Impact of bioactive compounds on the function of adipose tissue, using precision-cut adipose tissue slices as a model
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- Obesity can be linked to numerous health issues, including hypertension, dyslipidaemia, type II diabetes, cardiovascular disorders, and some cancers. Bioactive compounds, such as polyunsaturated fatty acids (PUFAs) and phytochemicals represent promising alternatives to drugs to prevent or treat obesity. Punicic acid (PunA) is a conjugated linolenic acid (CLnA), a type of PUFA. It has shown anti-obesity effects through β-oxidation, insulin sensitivity, inflammation, adipogenesis and lipogenesis. No study has investigated its impact on lipolysis, and few on adipokines expression. Yet, both pathways are relevant in this context. Indeed, excessive fat accumulation promotes the production of pro-inflammatory adipokines, such as TNF-alpha, which favours the deposition of ectopic fat via increased lipolysis. Another interesting bioactive compound is piceatannol (PIC), a polyphenol. It has shown anti-obesity effects through inflammation, adipogenesis, lipogenesis and insulin sensitivity. Its impact on lipolysis has been investigated in two studies. However, our laboratory discovered that PIC interferes with the enzymes of the kit used to quantify glycerol released during lipolysis, skewing the results obtained in previous studies. The effect of PIC alone but also in combination with PunA would be interesting to explore. Indeed, research has already reported that some PUFAs and polyphenols are able to interact synergistically to reduce comorbidities associated with obesity. In this context, the aim of our master’s thesis was to investigate the impact of PunA, PIC and their combination (PunA+PIC) on the function of adipose tissue, especially on lipolysis and adipokine gene expression using a pig precision-cut adipose tissue slices (PCATS) model was used. In addition to PunA and PIC, rumenic acid (RmA) and t10c12, both conjugated linoleic acids (CLAs), were studied. In fact, PunA is known to be biotransformed into RmA in animal tissues. Investigating the effects of RmA on adipose tissue is therefore relevant to see if the effects of Puna were due to PunA itself, or to it transformation into RmA. T10c12 was chosen as a positive control for lipolysis, as some studies have suggested that it increases lipolysis. Pig PCATS were first pre-incubated for 24 hours in media containing the bioactive compounds (PunA, RmA, and t10c12 at 100 µM, PIC at 500 µM and PunA+PIC at these same concentrations) and were then incubated for a further 24 hours with the bioactive compounds, in basal lipolysis and lipolysis induced with isoproterenol, a β-adrenergic receptor agonist. Only t10c12 showed a slightly significant increase in basal lipolysis, whereas none of the other treatments significantly affected lipolysis. However, trends towards inhibition of induced lipolysis in presence of PIC were reported (using the quantification of fatty acids released in the culture media by gas chromatography), which suggests a potential anti-lipolytic action of this polyphenol. In addition, PIC increased the proportion of palmitic acid, a saturated fatty acid and decreased the proportion of oleic acid, an unsaturated fatty acid. The analysis of TNF-α and adiponectin gene expression did not reveal any significant effect of the bioactive compounds. Finally, no clear interaction between PunA and PIC was reported.