Journal
MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 391, Issue 1-2, Pages 59-66Publisher
SPRINGER
DOI: 10.1007/s11010-014-1987-5
Keywords
TNF alpha; Wnt/beta-catenin signaling; Leptin receptor; Obesity; Adipocyte
Categories
Funding
- National Natural Sciences Foundation of China [81070685]
- Research Found for the Doctoral Program of Higher Education of China [20103704110002]
- Science and Technology Projects of Shandong [J06L11]
- Natural Sciences Foundation of Shandong
- Novo Nordisk Fonden [NNF14OC0009897] Funding Source: researchfish
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Tumor necrosis factor alpha (TNF alpha) is an adipokine involved in the regulation of cell differentiation and lipid metabolism, but its specific role has not been clearly understood. We validated a hypothesis that loss of TNF alpha function would inhibit Wnt/beta-catenin signaling and accelerate adipogenesis in adolescent genetic obese mice. Epididymal white adipose tissues (eWAT) from TNF alpha deficient (TNF alpha(-/-)), leptin receptor deficient (db/db) and double gene mutant (db/db/TNF alpha(-/-), DT) male mice were used for comparative analysis of key molecules in Wnt/beta-catenin signaling and adipogenic markers by qRT-PCR and western blot techniques. Compared with TNF alpha(-/-) and WT mice of 28 days old, an obese trait was observed in both db/db and DT mice, while the latter showed more significant body weight gain and eWAT hypertrophy. The mRNA level of key molecules in Wnt/beta-catenin pathway was reduced in both obese groups, while the DT group was the lowest. Expression of adipocyte-specific genes was up-regulated during obese development in the two obese groups, while the DT group revealed more correlation than that of db/db group. At the protein level, a down regulation of Wnt10b and beta-catenin in obese eWAT showed similar tendency with that of mRNA level. Compared with the lean groups, the levels of adiponectin and PPAR gamma 2 for the obese groups were down-regulated at 21-day-old age, while they were elevated at older age. Our results suggested that deficiency in TNF alpha inhibited Wnt/beta-catenin signaling of the obese eWAT and up-regulated expression of adipokines, and accelerated adipogenesis in genetic obese mice on a chow diet.
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