Key result
In high-fat diet-fed mice, LFABP deletion increased subcutaneous adipose tissue mass by markedly increasing the number of adipocytes (5-fold higher) rather than their size (4-fold smaller) compared to wild-type mice.
Why the study?
Obesity is a major risk factor for metabolic syndrome disorders, but the mechanisms underlying why high-fat diet-fed liver fatty acid-binding protein null mice become obese yet remain metabolically healthy were unclear.
Does LFABP deletion promote hyperplastic expansion of white adipose tissue in male mice on a high-fat diet?
Does LFABP deletion promote hyperplastic expansion of white adipose tissue in male mice on a high-fat diet?
Absolute Event Rate: 45.6% vs 222%
p-value: p=<0.001
LFABP deletion in mice promotes a metabolically healthy obese phenotype by driving hyperplastic rather than hypertrophic expansion of subcutaneous adipose tissue during high-fat diet feeding.
SAT hyperplasia may confer metabolic protection in obese mice; leaves open human relevance and therapeutic targeting.
Obesity is an important risk factor for the development of metabolic syndrome disorders. We previously showed that the liver fatty acid-binding protein null mouse (LFABP −/− ) becomes obese upon high-fat diet (HFD) feeding but remains metabolically healthy. Here we find that the obese LFABP −/− mouse increases subcutaneous adipose tissue (SAT) mass by markedly increasing the number rather than the size of adipocytes, as is typical with HFD. Indeed, while HFD-fed LFABP −/− mice had almost double the fat mass of WT, SAT adipocyte size was >4-fold smaller and adipocyte number was 5-fold higher in the LFABP −/− . Transcriptomic analysis of SAT revealed that Lfabp deletion alters the expression of multiple pathways that modulate adipose expansion and function including cholesterol biosynthesis, adipogenesis, and extracellular matrix remodeling. LFABP is expressed in liver and small intestine but not in adipose tissues, thus its ablation may promote interorgan crosstalk that drives hyperplastic expansion of metabolically beneficial SAT, contributing to the healthy obese phenotype of the LFABP −/− mouse.
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Diolintzi et al. (2025) studied Diet-induced obesity (n=40). Lfabp deletion (LFABP-/-) and high-fat diet vs. Wild-type mice on high-fat diet was evaluated on Inguinal white adipose tissue (iWAT) fat cell volume (pL) (p=<0.001). In high-fat diet-fed mice, LFABP deletion increased subcutaneous adipose tissue mass by markedly increasing the number of adipocytes (5-fold higher) rather than their size (4-fold smaller) compared to wild-type mice.
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