While the study confirmed most of the known diabetes "risk loci"-- sites on the genome where small DNA variations have been linked to altered, usually higher diabetes risk -- the researchers also uncovered 16 new risk factors.
The researchers also identified eight specific gene variants that are strongly linked to altered risk for both diseases.
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"Identifying these gene variants linked to both Type 2 diabetes and coronary heart disease risk in principle opens up opportunities to lower the risk of both outcomes with a single drug," said co-senior author Danish Saleheen, Assistant Professor at the University of Pennsylvania in the US.
"From a drug development perspective, it would make sense to focus on those pathways that are most strongly linked to both diseases."
Seven of these gene variants, as expected, appeared to increase risk for both Type 2 diabetes and coronary heart disease risk.
The eighth, a variant of the gene for the cholesterol-transport protein ApoE, turned out to be associated with higher diabetes risk but lower coronary heart disease risk.
On the whole, the genetic link between the diseases appears to work in one direction so that risk genes for Type 2 diabetes are much more likely to be associated with higher coronary heart disease risk than the other way around, the researchers explained in the paper published in the journal Nature Genetics.
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There could also be some pathways where pharmacological lowering of one disease increases the risk of the other.
"Using evidence from human genetics, it should be possible to design drugs for Type-2 diabetes that have either beneficial or neutral effects on coronary heart disease risk," Saleheen said.
The findings, published in the journal Experimental Physiology, show that people who sleep fewer than seven hours per night have lower blood levels of three physiological regulators, or microRNAs, which influence gene expression and play a key role in maintaining vascular health.
"This study proposes a new potential mechanism through which sleep influences heart health and overall physiology," said Christopher DeSouza, Professor at University of Colorado in the US.
For the study, the research team took blood samples from a small group of healthy men and women, age 44 to 62, who had filled out questionnaires about their sleep habits.
While half of the participants slept seven to 8.5 hours nightly, the other half slept five to 6.8 hours every night.
The research team measured the expression of nine microRNAs previously associated with inflammation, immune function or vascular health.
They found that people with insufficient sleep had 40 to 60 per cent lower circulating levels of miR-125A, miR-126, and miR-146a than those who slept enough.
"Why seven or eight hours seems to be the magic number is unclear. However, it is plausible that people need at least seven hours of sleep per night to maintain levels of important physiological regulators, such as microRNAs," DeSouza added.
"They are like cellular brakes, so if beneficial microRNAs are lacking that can have a big impact on the health of the cell," DeSouza said.
The results suggest that microRNAs in blood could be used as a marker of cardiovascular disease in people with insufficient sleep.
"The effect in this study was not only statistically significant but also has the potential to be clinically relevant by reducing risk of diabetic complications and death," said study researcher Xiqian Huo from Fuwai Hospital in China.
"Capitalising on the exponential growth in mobile phone usage over the past decade, a simple text messaging programme could increase the reach of diabetes self-management support," she added.
It may provide a means to better address the burgeoning healthcare demand-capacity imbalance.
For the study presented at the ESC Congress 2019 in France, the researchers enrolled 502 patients from 34 clinics in China and the patients were randomly assigned to the text messaging intervention or a control group for six months.
The intervention group received six messages per week, at random times of the day, from an automated system set up by the researchers.
The messages were designed to provide information and motivation and help patients set goals and manage stress.
The control group received two thank you text messages per month.
At six months, blood glycated haemoglobin (HbA1c) was significantly lower in the intervention group compared to the control group (6.7 per cent versus 7.2 per cent).
On an average, HbA1c fell by 0.2 per cent in the intervention group and rose by 0.1 per cent in the control group - a difference of 0.3 per cent between groups.
The change in fasting blood glucose was larger in the intervention, compared to control, group (-0.5 versus 0.1 mmol/L, respectively).
The intervention was acceptable to participants, 97 per cent found the text messages useful, readable and an appropriate method of contact.
The study, published in the European Heart Journal, also found that heart failure patients taking drugs targeting the renin-angiotensin-aldosterone system (RAAS), such as angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), did not have higher concentrations of ACE2 in their blood.
"Our findings do not support the discontinuation of these drugs in COVID-19 patients as has been suggested by earlier reports," said study co-author Adriaan Voors from the University of Groningen in the Netherlands.
Some recent research suggested that RAAS inhibitors might increase concentrations of ACE2 in plasma -- the liquid part of blood -- thereby increasing the risk of COVID-19 for cardiovascular patients taking these drugs.
The current study indicates that this is not the case, although it looked only at ACE2 concentrations in plasma, not in tissues such as lung tissue.
"ACE2 is a receptor on the surface of cells. It binds to the coronavirus and allows it to enter and infect healthy cells after it is has been modified by another protein on the surface of the cell, called TMPRSS2," Voors said.
"High levels of ACE2 are present in the lungs and, therefore, it is thought to play a crucial role in the progression of lung disorders related to COVID-19," he added.
For the findings, the researchers measured ACE2 concentrations in blood samples taken from two groups of heart failure patients from 11 European countries.
There were 1,485 men and 537 women in the first group, the index cohort, which was designed to test the researchers' hypotheses and research questions. Then the researchers validated their findings in the second group of 1,123 men and 575 women, the validation cohort.
The research team assessed the number of clinical factors that could play a role in ACE2 concentrations, including the use of ACE inhibitors, a history of chronic obstructive pulmonary disease, and coronary artery by-pass graft.
They found that male sex was the strongest predictor of elevated ACE2 concentrations. ACE2 is found not only in the lungs, but also the heart, kidneys and the tissues lining blood vessels, and there are particularly high levels in the testes.
The researchers speculate that its regulation in the testes might partially explain higher ACE2 concentrations in men, and why men are more vulnerable to COVID-19.
Last month, the study, published in the journal Frontiers in Public Health, found that men are more than twice as likely to die from the disease as compared to women.
Another study from the American Journal of Respiratory and Critical Care Medicine showed that males over 50 with non-communicable chronic diseases such as hypertension, diabetes and coronary heart disease are at greater risk of death from coronavirus.
(IANS)