Yerba Maté (Ilex paraguariensis) Supplement Exerts Beneficial, Tissue-Specific Effects on Mitochondrial Efficiency and Redox Status in Healthy Adult Mice

Abstract

Yerba maté, a herbal tea derived from Ilex paraguariensis, has previously been reported to be protective against obesity-related and other cardiometabolic disorders. Using high-resolution respirometry and reverse-phase high-performance liquid chromatography, the effects of four weeks of yerba maté consumption on mitochondrial efficiency and cellular redox status in skeletal muscle, adipose, and liver, tissues highly relevant to whole-body metabolism, were explored in healthy adult mice. Yerba maté treatment increased the mitochondrial oxygen consumption in adipose but not in the other examined tissues. Yerba maté increased the ATP concentration in skeletal muscle and decreased the ATP concentration in adipose. Combined with the observed changes in oxygen consumption, these data yielded a significantly higher ATP:O₂, a measure of mitochondrial efficiency, in muscle and a significantly lower ATP:O₂ in adipose, which was consistent with yerba maté-induced weight loss. Yerba maté treatment also altered the hepatic glutathione (GSH)/glutathione disulfide (GSSG) redox potential to a more reduced redox state, suggesting the treatment's potential protective effects against oxidative stress and for the preservation of cellular function. Together, these data indicate the beneficial, tissue-specific effects of yerba maté supplementation on mitochondrial bioenergetics and redox states in healthy mice that are protective against obesity.

Keywords: metabolism; mitochondria; nutraceuticals; obesity; yerba maté.

Figure 1

Yerba maté consumption prevents weigh gain in female and male mice. Body weight was measured weekly over the four weeks of yerba maté treatment and normalized to initial weights at week = 0. Female and male weights were assessed together (A), as well as separately (B,C). Female CON, n = 5; female MATÉ, n = 5; male CON, n = 5, male MATÉ, n = 5. * p < 0.05.

Figure 2

Yerba maté consumption increases the mitochondrial efficiency in skeletal muscle from male and female mice. Rates of mitochondrial oxygen consumption (A) were measured via a substrate–uncoupler–inhibitor–titration protocol from gastrocnemius tissue following four weeks of yerba maté supplementation. The protocol included the addition of glutamate and malate (GM), ADP (D), and succinate (S). ATP concentration was quantified (B) and ATP:O₂ flux ratios (C) were calculated (CON, n = 6; MATÉ, n = 6). Concentrations of reduced glutathione (GSH, (D)) and oxidized glutathione (GSSG, (E)) were quantified via reverse-phase high-performance liquid chromatography. GSH/GSSG E_h redox potentials were calculated ((F); CON, n = 8; MATÉ, n = 8). * p < 0.05, ** p < 0.01.

Figure 3

Yerba maté consumption decreases mitochondrial efficiency in white adipose tissue. Rates of mitochondrial oxygen consumption (A) were measured using a substrate–uncoupler–inhibitor–titration protocol from subcutaneous white adipose tissue following four weeks of yerba maté supplementation. The protocol included the addition of glutamate and malate (GM), ADP (D), and succinate (S). The ATP concentration was quantified (B), and ATP:O₂ flux ratios (C) were calculated (CON, n = 6; MATÉ, n = 6). Concentrations of reduced glutathione (GSH, (D)) and oxidized glutathione (GSSG, (E)) were quantified via reverse-phase high-performance liquid chromatography. GSH/GSSG E_h redox potentials were calculated ((F); CON, n = 8; MATÉ, n = 8). * p < 0.05.

Figure 4

Yerba maté consumption alters hepatic redox potential but not mitochondrial efficiency. Rates of mitochondrial oxygen consumption (A) were measured via a substrate–uncoupler–inhibitor–titration protocol from liver tissue following four weeks of yerba maté supplementation. The protocol included the addition of glutamate and malate (GM), ADP (D), and succinate (S). The ATP concentration was quantified (B) and ATP:O₂ flux ratios (C) were calculated (CON, n = 6; MATÉ, n = 6). Concentrations of reduced glutathione (GSH, (D)) and oxidized glutathione (GSSG, (E)) were quantified via reverse-phase high-performance liquid chromatography. GSH/GSSG E_h redox potentials were calculated (F); CON, n = 8; MATÉ, n = 8). * p < 0.05.