Causes and mechanisms of adipocyte enlargement and adipose expansion

Abstract

Adipose tissue plays a significant role in whole body energy homeostasis. Obesity-associated diabetes, fatty liver and metabolic syndrome are closely linked to adipose stress and dysfunction. Genetic predisposition, overeating and physical inactivity influence the expansion of adipose tissues. Under conditions of constant energy surplus, adipocytes become hypertrophic and adipose tissues undergo hyperplasia so as to increase their lipid storage capacity, thereby keeping circulating blood glucose and fatty acids below toxic levels. Nonetheless, adipocytes have a saturation point where they lose capacity to store more lipids. At this stage, when adipocytes are fully lipid-engorged, they express stress signals. Adipose depots (particularly visceral compartments) from obese individuals with a severe metabolic phenotype are characterized by the high proportion of hypertrophic adipocytes. This review focuses on the mechanisms of adipocyte enlargement in relation to adipose fatty acid and cholesterol metabolism, and considers how this may be related to adipose dysfunction.

Lmo4‐resistin signaling contributes to adipose tissue‐liver crosstalk upon weight cycling

“…Adipocyte hypertrophy is typical for individuals with overweight or obesity, while adipocyte hyperplasia usually occurs at late stage of weight gain, since adipocytes have a saturation point where they lose the capacity to store more lipids, and the hypertrophic adipocytes secrete certain adipokines to stimulate preadipocytes to proliferate in a paracrine way. 47 Under most circumstances, increased adipocyte hypertrophy is associated with chronic inflammation in WAT. 29 However, similar hypertrophy, but increased hyperplasia, associated with less inflammation in eWAT, has been found in the HF-LF cycled mice ( Figure 3A-D).…”

Oxygenation of adipose tissue: A human perspective

“…However, it has been suggested that there is a set number of pre‐adipocytes that can be recruited, which seems to be genetically determined . Adipocytes can substantially increase in size but do have a certain expansion limit, implying that these cells have a maximum capacity of storing TAG . What seems to be even more important than the maximal storage capacity is the ability to dynamically store lipids in the postprandial phase, the so‐called lipid buffering capacity, and to release fatty acids under fasting conditions .…”

“…As a consequence, more dietary lipids are diverted through the circulation to be stored in other tissues, which results in ectopic fat accumulation when lipid uptake exceeds lipid oxidation . The storage of excess lipids in non‐adipose tissues in obesity has important metabolic consequences, since this is closely associated with insulin resistance . Furthermore, hypertrophic adipocytes are characterized by a pro‐inflammatory phenotype, which may further aggravate insulin resistance .…”

Adipocyte hyperplasia: the primary mechanism of supraspinatus intramuscular fat accumulation after a complete rotator cuff tendon tear: a study in the rabbit

“…There is evidence for regional differences in adipocytes behaviour in human obesity. While adipocyte hypertrophy characterizes upper body sub-cutaneous fat, adipocytes cycling between hyperplasia and hypertrophy characterized deposits below the waist as obesity progresses upon high-fat feeding [23,25,34]. Our results indicate that expansion of IMF in the SSP muscle present significant similarities with subcutaneous fat deposits located below the waist; fat expansion resulted from adipocyte hyperplasia at least within the first 12 weeks after tendon detachment.…”