Curcumin, a naturally occurring plant polyphenolic compound, may have beneficial effects in nonalcoholic steatohepatitis (NASH) development. We examined whether curcumin supplementation could be used in both prevention and treatment of NASH with fibrosis. Female Wistar rats were provided ad libitum access to a “western diet” (WD) high in fat (43% kcal), sucrose (29% kcal), and cholesterol (2% w/v), as well as 15% fructose drinking water. Intraperitoneal CC14 injections (0.5 mL/kg) were also administered at weeks 1, 2, 4, and 6 to accelerate development of a NASH with fibrosis phenotype. Rats were randomized to four groups (n = 9–12/group) and fed ad libitum: (1) WD for 8‐weeks (8WD), (2) WD enriched with curcumin for 8‐weeks (8WD+C; 0.2% curcumin, BCM‐95, DolCas Biotech) to assess prevention, (3) WD for 12‐weeks (12WD), (4) WD for 8‐weeks followed by 4‐weeks WD+C (12WD+C) to assess treatment. Curcumin prevention (8WD vs. 8WD+C) attenuated (P < 0.05) histological liver inflammation, molecular markers of fibrosis (Col1a1 mRNA) and a serum marker of liver injury (AST). Curcumin treatment (12WD vs. 12WD+C) reduced (P < 0.05) hepatocellular inflammation, steatosis, NAFLD Activity Scores, and serum markers of liver injury (AST, ALP). Moreover, curcumin treatment also increased hepatic pACC/ACC, ApoB100, and SOD1 protein, and decreased hepatic FGF‐21 levels; whereas, curcumin prevention increased hepatic glutathione levels. Both curcumin prevention and treatment reduced molecular markers of hepatic fibrosis (Col1a1 mRNA) and inflammation (TNF‐α, SPP1 mRNA). Curcumin supplementation beneficially altered the NASH phenotype in female Wistar rats, particularly the reversal of hepatocellular inflammation.

EPC when used concurrently with HIIT and in subsequent recovery days reduces skeletal muscle markers of proteolysis.

Background: We examined the acute effect of a red spinach extract (RSE) (1000 mg dose; ~90 mg nitrate (NO3−)) on performance markers during graded exercise testing (GXT). Methods: For this randomized, double-blind, placebo (PBO)-controlled, crossover study, 15 recreationally-active participants (aged 23.1 ± 3.3 years; BMI: 27.2 ± 3.7 kg/m2) reported >2 h post-prandial and performed GXT 65–75 min post-RSE or PBO ingestion. Blood samples were collected at baseline (BL), pre-GXT (65–75 min post-ingestion; PRE), and immediately post-GXT (POST). GXT commenced with continuous analysis of expired gases. Results: Plasma concentrations of NO3− increased PRE (+447 ± 294%; p < 0.001) and POST (+378 ± 179%; p < 0.001) GXT with RSE, but not with PBO (+3 ± 26%, −8 ± 24%, respectively; p > 0.05). No effect on circulating nitrite (NO2−) was observed with RSE (+3.3 ± 7.5%, +7.7 ± 11.8% PRE and POST, respectively; p > 0.05) or PBO (−0.5 ± 7.9%, −0.2 ± 8.1% PRE and POST, respectively; p > 0.05). When compared to PBO, there was a moderate effect of RSE on plasma NO2− at PRE (g = 0.50 [−0.26, 1.24] and POST g = 0.71 [−0.05, 1.48]). During GXT, VO2 at the ventilatory threshold was significantly higher with RSE compared to PBO (+6.1 ± 7.3%; p < 0.05), though time-to-exhaustion (−4.0 ± 7.7%; p > 0.05) and maximal aerobic power (i.e., VO2 peak; −0.8 ± 5.6%; p > 0.05) were non-significantly lower with RSE. Conclusions: RSE as a nutritional supplement may elicit an ergogenic response by delaying the ventilatory threshold.