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.

The tropical freshwater zebrafish has recently emerged as a valuable model organism for the study of adipose tissue biology and obesity-related disease. The strengths of the zebrafish model system are its wealth of genetic mutants, transgenic tools, and amenability to high-resolution imaging of cell dynamics within live animals. However, zebrafish adipose research is at a nascent stage and many gaps exist in our understanding of zebrafish adipose physiology and metabolism. By contrast, adipose research within other, closely related, teleost species has a rich and extensive history, owing to the economic importance of these fish as a food source. Here, we compare and contrast knowledge on peroxisome proliferator-activated receptor gamma (PPARG)-mediated adipogenesis derived from both biomedical and aquaculture literatures. We first concentrate on the biomedical literature to (i) briefly review PPARG-mediated adipogenesis in mammals, before (ii) reviewing Pparg-mediated adipogenesis in zebrafish. Finally, we (iii) mine the aquaculture literature to compare and contrast Pparg-mediated adipogenesis in aquaculturally relevant teleosts. Our goal is to highlight evolutionary similarities and differences in adipose biology that will inform our understanding of the role of adipose tissue in obesity and related disease.

Adipose tissues often exhibit subtle, quantitative differences between individuals, leading to a graded series of adiposity phenotypes at the population level. Robust, quantitative analyses are vital for studying these differences. In this Commentary we highlight two articles from our lab that employ sensitive new methods in zebrafish capable of delineating complex and quantitative adiposity phenotypes. In the first article, we utilized in vivo imaging to systematically quantify zebrafish adipose tissues. We identified 34 regionally distinct zebrafish adipose tissues and developed statistical models to predict the size and variance of each adipose tissue over the course of zebrafish growth. We then employed these models to identify effects of strain and diet on adipose tissue growth. In the second article, we employed deep phenotyping to study complex disease-related adiposity traits. Using this methodology, we identified that adipose tissues have unique capacities to re-deposit lipid following food restriction and re-feeding. These distinct re-deposition potentials led to widespread fat distribution changes following refeeding. We discuss how these novel findings may provide relevance to health conditions such as anorexia nervosa. Together, the strategies described in these two articles can be used as unbiased and quantitative methods to uncover new relationships between genotype, diet and adiposity.

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