramides, the enzyme fatty acid synthase (FAS), high amounts of carbohydrates.
Now, to add to the burgeoning list, here is another candidate, a protein called Galectin-3.
A collaborative effort between laboratories in China and USA has uncovered the potential of Galectin-3 in inhibiting the action of the insulin receptor.
Galectin-3 is produced in cells involved in inflammation (the macrophage). In obese individuals, inflammation is cited as a cause for insulin resistance. One of the proteins that have been discovered in this inflammatory state by researchers is Galectin-3 or Gal3.
The study was conducted in obese mice and it was found that when Gal3 was blocked by a drug or by genetic modification, it allowed normal insulin signaling.
Galectin-3 binds to the insulin receptor (it recognizes insulin protein) and blocks the insulin protein from binding to the receptor. Through this action the effect of insulin is negated.
The inflammatory cells (macrophages) secrete Gal3 and the secretion has been observed in bone marrow macrophages. The effect of Gal3 can be observed in fat cells, liver, and muscle.
The study aims to promote further research on drugs that can target Gal3 and thus rescue insulin function.
