Size matters when it comes to fat cells

Science by Dr. Ben Bikman

Few cells in the body receive more attention than the fat cell–it’s the cell everyone loves talking about. Despite this enthusiasm (and disdain?!) for fat, few people appreciate its role in regulating healthy metabolic function within the body.

The standard view of fat tissue is that it’s bad. We all know that if you have too much fat on your body, the risk of myriad chronic diseases climbs, such as heart disease [1], diabetes [2], and more. But this view has resulted in a degree of wrong-thinking–we erroneously conclude that the amount of fat is what matters. In reality, much of the disease risk that comes from excess fat is the size of the fat cell.

During development, from infancy through adolescence, our bodies are busily making fat cells through a process called hyperplasia. This obviously accounts for some of the amount of fat a body has, but it’s not the main reason a body gains or loses fat. Weight gain (in adulthood) is much more a matter of fat cells growing, a process called hypertrophy. Accordingly, when we lose weight, it’s the result of fat cells shrinking, not fat cells dying.

But all this focus on growing and shrinking fat cells somewhat diminishes the broader role of the fat cell in the body. In addition to acting as a reservoir for energy (i.e., storing fat), fat tissue is an endocrine organ, actively producing and releasing hormones. When you think of an endocrine organ, you likely think of the classic glands, such as the thyroid or adrenal glands. However, fat is right up there in hormone-producing potential, contributing to a greater variety of hormones than either.



Leptin is one such product. Leptin is famous–everyone knows of its ability to influence appetite; when leptin climbs, appetite goes down. Ideally. Unfortunately, the larger the fat cells get, the more leptin they continue to produce. This continues until the body begins to become resistant to leptin [3]. There’s just been too much leptin for too long and the cells of the body become deaf to the incessant shouts. (As an aside, leptin is involved in many other processes outside of appetite, including puberty and fertility.)

Another relevant fat-produced hormone is adiponectin. Adiponectin elicits a host of metabolically-favorable effects, including improving insulin sensitivity and promoting weight loss [4]. Unlike leptin, adiponectin production goes down as fat cells grow–despite their size, the enlarged fat cell releases less adiponectin.

The combination of these two changes–reduced leptin action (despite a great amount) and lower adiponectin production–contributes significantly to the metabolic disruption that accompanies fat gain. They’re also a perfect reflection of fat cells that are getting too large. As adiponectin drops and leptin continues to climb, this is metabolic evidence that fat cells have expanded to an unhealthy point. Accordingly, it’s little surprise that this ratio not only predicts insulin resistance [5], but myriad metabolic problems, including polycystic ovary syndrome [6].

The key to resolving the adiponectin:leptin ratio is shrinking fat cells through lowering insulin. Insulin has a uniquely powerful ability to enlarge fat cells [7], and lowering insulin eases the pressure, allowing fat cells to shrink. By controlling carbohydrate consumption by restricting refined starches and sugars, while focusing on protein and fat, you can nourish the body (i.e., not be hungry) while keeping insulin low.




This article is for informational and educational purposes only. It is not, nor is it intended to be substitute for professional medical advice, diagnosis, or treatment and should never be relied upon for specific medical advice.