You see it in the news all the time: more and more people around the world are obese and as a result they’re at a higher risk for diabetes, heart disease and cancer. In fact, 90% of individuals with type 2 diabetes are overweight or obese.
“Healthy” obese individuals protected from diabetes and other complications
A fascinating observation is that despite this tight association between weight and diabetes, some obese people are somehow shielded from the increased risks for diabetes and other associated diseases. Considering these conditions are among the leading causes of preventable death in the U.S., understanding how exactly these “healthy” obese individuals are protected could benefit millions of people.
A new study by researchers at the University of Bristol and Anti-Doping Laboratory Qatar (ADLQ) suggests that fat stem cells may hold the key to unlocking this mystery. Reporting in Diabetologia, the team found that fat stem cells from “healthy” obese people were better at storing fat compared to these same cells in people with increased risk for diabetes.
Belly fat and the development of diabetes
To delve deeper into the study, let’s take a closer look at the cellular biology of obesity and diabetes. The accumulation of fat in obese individuals initially leads to bigger fat cells but eventually causes the recruitment of fat stem cells. These additional fat cells can deposit as so-called visceral fat (aka belly fat) which accumulates within larger organs like the liver, heart and muscle instead of under the skin. Now, when a carbohydrate meal is eaten, the food is broken down into simple sugars which enter the blood. This rise in blood sugar is temporary because our organs like the liver and muscle use the sugar for energy. The blood sugar enters muscle and liver cells with the help of the hormone, insulin. But visceral fat mucks up these organs’ ability to sense insulin – they’re called insulin resistant – and blood sugar levels stay elevated which is the hallmark of type 2 diabetes (in type 1 diabetes the body doesn’t make any insulin).
In the study, the research team collected blood samples and isolated fat stem cells from 57 severely obese individuals undergoing liposuction. Some of the volunteers were insulin resistant (their organs had a hard time taking up blood sugar despite the presence of insulin) and had obesity-related conditions like diabetes, hypertension and heart disease. The others were insulin sensitive (their organs could take in blood sugar) and had no signs of obesity-related conditions.
Obesity-related complications and faulty fat stem cells
It turned out that the fat stem cells from obese individuals with insulin resistance (increased risk of complications) did not store fat as well as the fat stem cells from the “healthy” obese subjects. It’s this inefficient fat storage that likely leads to the build-up of visceral fat.
So why the difference? A comparison of various proteins in the blood of the two groups, showed that IL-6 – a protein secreted by the white blood cells of our immune system – was higher in the insulin resistant subjects. Back in the lab, the team found that the elevated IL-6 played a role in the cells’ reduced ability to store fat. Mohamed Elrayess, one of the authors from ADLQ, summarized the results in a press release:
“In this study we have shown that the impaired ability of fat stem cells to store excess fat was partially due to increased levels of the inflammatory marker interleukin-6 in the blood. Indeed, when fat stem cells isolated from healthy obese individuals were exposed to interleukin-6 in the laboratory, they behaved like those obtained from individuals with risk of diabetes.”
With this new piece of the obesity puzzle, the researchers are now focused on how they can make the fat stem cells from at risk individuals better at storing fat as a means to prevent the onset of diabetes.
One thought on “Faulty fat stem cells & obesity-related diabetes”
I see two problems here. First stem cells do not store fat. They must first differentiate and then become adipocytes then they can store fat.
Second it is well known that inflammation disrupts insulin receptors. So is IL-6 the chicken or the egg or simply a marker of another process and not the cause.