Following my introduction to fat accumulation (read more), I’m diving deeper into the science of fat growth. This post explores two key processes driving the physical increase in fat: adipose hypertrophy and mitosis. Understanding these mechanisms can help us grasp why fat accumulates, offering insights into managing a healthy body fat percentage for sustainable weight loss and overall wellbeing.

Let’s begin with adipose hypertrophy, the primary way fat increases in our bodies. This process occurs when existing fat cells, or adipocytes, grow larger by storing more lipids. Think of a balloon inflating—each adipocyte expands as it packs in more triacylglycerols (TAGs) into its lipid droplet. The Energy Balance Model suggests that hypertrophy is triggered by an energy imbalance: consuming more calories than we burn, often due to a high-calorie diet or sedentary lifestyle. Research indicates that hypertrophy is the dominant method in adults, particularly during gradual weight gain, as the body tends to enlarge existing fat cells before creating new ones [1][2].

Next, let’s define mitosis in this context. Mitosis happens when adipocytes divide, increasing the total number of fat cells, a process known as hyperplasia. Imagine not just inflating a balloon, but adding more balloons to the bunch. This process is more common in childhood and adolescence, setting the body’s baseline number of fat cells, but can also occur in adults under extreme conditions like severe obesity, where existing fat cells reach their storage limit, leading to the creation of new adipocytes to manage excess energy [3][2].

How do these processes compare? Hypertrophy focuses on expansion—fat cells growing larger—while mitosis is about multiplication, creating more fat cells. Studies suggest that hypertrophy is the body’s preferred method in adults, handling most fat increases, while mitosis plays a smaller role, mainly in extreme cases like severe obesity. There’s ongoing debate about their exact contributions, as the balance can vary based on factors like genetics and the extent of obesity [1][2].

What triggers hypertrophy and mitosis? Genetics play a significant role—twin studies show that some individuals may be more prone to hypertrophy or mitosis based on genetic predisposition, affecting how their body handles excess energy [4]. Lifestyle factors are also crucial: a consistent energy surplus, often from a high-calorie diet, drives hypertrophy, while long-term overeating can push the body towards mitosis, especially when fat cells can’t expand further. Research also points to inflammation as a trigger for fat growth, with obese adipose tissue showing increased inflammatory markers that may influence cell dynamics [5]. Additionally, hormonal imbalances, such as elevated cortisol from stress, are linked to increased abdominal fat accumulation, further contributing to fat growth [6].

Scientists are exploring drugs that induce mitosis to manage metabolic syndrome. These drugs aim to create smaller, more insulin-sensitive fat cells, improving insulin sensitivity and reducing strain on existing cells. Thiazolidinediones, like pioglitazone, are among the drugs studied, shown to increase whole-body adiposity by creating more but smaller adipocytes, which may contribute to their clinical benefits [7][8]. However, this approach can increase overall fat storage, as more cells mean greater capacity—a challenge for weight management.

This exploration of adipose hypertrophy and mitosis sets the stage for a deeper understanding of fat. Next, we’ll examine the contents of a lipid droplet within individual adipocytes, revealing components beyond TAGs, such as proteins and vitamins.

References:

1. Spalding KL, Arner E, Westermark PO, et al. Dynamics of fat cell turnover in humans. Nature. 2008;453(7196):783-787. doi:10.1038/nature06902. Available at: https://www.ncbi.nlm.nih.gov/pubmed/18454136
2. Salans LB, Cushman SW, Weismann RE. Studies of human adipose tissue. Adipose cell size and number in nonobese and obese patients. J Clin Invest. 1973;52(4):929-941. doi:10.1172/JCI107258. Available at: https://www.ncbi.nlm.nih.gov/pubmed/4693656
3. Hirsch J, Knittle JL. Cellularity of obese and nonobese human adipose tissue. Fed Proc. 1970;29(4):1516-1521. Available at: https://pubmed.ncbi.nlm.nih.gov/5459900/
4. Loos RJ, Bouchard C. Obesity—is it a genetic disorder? J Intern Med. 2003;254(5):401-425. doi:10.1046/j.1365-2796.2003.01242.x. Available at: https://pubmed.ncbi.nlm.nih.gov/14535962/
5. Cancello R, Clément K. Is obesity an inflammatory illness? Role of low-grade inflammation and macrophage infiltration in human white adipose tissue. BJOG. 2006;113(10):1141-1147. doi:10.1111/j.1471-0528.2006.01004.x. Available at: https://pubmed.ncbi.nlm.nih.gov/16903845/
6. Björntorp P. Do stress reactions cause abdominal obesity and comorbidities? Obes Rev. 2001;2(2):73-86. doi:10.1046/j.1467-789x.2001.00027.x. Available at: https://www.ncbi.nlm.nih.gov/pubmed/12119665
7. de Souza CJ, Eckhardt M, Gagen K, et al. Effects of pioglitazone on adipose tissue remodeling within the setting of obesity and insulin resistance. Diabetes. 2001;50(8):1863-1871. doi:10.2337/diabetes.50.8.1863. Available at: https://pubmed.ncbi.nlm.nih.gov/11473050/
8. Mudaliar S, Henry RR. New oral therapies for type 2 diabetes mellitus: The glitazones or insulin sensitizers. Annu Rev Med. 2001;52:239-257. doi:10.1146/annurev.med.52.1.239. Available at: https://www.ncbi.nlm.nih.gov/pubmed/11160777