Omics & gene networks

Functional dissection of Junb in Ucp1-independent thermogenic regulation in porcine adipose tissue

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Abstract

In mammals, adipose tissue stores energy and regulates body temperature. White adipose tissue (WAT) accumulates lipids, while brown (BAT) and beige adipocytes generate heat via UCP1-mediated non-shivering thermogenesis. Pigs lack BAT and functional UCP1, leading to reduced cold tolerance and 10à¢â‚¬â€œ20% neonatal mortality in winter. While pigs mainly rely on muscle shivering, recent data suggest adipocytes can support non-shivering thermogenesis. This study investigates cold-induced thermoregulation in pig adipose tissue and compares it with Ucp1-knockout mice to uncover UCP1-independent mechanisms. Seven 2-month-old Xiangzhu minipigs were used. Four pigs were exposed to a cold room (4à¢â‚¬â€œ10à¢â‚¬Â¯°C) for 14 days, while three remained outdoors (26à¢â‚¬â€œ31.5à¢â‚¬Â¯°C). Samples were collected only after cold exposure, and no paired samples were obtained before cold stimulation. Histological analysis, qPCR, and western blotting were performed to detect thermogenic and beige adipocyte marker genes. Cold exposure induced a distinct beige-like phenotype and activated thermogenic gene expression in pig adipose tissue. scRNA-seq of neck white adipose tissue further revealed an increased population of Junbà¢ÂÂº cells after cold exposure, and in vitro experiments confirmed a marked upregulation of Junb expression. To explore Junb's functional role, an immortalized porcine adipocyte cell line overexpressing Junb was established. Junb overexpression significantly enhanced lipogenesis, likely by promoting long-chain fatty acid synthesis, leading to increased lipid accumulation. In contrast, Junb silencing or overexpression in primary white adipocytes derived from Ucp1-knockout mice revealed that Junb may regulate Ucp1-independent thermogenesis by regulating lipolytic pathways. These findings suggest that Junb exerts distinct regulatory effects on non-Ucp1-dependent thermogenesis between Ucp1-deficient species (pigs) and Ucp1-knockout models (mice). Specifically, while Junb in pigs primarily facilitates lipid storage and thermal insulation under cold stress, it contributes to free fatty acid mobilization within compensatory thermogenic pathways in Ucp1-KO mice. This study constructs a thermogenic signaling network of Junb in adipose tissue. It provides molecular targets for improving piglet cold resistance and breeding cold-resistant pig breeds, with significant scientific and industrial application value.

Keywords: 2026

How to Cite:

Li, J., Hu, X. & Nedergaard, J., (2026) “Functional dissection of Junb in Ucp1-independent thermogenic regulation in porcine adipose tissue”, World Congress on Genetics Applied to Livestock Production Digital Archive 2026(1): 2285350. doi: https://doi.org/10.31274/wcgalp.23651

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