Mechanisms underlying fat pad remodeling induced by fasting: role of PAF receptor

Fasting has long been practiced for political and religious reasons and to lose weight. However, biological responses during fasting have yet to be fully understood. Previous studies have shown that cytokines may control fat pad expansion, at least in part, owing to the induction of lipolysis. Indeed, we have previously shown that mice with a lower inflammatory response, such as platelet-activating factor receptor knockout mice (PAFR^-/-), are prone to gain weight and adiposity. The aims of this study were to determine whether adipose tissue becomes inflamed after fasting and to evaluate whether the PAF signaling is a factor in the fat loss induced by fasting.

Wild-type (WT) and PAFR^-/- mice were fasted for 24 h. Adiposity, leukocyte recruitment, and cytokine levels were evaluated. Multiple comparisons were performed using two-way analysis of variance and post hoc Fisher exact test.

After fasting, male WT mice showed lower adiposity (P < 0.001), higher recruitment of immune cells (P < 0.001), and increased cytokine levels (P < 0.05) in adipose tissue. Although WT mice lost ~79% of their adipose tissue mass, PAFR^-/- mice lost only 36%. Additionally, PAFR^-/- mice did not show enhanced cytokine and chemokine levels after fasting (P > 0.05).

Despite low-grade inflammation being associated with metabolic syndrome, at least in part, the inflammatory milieu is also important to induce proper fat mobilization and remodeling of adipose tissue.