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Unilocular adipocytes, or white adipocytes, are found in the adipose tissue, although they are also observed scattered in the connective tissue. The white color, sometimes yellowish, is the color of fresh white fat. Adipocytes are specialized cells in storing energy as neutral fatty acids when the energy balance is positive. Most adipocytes of the body are white adipocytes. Unilocular means that the majority of the cell cytoplasm is occupied by a very large lipid droplet. There are other types of adipocytes like multilocular or brown adipocytes, and beige and pink adipocytes.

1. Morphology

Unilocular adipocytes are usually rounded in shape. The cell size is variable, and they can be up to 100 to 150 µm in diameter when they are filled with storing substances (Figures 1 and 2). Adipocyte diameter changes during development. In humans, they are 40 to 50 µm in the fetus, 50 to 80 µm in newborns, 90 to 130 µm in babies, 50 to 200 µm in normal adults, and 90 to 270 µm in obese adults. The maximum size is limited by oxygen diffusion and by interaction with the extracellular matrix.

Figure 1. On the left: adipose tissue around the uterus of a rat, stained with Masson trichrome. On the right: adipose tissue of the posterior part of the rat tongue, stained with haematoxylin-eosin.
Figure 2. Unilocular adipocytes separated by connective tissue septa. Trichrome staining.
Adipose tissue
Adipose tissue

White fat tissue
White fat tissue

Brown fat tissue
Brown fat tissue

Lipid droplets
Lipid droplets

White fat adipocytes show a large lipid droplet that occupies most of the cytoplasm. Lipid droplets are found in all eukaryote cells, which means they perform an essential function for the cell. They are not limited by a bi-layered membrane , but by a lipidic membrane monolayer of about 5 nm in thickness, which is derived from the endoplasmic reticulum membrane, and it is covered by a network of vimentin filaments. Lipid droplets may be in contact with endoplasmic reticulum and mitochondria favoring sterification and degradation triacylglycerol, respectively. Some cisterns of endoplasmic reticulum have sometimes been observed inside the lipid droplets, indicating the origin of these lipid organelles. The remaining organelles and the nucleus are pressed against the plasma membrane. Unilocular adipocytes contain the normal set of organelles than other cells have, like endoplasmic reticulum, Golgi apparatus, and mitochondria. These cells show an intense endocytic flux mediated by caveolae during the formation of the lipid droplet, which can be observed at transmission electron microscopy. Caveolae may be up to 30 % of the total membrane of the adipocyte.

Inside a group, there are cell-cell connections by gap junctions that allow them to respond in a coordinated manner to electrical inputs. It is unknown if these cytoplasm-cytoplasm connections also happens between adipocytes of different groups.

Covering the external surface of the adipocyte plasma membrane, there is a layer of extracellular matrix (known as external layer) with similar features than the basal lamina of epithelia. The external layer may function as a selective barrier or as a mechanical scaffold, or both. It contains collagen IV, laminin and heparan sulfate, but lacks fibronectin. Fibronectin is present, however, in non-mature adipocytes and it is later exchanged for laminin.

Extracellular matrix is very important for the adipocyte since it influences cell size and differentiation. For instance, it has been suggested that abundant collagen IV is involved in regulating adipocyte cellular size, and pre-adipocytes are not differentiated into mature adipocytes if they cannot release MT1-MMP metalloproteases. Metalloproteases degrade extracellular matrix. Thus, extracellular matrix may physically regulates the cell hipertrophic growth. Adipocyte are connected to the extracellular matrix through integrins, which bind laminin, fibronectin and collagen. There are changes in the integrin expression that guide adipocytes during cell differentiation. Integrins may also be a cell size sensor.

2. Grow and proliferation

During embryo development, there are cells with small lipid droplets in the hipodermis and among viscera, visible at 6 months of pregnancy. They increase in size from 15 µm to 80 µm during birth time.

Adipose tissue can grow by increasing the size of adipocytes: hypertrophy, and by increasing the number of adipocytes: hyperplasia or adipogenesis. Both mechanisms happen when the net body energy is positive.

Increasing the size of adipocytes is the first step to obesity, and hyperplasia happens during severe obesity. Adipocytes can grow to a maximum size, so they can store a limited amount of energy. If energy is still coming, adipose tissue response is to proliferate adipocytes. That is why hypertrophy precedes hyperplasia. Large size adipocytes release substances in a paracrine way that stimulate pre-adipocytes to proliferate. Large adipocytes do not response properly to insulin hormone.

Adipogenesis is produced from fibroblast-like mesenchymal stem cells found in the adipose tissue in both young and adult individuals. Mesenchymal cells are found near the blood vessels of adipose tissue and may derived from embryo neural crests or mesoderm. There are two differentiation steps. Commintment: mesenchymal cell becomes pre-adipocyte, and differentiation: pre-adipocyte becomes adipocytes. However, during early stages of development, the number of adipocytes is genetically determined.

Proliferation of adipocytes in different body fat depots depends on several factors like precursor adipocyte population present in the depot, blood perfusion and nervous innervation density. For example, there is an inverse relation between nervous innervation density and increase of adipocyte proliferation. Likewise, some hormones like insulin and testosterone influence adipocytes behavior, but appear to have more impact on the adipocyte size than in proliferation. There are two main white fat depots in the body: subcutaneous and visceral. Hyperplasia is more frequent in subcutaneous and hypertrophy is prevailing in the visceral depot. The origin of these two depots is different and their physiology and function are also different.

3. Functions

The main function of adipocytes is to store energy as lipid molecules. However, they are also involved in regulating levels of glucose and lipids in the organism. Furthermore, depending on the white fat depot, the functions are different.

Energy storage

Adipocytes storage nutrients as neutral triacylglycerols, so that they can be released during exercise or in periods of lack of food. From the extracellular space, adipocytes can also get fatty acids, cholesterol and glucose that is converted in fatty acids. Adipocytes are very flexible when storing / releasing energy. Lipids are stored more easily than for example glycogen because they are not soluble molecules. Furthermore, a quantity of lipids can contain double amount of energy that the same quantity of glucose. One gram of lipids stores 38 KJ. The storing process is not just to accumulate energy but also for clearing circulating fat and avoiding ectopic lipid depots. An excess of lipids is toxic (lipotoxicity), particularly dangerous for muscle and liver.

About 80 % of free cholesterol (non-esterified cholesterol) is found in the membranes of lipid droplets. Fat depots work as a sink of cholesterol in normal adult humans. Around 25 % of the total cholesterol of the human body is found in fat depots. Caveolae are abundant in adipocytes, which contain the same amount of caveolin 1 than caveolin 2 proteins. The interactions of the two caveolins is important for caveolae formation in adipocytes, and it is mediated by cholesterol. Insulin receptor is found in caveolae membranes. During lipid droplet growing, caveolins are moved from the plasma membrane to the lipid droplet membrane, at the same time that much cholesterol is incorporated. Actually, it is cholesterol that activates the caveolins transfer to facilitate the lipid droplet expansion.

Lipogenesis is the process for incorporating and storing triacylglycerols in adipocytes (Figure 3). The major pathway for synthesizing lipids starts from sn-glycerol 3-phosphate, which is transformed in mono-, di-, or triacylglycerols by fatty acid esterification, which happens in the endoplasmic reticulum. The hormone insulin favors this process by increasing the absorption of glucose by adipocytes. Glycerol 3-phosphate is synthesized from glucose, although it can also be produced from other sources like lactate and some amino acids. Insulin has an additional role by inhibiting lipolysis. Glucose crosses the adipocyte plasma membrane through the GLU4 glucose transporter. This receptor is removed from the plasma membrane by endocytic vesicles and stored in endosomes when insulin levels are low. When insulin concentration increases again, GLU4 is moved to the plasma membrane again.

Figure 3. Lipogenesis and lipolysis (adapted from Rutkowski et al., 2015).

Lipolysis is the degradation of triacylglycerols of the lipid droplet into fatty acids (Figure 3). The enzymes involved in lipolysis are found associated to the surface of the lipid droplet, and after a hormonal stimulus they are recruited in larger number from the cytosol. Fatty acids are released to the extracellular space.


Besides the energy storing function, adipocytes are very active cells releasing proteins and hormones, altogether known as adipocines. Adipose tissue is the largest endocrine structure of the body and can release more than 500 active molecules. Some of them have inflammatory activity. Leptin and adiponectin are involved in the metabolism. Leptin regulates food intake by acting on the hypothalamus. Adiponectin induces sensibility to insulin in the liver and in muscles. Adipcytes release molecules that influence immune system, blood vessel formation and remodeling of the extracelular matrix.


The subcutaneous depot of fat works as temperature insulation tissue at lower temperatures. Furthermore, subcutaneous fat depots soften mechanical strokes on the integument of animals.


Haczeyni H, Bell-Anderson KS, Farrell GC. 2018. Causes and mechanisms of adipocyte enlargement and adipose expansion. Obesity review. 19: 406-420.

Hausman DB, DiGirolamo M. Bartness TJ. Hausman G J, Martin RJ. 2001. The biology of white adipocyte proliferation. Obesity review. 2: 239-254. Read  the paper

Pope BD, Warren CR, Parker KK, Cowan CA. 2016. Microenvironmental Control of Adipocyte Fate and Function. Trends in cell biology. 26:745-5

Rutkowski JM, Stern JH, Scherer PE. 2015. The cell biology of fat expansion. Journal of cell biology. 208: 501-512.

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