Differences in the cells that store fat in the body could explain why some people are more prone to obesity-related conditions, such as type 2 diabetes.
Scientists at the University of Melbourne, in Australia, led an investigation that examined human white fat cells from samples that volunteers had donated.
The samples came from white fat tissues in different parts of the body.
White fat cells are the cells that store energy in fat molecules called triglycerides.
The human body has reservoirs of regenerative cells, called adipose progenitor cells (APCs), which mature into white fat cells.
Using tools that assessed genes, proteins, and metabolism, the study is the first to identify three distinct subtypes of APCs.
In a recent Cell Reports paper, the authors explain how the APC subtypes differ in the ways that they deal with energy and hormones.
The findings suggest that the makeup and distribution of white fat in the body, in terms of the APC subtypes, could predict a person’s risk of developing type 2 diabetes and other metabolic diseases.
The first APC subtype matures into fat cells that discharge lots of fat molecules into the bloodstream, while the second type leads to cells that burn energy fast. The third subtype has a more “neutral” profile and behaves more like scientists might expect a fat cell to behave, if rather more slowly.
Senior study author Prof. Matthew J. Watt, who heads the physiology department in the School of Biomedical Sciences at the University of Melbourne, suggests that the first subtype could be one that promotes fat deposits on organs and in other parts of the body. This could happen in people of healthy weight as well as in those who are overweight.
He suggests that the second APC subtype could be one that stops people from gaining weight.
In the United States, figures from the Centers for Disease Control and Prevention (CDC) reveal that 40% of adults, amounting to some 93.3 million people, had obesity in 2015–2016.
Obesity-related health conditions such as heart disease and type 2 diabetes account for a large number of preventable early deaths.
In their study paper, Prof. Watt and his colleagues note that obesity and dysfunction of fat tissues are “inextricably linked to the development of metabolic diseases, such as dyslipidemia and type 2 diabetes.”
Given the rising tide of worldwide obesity, “There remains intense interest,” they write, in furthering knowledge of how fat cells develop and how their energy and hormone mechanisms work, especially in relation to overeating.
When they examined the fat tissue samples, the researchers found all three APC subtypes in all the samples. There was no part of the body in which white fat tissue did not have all three.
However, they did find that the distribution of the subtypes differed among individuals: Some subtypes were more abundant, while others were less so.
Prof. Watt remarks that this could mean that the makeup of people’s APC subtypes in their white fat tissues could be a factor in their metabolic health.
He imagines, for example, that future weight loss treatments could involve switching off the fat-releasing APCs and switching on the fast-burners.
Drugs that do this could potentially help to prevent obesity-related conditions and offer less invasive alternatives to surgery.
However, Prof. Watt cautions that there is still a lot of work to do, and it could be 10 years or more before such treatments become available.
Further studies should, for example, confirm whether having more or less of certain APC subtypes actually raises or lowers risk of specific metabolic diseases.
They then need to find out whether increasing or decreasing certain cell types can affect disease outcomes.
Even if treatments that alter APCs become available, Prof. Watt predicts that people will likely still need to adopt healthful lifestyles, reduce food consumption, and increase physical activity.
“The discovery is important because it tells us that not all fat cells are the same and that by understanding the fat subtypes in a human, we might be able to predict their future metabolic health.”
Prof. Matthew J. Watt