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Updated: May 1, 2026
Isolating Brown Adipocytes from Murine Interscapular Brown Adipose Tissue for Gene and Protein Expression Analysis
Published on: March 12, 2021
Expression profiling of PPARγ-regulated microRNAs in human subcutaneous and visceral adipogenesis in both genders
Jing Yu1, Xiaocen Kong, Juan Liu
1Department of Geratology (J.Y., X.K., J.L., Y.L., Y.S., S.L., W.D., C.W., G.D.) and Department of General Surgery (F.Z.), the First Hospital Affiliated to Nanjing Medical University, Nanjing, People's Republic of China.
Abstract:
Clinical evidence shows that visceral fat accumulation decreases whereas sc fat increases in patients treated with thiazolidinediones (TZDs), a type of peroxisome proliferator-activated receptor (PPAR)γ agonist. To clarify the molecular mechanism of the differential effects of PPARγ agonists on sc and visceral adipose, we investigated expression profiling of PPARγ-regulated micro-RNAs (miRNAs) using miRNA microarray. The level of 182 miRNAs changed in human sc adipose treated with pioglitazone, whereas only 46 miRNAs changed in visceral adipose. Among these miRNAs, 27 miRNAs changed in both human sc and visceral adipocytes. Specifically, 7 miRNAs changed at the same direction in sc and visceral adipocytes, whereas 20 miRNAs changed at opposite directions in these two fat depots. Bioinformatics analysis showed that these miRNAs and the predicted target genes were involved in TGF-β-, Wnt/β-catenin-, and insulin-signaling pathways and related to metabolic regulation or cell cycle. Among the miRNAs changed at the same direction in sc and visceral adipocytes, miR-378, located in the first intron of PPARγ coactivator 1β (PGC1β), was coordinately expressed with PGC1β during adipogenesis. Moreover, miR-378 and PGC1β were both up-regulated by PPARγ agonist. We also provided evidence that miR-378 promoted adipogenesis in sc fat, but not in visceral fat. These results display miRNAs expression profiling altered in sc and visceral adipogenesis regulated by PPARγ and suggest a potential mechanism underlying the differential effects of TZDs on the 2 fat depot accumulations.
Insights
Thiazolidinediones (TZDs) differentially affect fat depots by altering micro-RNA (miRNA) expression. This study reveals specific miRNAs, like miR-378, mediate these effects, impacting subcutaneous fat but not visceral fat accumulation.
Area of Science:
- Endocrinology
- Molecular Biology
- Metabolic Research
Background:
- Thiazolidinediones (TZDs), peroxisome proliferator-activated receptor (PPAR)γ agonists, are known to decrease visceral fat and increase subcutaneous (sc) fat.
- The precise molecular mechanisms driving these differential effects on adipose tissue depots remain incompletely understood.
Purpose of the Study:
- To elucidate the molecular mechanisms behind the differential effects of PPARγ agonists on sc and visceral adipose tissue.
- To investigate the expression profiling of PPARγ-regulated micro-RNAs (miRNAs) in response to PPARγ agonism.
Main Methods:
- Utilized miRNA microarray to profile miRNA expression in human sc and visceral adipose tissue treated with pioglitazone (a TZD).
- Performed bioinformatics analysis to identify pathways and functions associated with differentially expressed miRNAs.
- Investigated the role of specific miRNAs, such as miR-378, in adipogenesis in different fat depots.
Main Results:
- Pioglitazone altered the expression of 182 miRNAs in sc adipose tissue and 46 miRNAs in visceral adipose tissue.
- 27 miRNAs showed altered expression in both depots, with 7 changing in the same direction and 20 in opposite directions.
- miR-378, co-expressed with PGC1β and upregulated by PPARγ agonists, promoted sc adipogenesis but not visceral adipogenesis.
Conclusions:
- PPARγ activation leads to distinct miRNA expression profiles in sc and visceral adipose tissue.
- Specific miRNAs, including miR-378, play a role in the differential regulation of fat depot accumulation by TZDs.
- Findings suggest a potential mechanism for the divergent effects of TZDs on subcutaneous and visceral fat.
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