Mechanism of the antiadipogenic-antiobesity effects of a rice hull smoke extract in 3T3-L1 preadipocyte cells and in mice on a high-fat diet

Abstract

The present study investigated the inhibitory effects of a rice hull smoke extract (RHSE) against adipogenesis in 3T3-L1 preadipocyte cells and in mice fed high fat (HFD) and normal (ND) diets. At concentrations of 0.1% and 0.5%, RHSE was shown to reduce the cellular lipid content in MDI-induced 3T3-L1 cells by about 72% and 88%, respectively, compared to that in control cells without RHSE, indicating a strong antiadipogenic effect. This result was supported by the finding that the expression of the adipocyte differentiation marker adiponectin was suppressed. MTT and lactate dehydrogenase (LDH) release assays showed that RHSE doses of up to 0.5% (v/v) were not cytotoxic to the 3T3-L1 cells. RHSE activates AMP-activated protein kinase (AMPK) through raising the phosphorylated ratio during the early phase of cell differentiation, and western blot analysis showed that it dose-dependently inhibited the expression of the peroxisome proliferator-activated receptor-γ (PPARγ), CCAAT-enhancer binding protein (C/EBPα), and sterol regulatory element-binding protein 1c (SREBP-1c) at the late stage of differentiation. The antiadipogenic properties of RHSE were confirmed in vivo using experimental obese mice on a high-fat diet. Dietary supplementations of 0.5% and 1% RHSE resulted in a reduction at the end of the 7-week feeding study of body weight gain of 66.9% and 72.5%, respectively, a reduction of epididymal white adipose tissue weight by up to 87.9%, restoration of elevated total cholesterol and triglyceride levels in plasma and liver to those observed in the ND-fed mice, normalization of distorted serum leptin and adiponectin levels, and restoration of liver weight and glutamate oxaloacetate transaminase/glutamate pyruvate transaminase (GOT/GPT) enzymes, blood urea, and serum creatinine to the normal control levels observed in the ND-fed mice. As was found in the 3T3-L1 cells, RHSE up-regulated AMPK phosphorylation and down-regulated PPARγ, C/EBPα and SREBP-1c protein expression in the epididymal white adipose tissues. These results indicate that RHSE inhibits the AMPK signaling pathway in mice and might serve as an antiobesity multifunctional food additive.

Acrylamide Content of Experimental Flatbreads Prepared from Potato, Quinoa, and Wheat Flours with Added Fruit and Vegetable Peels and Mushroom Powders

“…We are also engaged in a parallel effort designed to define the potential health benefits of antioxidative fruits and vegetable peels, as well the peel (hull) from rice, which are often discarded as a food-processing waste product [9,10,11]. As part of this effort, we have shown that (a) the dietary supplementation of potato peel powders reduced weight gain in mice on a high-fat diet [12]; (b) potato peel powders inhibited the growth of pathogenic trichomonads (protozoa) that cause sexually transmitted diseases in humans and cattle [13]; (c) apple, orange, and potato peel powders inhibited the outgrowth of pathogenic Bacillus cereus bacteria from spores in cooked rice [14]; and (d) a rice hull smoke extract reduced weight gain in mice on a high-fat diet [15]. We also recently determined the content of phenolic and flavonoid compounds and antioxidative activities of 12 melon peel powders [16].…”

The Absence of Adiponectin Alters Niacin’s Effects on Adipose Tissue Inflammation in Mice

“…The time at which HFD-fed mice develop decreased serum or plasma adiponectin concentrations varies in the literature. Some studies, using a range of diets that contain anywhere from 40% to 60% lard, demonstrate decreased adiponectin concentrations by as early as 4 weeks on the diet [ 50 , 51 , 52 ]. However, another study similar to ours did not observe an HFD-mediated decrease in adiponectin after 10 weeks on an HFD that consisted of 60% lard [ 53 ].…”

Anti-adipogenic and anti-obesity activities of purpurin in 3T3-L1 preadipocyte cells and in mice fed a high-fat diet

“…Cell viability was assessed using the MTT staining assay following the method of Mosmann [26]. This method has previously been applied to 3T3-L1 cells [27, 28]. Briefly, cells were treated with serial concentrations of purpurin (0, 1, 10, 50, 100, 250 μM) for 24 h or 48 h at 37 °C in humidified air with 5% CO 2 .…”

“…Cells were induced to differentiate according to methods used previously [27, 28]. Briefly, 3T3-L1 murine pre-adipocyte cells were stimulated to differentiate by culturing in MDI medium in the presence and absence of purpurin for 2 days.…”