Adipose morphology and metabolic disease

Abstract

Adipose morphology is defined as the number and size distribution of adipocytes (fat cells) within adipose tissue. Adipose tissue with fewer but larger adipocytes is said to have a 'hypertrophic' morphology, whereas adipose with many adipocytes of a smaller size is said to have a 'hyperplastic' morphology. Hypertrophic adipose morphology is positively associated with insulin resistance, diabetes and cardiovascular disease. By contrast, hyperplastic morphology is associated with improved metabolic parameters. These phenotypic associations suggest that adipose morphology influences risk of cardiometabolic disease. Intriguingly, monozygotic twin studies have determined that adipose morphology is in part determined genetically. Therefore, identifying the genetic regulation of adipose morphology may help us to predict, prevent and ameliorate insulin resistance and associated metabolic diseases. Here, we review the current literature regarding adipose morphology in relation to: (1) metabolic and medical implications; (2) the methods used to assess adipose morphology; and (3) transcriptional differences between morphologies. We further highlight three mechanisms that have been hypothesized to promote adipocyte hypertrophy and thus to regulate adipose morphology.

Relationship between epicardial adipose tissue thickness and epicardial adipocyte size with increasing body mass index

“…Finally, as mentioned earlier, adipose tissue also expands by adipocyte hyperplasia [8]. Recent prospective studies using adipocyte deuterium incorporation over an 8-week period have found independent correlations of new-adipocyte formation with body fat percentage and BMI [34,35].…”

“…Adipose expansion in obesity occurs by two main morphological alterations to the constituent adipocytes: an increase in cell size (hypertrophy) and an increase in cell number (hyperplasia) [8]. The relative contributions of trophic and plastic remodelling vary between different subcutaneous (SAT) and visceral adipose tissue (VAT) depots; however, hypertrophic growth seems to be the predominant mechanism in obesity [8].…”

“…Adipose expansion in obesity occurs by two main morphological alterations to the constituent adipocytes: an increase in cell size (hypertrophy) and an increase in cell number (hyperplasia) [8]. The relative contributions of trophic and plastic remodelling vary between different subcutaneous (SAT) and visceral adipose tissue (VAT) depots; however, hypertrophic growth seems to be the predominant mechanism in obesity [8]. Consistently, an increase in the volume of various SAT depots, including at abdominal, femoral, and gluteal sites has been found to not only correlate with indices of obesity, like body mass index (BMI) and body fat percentage but also with the size of the adipocytes comprising each depot [9][10][11][12][13][14][15][16].…”

Adipose tissue dysfunction in obese horses with equine metabolic syndrome

“…Our data demonstrate that adipocyte hypertrophy, inflammation and increased CCL2 expression are features of obese adipose tissue in horses but that fibrosis and altered adipose tissue expression of insulin signalling genes are not consistent features. Increased adipocyte size, hypertrophy, in response to excess calorie intake is associated with insulin resistance and dyslipidaemia in humans whereas increasing adipocyte number, hyperplasia, is associated with a favourable metabolic profile [3]. Hypertrophy occurs when there is an imbalance between lipid storage and lipolysis.…”

Dihydropyranocoumarins Exerted Anti-Obesity Activity In Vivo and its Activity Was Enhanced by Nanoparticulation with Polylactic-Co-Glycolic Acid

“…On the one hand, hypertrophy of adipocytes can increase hypoxia and mechanical stress to neighboring cells and the extracellular matrix, resulting in decreased adipose tissue function, which contributes to the early onset of metabolic disease, and persistently elevated levels of nutrients in the blood, which cause toxic lipid deposits in other tissues, such as muscle and the liver [20,21]. On the other hand, hyperplastic growth is considered to be a healthy and adaptive mechanism by which to maintain proper vascularization, responses to anti-inflammatory hormone adiponectin, and insulin-sensitizing and other metabolism-modulatory adipokines [20,22]. Indeed, although treatment with thiazolidinediones, an insulin-sensitizing drug, leads to enhancement of overall adipose tissue growth, it induces the conversion of hypertrophic into hyperplastic adipose tissue, which results in a greater number of small adipocytes and a significant decrease in large adipocytes [23].…”