<p>In studies on mice and humans, a team of researchers at the Sanford-Burnham Medical Research Institute in the US found that high levels of fat disrupted two key proteins that turn genes on and off.<br /><br />The "transcription factors" FOXA2 and HNF1A activate a pancreatic enzyme that in healthy people prevents diabetes developing, the Daily Mail reported.<br /><br />When the proteins stop working, the enzyme is shut down, which in turn upsets the ability of insulin-secreting beta cells in the pancreas to monitor blood sugar levels.<br />Without this glucose sugar-sensing mechanism, blood sugar cannot be regulated properly.<br /><br />The discovery, published in the journal Nature Medicine, helps explain why Type 2 diabetes is so often linked to obesity and it could also lead to a potential cure for the condition, the researchers said.<br /><br />Study leader Dr Jamey Marth said: "Now that we know more fully how states of over-nutrition can lead to Type 2 diabetes, we can see more clearly how to intervene.<br />"The identification of the molecular players in this pathway to diabetes suggests new therapeutic targets and approaches towards developing an effective preventative or perhaps curative treatment.<br /><br />"This may be accomplished by beta cell gene therapy or by drugs that interfere with this pathway in order to maintain normal beta cell function." <br /><br />Experiments in mice showed that preserving the function of the enzyme affected by FOXA2 and HNF1A blocked the onset of diabetes, even in obese animals.<br />Diminished glucose sensing by beta cells was an important factor in both the development and severity of the disease.<br /><br />Dr Marth and his team are now looking at ways to augment the enzyme's activity in humans.<br /><br />More than two million people in the UK have Type 2 diabetes, the most common form of the disease.<br /><br />Insulin-dependent or Type 1 diabetes is a quite different condition caused by an autoimmune disorder.</p>
<p>In studies on mice and humans, a team of researchers at the Sanford-Burnham Medical Research Institute in the US found that high levels of fat disrupted two key proteins that turn genes on and off.<br /><br />The "transcription factors" FOXA2 and HNF1A activate a pancreatic enzyme that in healthy people prevents diabetes developing, the Daily Mail reported.<br /><br />When the proteins stop working, the enzyme is shut down, which in turn upsets the ability of insulin-secreting beta cells in the pancreas to monitor blood sugar levels.<br />Without this glucose sugar-sensing mechanism, blood sugar cannot be regulated properly.<br /><br />The discovery, published in the journal Nature Medicine, helps explain why Type 2 diabetes is so often linked to obesity and it could also lead to a potential cure for the condition, the researchers said.<br /><br />Study leader Dr Jamey Marth said: "Now that we know more fully how states of over-nutrition can lead to Type 2 diabetes, we can see more clearly how to intervene.<br />"The identification of the molecular players in this pathway to diabetes suggests new therapeutic targets and approaches towards developing an effective preventative or perhaps curative treatment.<br /><br />"This may be accomplished by beta cell gene therapy or by drugs that interfere with this pathway in order to maintain normal beta cell function." <br /><br />Experiments in mice showed that preserving the function of the enzyme affected by FOXA2 and HNF1A blocked the onset of diabetes, even in obese animals.<br />Diminished glucose sensing by beta cells was an important factor in both the development and severity of the disease.<br /><br />Dr Marth and his team are now looking at ways to augment the enzyme's activity in humans.<br /><br />More than two million people in the UK have Type 2 diabetes, the most common form of the disease.<br /><br />Insulin-dependent or Type 1 diabetes is a quite different condition caused by an autoimmune disorder.</p>