Background/Objective: β-Carotene is often used as a marker for the amount of fruit and vegetables consumed, but little is known about plasma β-carotene concentrations in subjects whose habitual (long-term) diets are characterized by different amounts of foods of plant origin. We compared dietary β-carotene intake and plasma concentrations in women on habitual diets differing in the consumed amounts of foods of plant origin. Methods: A comparison of dietary β-carotene intakes and plasma β-carotene concentrations in women adhering to an average Western diet (n = 172), wholesome nutrition (following preventive recommendations) (n = 238) or a raw food diet (n = 104). Results: Dietary β-carotene intake was 5.5, 9.3, 14.7 mg/day for women adhering to an average Western diet, wholesome nutrition and raw food diet, respectively (p < 0.001). Corresponding multivariate adjusted plasma β-carotene concentrations were 1.07, 1.65, and 1.16 µmol/l, respectively (p < 0.001). Comparable dietary β-carotene intake resulted in lower multivariate adjusted plasma β-carotene in women adhering to a raw food diet and average Western diet compared to those on wholesome nutrition (p < 0.001 for all intake groups up to 20 mg/day). The amount of fruit and vegetable intake did not predict plasma β-carotene levels in women consuming a raw food diet. Conclusions: Plasma β-carotene concentrations differed among the diet groups, with highest plasma levels in women adhering to wholesome nutrition. Plasma β-carotene concentrations may not reflect β-carotene intake and the amount of fruit and vegetables consumed.
Alcoholic liver diseases are classified as one of the major reasons for worldwide morbidity and mortality. Curcuminoids exhibit a wide range of pharmacological activities that are beneficial for health, including hepatoprotective effects, but its clinical significance is limited due to poor oral bioavailability. In the present study, a novel formulation of curcumin as curcumin-galactomannosides (CGM) with enhanced oral bioavailability alleviated alcohol-induced liver damage in wistar rats with an increased potency compared to the unformulated natural curcuminoids (CM). Ethanol administration significantly elevated liver toxicity markers, lipid peroxidation and inflammatory markers with a simultaneous reduction in antioxidant defenses.Supplementation of CGM reversed all of the pathological effects of alcohol administration, almost close to the normal level, when compared with CM.
Background/objectives
Type 2 diabetes (T2D) is a global pandemic, and contributes significantly to the increasing incidence of conditions such as cardiovascular disease (CVD). Postprandial plasma glucose measured 2-h after the start of a meal is a good indicator of the overall status of glucose homeostasis. Clove (
Syzygium aromaticum L.
) and its essential oils (eugenol and acetyl eugenol) have been shown in preclinical studies to modulate pathways involved in glucose homeostasis. In addition, a water-soluble polyphenolic extract of unopened clove buds was recently shown to benefit liver function and redox status. Therefore, we conducted an open-label pilot study to test whether this polyphenolic clove extract (PCE) could influence glucose metabolism.
Methods
We evaluated the effect of PCE supplementation (250 mg once daily for 30 days) on preprandial glucose levels and 2-h postprandial glucose levels in 13 otherwise healthy volunteers who were stratified into two groups according to their initial preprandial glucose levels: Group I (
n
= 7) ≤100 mg/dL, Group II (
n
= 6) – between 101 and 125 mg/dL. In an effort to elucidate the molecular mechanisms of PCE action, we tested in vitro the effects of PCE on glucose uptake, hepatocyte glucose production, and carbohydrate hydrolyzing enzymes.
Results
At day 12 of supplementation, we observed statistically significant reductions in mean postprandial glucose levels in both groups [(Group I: Initial - Day 12 PPG = 13.29 mg/dL, 95% CI: 3.329–23.24) (Group II: Initial – Day 12 PPG = 16.67 mg/dL, 95% CI: 4.687–28.65,
P
= 0.0159)], which continued through study completion at day 30. PCE supplementation significantly decreased mean preprandial glucose levels only in Group II at Days 24 (Initial – Day 24 = 13.00 mg/dL, 95% CI: 1.407–24.59,
P
= 0.0345) and 30 (Initial – Day 30 = 13.67 mg/dL, 95% CI: 5.766–21.57,
P
= 0.0067). In cell-based assays, PCE enhanced glucose uptake in L6 myocytes and inhibited hepatocyte glucose production HepG2 cells. In cell-free assays, PCE inhibited α-amylase activity and α-glucosidase activity.
Conclusions
These findings underscore the therapeutic utility of PCE for maintaining healthy glucose metabolism and warrant further larger-scale clinical trials.
Trial registration
This trial was retrospectively registered in the ISRCTN registry on September 29, 2018 (
ISRCTN15680985
).
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