Effect of short chain fatty acids on the expression of free fatty acid receptor 2 (Ffar2), Ffar3 and early-stage adipogenesis.

Adipose tissue has a major influence on insulin sensitivity. Stimulation of free fatty acid receptor 2 (FFAR2) has been proposed to influence adipocyte differentiation. We hypothesised that exposing preadipocytes to short chain fatty acids would induce earlier expression of nuclear receptors that co-ordinate adipogenesis, triglyceride accumulation and leptin secretion. 3T3-L1 preadipocytes were differentiated in the presence of 1 µM acetate, 0.1-10 µM propionate or vehicle control. In experiment 1, expression of Ffar2 and nuclear receptor mRNA was measured by quantitative PCR over 48 h following onset of differentiation. In experiment 2, extracellular leptin concentration and intracellular triglyceride content were measured at days 0, 2, 4, 6, 8 and 10 following the onset of differentiation. Control cells exhibited similar temporal dynamics of gene expression, triglyceride accumulation and leptin secretion as reported previously. We were unable to detect expression of Ffar3 mRNA at any stage of differentiation. Consistent with a lack of Ffar2 expression in the first 24 h of differentiation, acetate and propionate had no significant effect on nuclear receptor expression. Furthermore, acetate or propionate treatment did not alter leptin concentration or triglyceride content. In conclusion, we observed no significant effect of propionate or acetate on adipogenesis in 3T3-L1 cells using validated quantitative techniques.

Adipose tissue, adipocytes and the circadian timing system.

Circadian clocks time the daily occurrence of multiple aspects of behaviour and physiology. Through studies of chronic misalignment between our internal clocks and the environment (e.g. during shift work), it has long been postulated that disruption of circadian rhythms is detrimental to human health. Recent advances in understanding of the cellular and molecular basis of mammalian circadian timing mechanisms have identified many key genes involved in circadian rhythm generation and demonstrated the presence of clocks throughout the body. Furthermore, clear links between sleep, circadian rhythms and metabolic function have been revealed, and much current research is studying these links in more detail. Here, we review the evidence linking circadian rhythms, clock genes and adipose biology. We also highlight gaps in our understanding and finally suggest avenues for future research.