Adipose Tissue Develops Similarly In The Early & Later Phases Of Obesity

Adipose Tissue Develops Similarly In The Early & Later Phases Of Obesity

From the latest study published in the International Journal of Obesity, it is uncovered that the growth of excess weight or obesity is accompanied by changes like fat cell size in the cellular properties of white adipose tissue(WAT) and lipid metabolism, especially lipolysis. These transformations are not known and are currently being investigated if they vary between early/puberty(EOO <18 years) or late-onset obesity(LOO).

Adipose Tissue Develops Similarly In The Early & Later Phases Of Obesity

White adipose tissue is one of the two adipose tissue which is composed of monocular adipocytes. The nutritional quantity of adipose tissues may vary as people age. In adult men, it composes between 6-25% of body weight and in adult women, it is 14-35%. WAT is used as energy storage and has receptors for insulin, sex hormones, norepinephrine, and glucocorticoids.Adipose Tissue Develops Similarly In The Early & Later Phases Of Obesity

They were regarded as inactive tissue that mainly functions as thermal insulation. By the middle of the twentieth century, it became very much clear that WAT was significant in energy homeostasis because it could use glucose as well as store and release energy-rich fatty acids.

Lipids are mainly accumulated in the form of triacylglycerol(TAG), in a single lipid drop ingrown white adipocytes, or multiple lipid drops in most cell types, including brown adipocytes.

The WAT advances by growth in the size of the fat cells. Several other studies proposed that WAT develops in childhood/adolescence due to the mix of size and number of growing fat cells, and growth during adolescence is associated only with the development of pre-existing fat cells.

Some further analyses contradict this view and show that weight gain or recovery over time in adults is also associated with an accumulation in the number of fat cells.

The researchers included 439 subjects with a confirmed BMI at the age of 18 and studied between 1996 and 2020. According to the data collected, the subjects were divided into separate groups, such as those who have never been overweight (BMI <25 kg/m2), EOO, and LOO. The size, number, morphology (size relative to body fat), and lipolysis of adipocytes in the subcutaneous abdominal cavity were defined.

This latest study proves the effects of the early or late beginning of obesity on human white adipose tissue. However, the BMI and total body fat levels were more elevated in the early outset form, there was no discrepancy between the two conditions regarding the potential cellular mechanism behind fat enlargement.

The feasible reasons behind the discrepancies may be an abrupt increase in body weight during adolescence when surplus body fat evolves earlier in life. Discrepancies in BMI continued after the correction for the adherence period.

In excess weight/obesity, the accumulation in body fat at least in the subcutaneous WAT of the abdomen is defined by an increase in both the size and number of fat cells. In the complete sense, these values ​​were higher in EOO than in LOO, which is probably due to the greater ESAT mass in the first group.

Surprisingly, the increase in BMI over time from the age of 18 is positively correlated with the size/number of fat cells in all groups. When the WAT morphology was quantified (delta value), only small discrepancies were observed between the three groups.

Damaged lipolysis can lead to the development of excess body fat. As mentioned earlier, the results of the study of the lipolysis of fat cells in the presence of excess body fat depending on how the rate is defined(the weight of lipids or the number of fat cells).

According to these previous studies, lipolysis rates decreased in excess weight/obesity when defined per lipid weight, but raised when associated with the number of fat cells.

Except for lipolysis data on the number of fat cells, age did not affect the onset of overweight/obesity. Other factors related to BMI, such as heredity/genetics, lifestyle, pancreatic beta-cell function, incretins, and currently unexplored microbiota, may be affected by the onset of excess weight/obesity and its effect on clinical phenotype.

As a result, subjects with the early or late beginning of excess weight/obesity had comparable disorders in WAT function in terms of cellularity, morphology, and lipolysis, except for some small differences in visceral fat mass and lipolysis in men.

The most significant discrepancy is at least partial subcutaneous WAT accumulation in the early-onset form, which may be due to the faster accumulation of body fat in adolescent obesity.

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