Key result
Phosphorus supplementation reversed localized perivascular adipose tissue inflammation and early cardiovascular consequences in a dose-dependent manner in a prediabetic rat model.
Why the study?
Perivascular adipose tissue inflammation is implicated as an early instigator of cardiovascular deterioration, but structured interventions targeting root metabolic pathologies are lacking.
Does phosphorus supplementation mitigate perivascular adipose inflammation and early cardiovascular consequences in a prediabetic rat model?
Does phosphorus supplementation mitigate perivascular adipose inflammation and early cardiovascular consequences in a prediabetic rat model?
Phosphorus supplementation may reverse perivascular adipose tissue inflammation and early cardiovascular consequences in metabolic impairment.
Hypothesis-generating in prediabetic models; leaves open whether phosphorus supplementation mitigates perivascular inflammation or cardiovascular risk in humans.
Background The complexity of the interaction between metabolic dysfunction and cardiovascular complications has long been recognized to extend beyond simple perturbations of blood glucose levels. Yet, structured interventions targeting the root pathologies are not forthcoming. Growing evidence implicates the inflammatory changes occurring in perivascular adipose tissue (PVAT) as early instigators of cardiovascular deterioration. Methods and Results We used a nonobese prediabetic rat model with localized PVAT inflammation induced by hypercaloric diet feeding, which dilutes inorganic phosphorus (Pi) to energy ratio by 50%, to investigate whether Pi supplementation ameliorates the early metabolic impairment. A 12-week Pi supplementation at concentrations equivalent to and twice as much as that in the control diet was performed. The localized PVAT inflammation was reversed in a dose-dependent manner. The increased expression of UCP1 (uncoupling protein1), HIF-1α (hypoxia inducible factor-1α), and IL-1β (interleukin-1β), representing the hallmark of PVAT inflammation in this rat model, were reversed, with normalization of PVAT macrophage polarization. Pi supplementation restored the metabolic efficiency consistent with its putative role as an UCP1 inhibitor. Alongside, parasympathetic autonomic and cerebrovascular dysfunction function observed in the prediabetic model was reversed, together with the mitigation of multiple molecular and histological cardiovascular damage markers. Significantly, a Pi-deficient control diet neither induced PVAT inflammation nor cardiovascular dysfunction, whereas Pi reinstatement in the diet after a 10-week exposure to a hypercaloric low-Pi diet ameliorated the dysfunction. Conclusions Our present results propose Pi supplementation as a simple intervention to reverse PVAT inflammation and its early cardiovascular consequences, possibly through the interference with hypercaloric-induced increase in UCP1 expression/activity.
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Dwaib et al. (2021) studied Early metabolic impairment. Phosphorus (Pi) supplementation vs. Control diet was evaluated on PVAT inflammation and cardiovascular dysfunction. Phosphorus supplementation reversed localized perivascular adipose tissue inflammation and early cardiovascular consequences in a dose-dependent manner in a prediabetic rat model.
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