medwireNews: An oral glucose tolerance test (OGTT) may identify youths with a more adverse cardiometabolic profile than a fasting plasma glucose (FPG) test does, say researchers.

Ming Li (Peking Union Medical College Hospital, Beijing, China) and colleagues found “surprisingly poor agreement between FPG and OGTT in the classification of pre-diabetes and diabetes when compared with previous reports in older adults.”

The team studied 542 participants of the Beijing Child and Adolescent Metabolic Syndrome study, who were aged 14–28 years and had at least one metabolic syndrome component. Of these, 10.0% had prediabetes according to at least one of FPG and OGTT, and 1.9% had type 2 diabetes.

However, they found that FPG failed to identify six of the 10 type 2 diabetes cases identified with an OGTT, as well as 32 of the 33 prediabetes cases. Conversely, the OGTT missed 21 of the 26 people who had impaired fasting glucose.

This is consistent with a study in obese Italian youth, say Li and team, and suggests that “FPG is inadequate as a screen for the pre-diabetes phenotype” in the presence of metabolic syndrome factors.

But the OGTT results identified a subgroup of young people with a more adverse cardiometabolic profile, as evidenced by the fact that 46.9% had metabolic syndrome, having at least three of its components, namely overweight/obesity, dysglycemia, raised blood pressure, elevated triglycerides, or low levels of high-density lipoprotein cholesterol. By contrast, metabolic syndrome rates were 14.3% among those with isolated impaired FPG and 7.5% among those with normal glucose tolerance.

Youth with isolated impaired glucose tolerance also had the highest prevalence of moderate-to-severe non-alcoholic fatty liver disease, at corresponding rates of 28.1%, 14.3%, and 9.0%.

Participants with impaired FPG had the highest insulin resistance according to HOMA-IR, which the researchers say “mainly reflects hepatic” insulin resistance, whereas those with impaired glucose tolerance scored lowest on the insulin sensitivity index, which “reflects both hepatic and peripheral (ie, muscle) insulin sensitivity.”

Beta-cell function as measured by HOMA-β was most aberrant in the impaired FPG group, but the impaired glucose tolerance group had the worst function as indicated by the insulinogenic index (reflecting early-phase insulin secretion) and by the oral disposition index.

This led the researchers to conclude that impaired glucose tolerance “was more indicative than [impaired fasting glucose] of profound [insulin resistance], β-cell dysfunction and an adverse cardiometabolic profile.”

They believe therefore that among young Chinese people, rather than an FPG test, “a 2-hour OGTT is necessary to adequately identify pre-diabetes in the subset of subjects with risk factors for [metabolic syndrome], even in the absence of obesity.”

The post Glucose tolerance test may be best for type 2 diabetes diagnosis in youth appeared first on MyMedicPlus.

Research led by the University of California, Los Angeles (UCLA) has uncovered a new process that may help explain how Type 2 diabetes develops. In tests on live mice and human cells in the lab, the team found a new mechanism besides insulin resistance and high glucose levels that triggers pancreatic cells to begin overproducing insulin.

Type 2 diabetes is the form of the disease that’s usually a result of lifestyle choices, such as poor diet and not enough exercise. It involves a kind of vicious cycle of insulin – beta cells in the pancreas produce too much insulin, which causes the body to become resistant to it. That in turn means the beta cells could produce even more to compensate.

It was long thought that high glucose levels – most commonly caused by eating too much sugary and fatty foods – was the trigger for the beta cells to begin overproducing insulin. But it’s also been shown in the past that even beta cells isolated in a lab dish can over-secrete insulin, without glucose playing a part.

So the team on the new study investigated what else could be causing beta cells to overproduce insulin. In tests on obese, pre-diabetic mice, the researchers discovered a new, separate molecular pathway that can induce insulin secretion without glucose. Instead, the trigger appears to be fatty acids.

When levels of these fatty acids rose too high in the mice, a protein called Cyclophilin D (CypD) caused protons to “leak” into the mitochondria of the beta cells. This triggers them to boost production of insulin.

To check the mechanism, the team then engineered mice without the gene that codes for CypD, and found that their insulin stayed at regular levels.

The researchers also investigated whether the same mechanism could be occurring in humans, by testing human pancreas cells isolated in the lab. When exposed to high levels of fatty acids – levels found in obese humans – the cells began to produce more insulin. Again, there was no glucose present.

The post New research uncovers potential trigger for Type 2 diabetes appeared first on MyMedicPlus.