When we increase our body fat, our subcutaneous adipose tissue increases, but when this is not enough to accommodate this excess energy converted into triglycerides, visceral adipose tissue begins to grow (or both at the same time), which, having less adipogenic capacity, grows by hypertrophy, that is, by increasing the size of adipocytes (cells that store fat).

When the expansion of adipose tissue from the differentiation of preadipocytes (adipogenesis) is limited, adipose tissue can only expand through hypertrophy of the adipocyte itself, in order to accommodate excess triglycerides. But its capacity is partially limited, and so a process of adipogenesis is initiated that prevents the adipocyte from expanding further by hypertrophy to critical limits. At that moment hyperplasia of the adipocyte occurs from a preadipocyte (not that the adipocyte divides in two as it is thought hehehe).

This process of hyperplasia could be considered as negative, as it allows the adipose tissue to continue increasing, but thanks to hyperplasia it is possible to continue storing energy (fattening) without any metabolic problems. But if the causes that trigger the increase in lipogenesis (such as a positive energy balance) continue, the adipose tissue becomes incompetent at storing triglycerides, making the main mode of expansion happen through adipocyte hypertrophy, which leads to health problems.

As adipocyte hypertrophy occurs, they begin to secrete proinflammatory cytokines ultimately leading to lipoinflammation and then chronic inflammation. However, hyperplasia gives us better insulin sensitivity and glucose levels are reduced, decreasing the production of pro-inflammatory cytokines.

A problem with excessive adipocyte hyperplasia is that when a fat loss process is initiated, let’s say that these adipocytes lose their triglyceride content as we lose weight, but are not eliminated in number, making it easier to regain the lost weight later on.

Leave a Reply