Diabetes: Cellular News

Diabetes: Cellular News: We’ve reported previously that high birth-weight babies are susceptible to diabetes later in life. New research indicates the same may be true for low birth-weight babies although the underlying reasons may be different.

The issue with low birth-weight babies has to do with a duo of gene variants. If an infant has these variants it can lead to both low birth-weight and a greater likelihood of diabetes.

According to BabyChums.com, “The collaborative effort of scientists from Britain, Finland, the Netherlands and the United States has yielded important research which could change the way diabetes is dealt with in the future.”

Researchers analyzed nearly 20 studies covering more than 38,000 European patients. Jim Wilson, a Scotland medical researcher said: “Finding two gene variants that decrease birth-weight is the first exciting step to unraveling the well known associations between birth-weight and killer diseases in later life. It is particularly interesting that one of these variants is also a risk factor for Type 2 diabetes.

“These genes will begin to reveal the biology behind how low birth-weight increases the risk of adult-onset diabetes, heart disease and high blood pressure,” Wilson is quoted by BabyChums.com.

One of these genes is known as Adenylate cyclase type 5 (ADCY5) and, “According to the researchers’ data, people who inherit two copies of this gene in two specific genetic regions have a 25 percent increased chance of developing diabetes later in adulthood,” said Babychums.com.

It seems relevant that certain genetic markers exist that can pose a potential problem for development potential in diabetes.

However, other researchers have cautioned that low birth-weight can be attributed to multiple circumstances and that simply because a new baby may be born with low birth-weight one cannot simply assume that diabetes will always be the outcome.

Meanwhile, Leptin is back in the news. UT Southwestern Medical Center researcher Dr. Joel Elmquist, senior author of a recent study said, “Our findings indicate that [obesity-linked diabetes] is not necessarily the case, at least in mice. We can make the animals very diabetic without obesity, suggesting that there may be a circuit or path of resistance to these signals in the brain that helps explain the powerful anti-diabetic actions of leptin.”

This researcher notes that Type 2 diabetes may not be directly attributable to obesity as he found similar issues in mice that were not obese and yet because they were leptin deprived they struggled with life threatening diabetic symptoms.

Interesting a single shot of leptin caused diabetic mice to reverse course in diabetes. “In the current study,” according to DNAIndia.com, “the researchers genetically engineered mice to lack both leptin and insulin receptors in their POMC neurons. Both receptors remained intact in all other cell types and tissues, including the liver and ovaries.”

What was the result? Well, according to the same report, “The researchers found that when they removed both receptors from these particular neurons the mice displayed systemic insulin resistance and became severely diabetic but not obese. Dr. Elmquist said the findings suggest that leptin and insulin – when acting on these neurons in the brain – are both necessary and can compensate for each other if there’s a shortage of one.”

Elmquist concluded by saying, “There seems to be what I call a functional redundancy in these neurons as it relates to blood sugar regulation. We don’t know if the same neurons respond to both leptin and insulin, but it is clear that functionally leptin can compensate for a lack of insulin and vice versa.”