Obesity has become a public health concern due to its positive association with the incidence of many diseases, and coffee components including chlorogenic acid (CGA) and caffeine have been demonstrated to play roles in the suppression of fat accumulation. To investigate the mechanism by which CGA and caffeine regulate lipid metabolism, in the present study, forty mice were randomly assigned to four groups and fed diets containing no CGA or caffeine, CGA, caffeine, or CGA þ caffeine for 24 weeks. Body weight, intraperitoneal adipose tissue (IPAT) weight, and serum biochemical parameters were measured, and the activities and mRNA and protein expression of lipid metabolism-related enzymes were analysed. There was a decrease in the body weight and IPAT weight of mice fed the CGA þ caffeine diet. There was a significant decrease in the serum and hepatic concentrations of total cholesterol, TAG and leptin of mice fed the CGA þ caffeine diet. The activities of carnitine acyltransferase (CAT) and acyl-CoA oxidase (ACO) were increased in mice fed the caffeine and CGA þ caffeine diets, while the activity of fatty acid synthase (FAS) was suppressed in those fed the CGA þ caffeine diet. The mRNA expression levels of AMP-activated protein kinase (AMPK), CAT and ACO were considerably up-regulated in mice fed the CGA þ caffeine diet, while those of PPARg2 were down-regulated. The protein expression levels of AMPK were increased and those of FAS were decreased in mice fed the CGA þ caffeine diet. These results indicate that CGA þ caffeine suppresses fat accumulation and body weight gain by regulating the activities and mRNA and protein expression levels of hepatic lipid metabolism-related enzymes and that these effects are stronger than those exerted by CGA and caffeine individually.

Alzheimer's disease (AD) is a neurodegenerative disease associated with amyloid-β (Aβ) deposition, leading to neurotoxicity (oxidative stress and neuroinflammation) and gut microbiota imbalance. Resveratrol (Res) has neuroprotective properties, but its bioavailability in vivo is very low. Herein, we developed a small Resselenium-peptide nanocomposite to enable the application of Res for eliminating Aβ aggregate-induced neurotoxicity and mitigating gut microbiota disorder in aluminum chloride (AlCl 3 ) and D-galactose(D-gal)-induced AD model mice. Res functional selenium nanoparticles (Res@SeNPs) (8 ± 0.34 nm) were prepared first, after which the surface of Res@SeNPs was decorated with a blood−brain barrier transport peptide (TGN peptide) to generate Res-selenium-peptide nanocomposites (TGN-Res@SeNPs) (14 ± 0.12 nm). Oral administration of TGN-Res@SeNPs improves cognitive disorder through (1) interacting with Aβ and decreasing Aβ aggregation, effectively inhibiting Aβ deposition in the hippocampus; (2) decreasing Aβ-induced reactive oxygen species (ROS) and increasing activity of antioxidation enzymes in PC12 cells and in vivo; (3) down-regulating Aβ-induced neuroinflammation via the nuclear factor kappa B/mitogen-activated protein kinase/Akt signal pathway in BV-2 cells and in vivo; and (4) alleviating gut microbiota disorder, particularly with respect to oxidative stress and inflammatory-related bacteria such as Alistipes, Helicobacter, Rikenella, Desulfovibrio, and Faecalibaculum. Thus, we anticipate that Res-selenium-peptide nanocomposites will offer a new potential strategy for the treatment of AD.

In order to investigate the mechanisms by which puerarin from kudzu root extract regulates lipid metabolism, fifty mice were randomly assigned to five groups: normal diet, high-fat diet (HFD), and HFD containing 0.2%, 0.4% or 0.8% puerarin for 12 weeks. Body weight, intraperitioneal adipose tissue (IPAT) weight, serum biochemical parameters, and hepatic and feces lipids were measured. Activity and mRNA and protein expressions of hepatic lipid metabolism-related enzymes were analyzed. Compared with HFD, 0.4% and 0.8% puerarin significantly decreased body and IPAT weight. There was a significant decrease in the serum and hepatic concentrations of total cholesterol, triglycerides and leptin in mice fed the 0.4% and 0.8% puerarin diets compared with HFD. Fatty acid synthase activity was suppressed in mice fed the 0.4% and 0.8% puerarin diets, while the activities of AMP-activated protein kinase (AMPK), carnitine acyltransferase (CAT) and hormone-sensitive lipase (HSL) were increased. mRNA expression of peroxisome proliferator-activated receptor γ 2 (PPARγ 2) was down-regulated in liver of mice fed the 0.8% diet compared with HFD, while mRNA expression of CAT and HSL was considerably up-regulated by 0.4% and 0.8% puerarin diets. The protein expression of PPARγ2 in liver was decreased and those of p-AMPK, HSL and p-HSL were increased in mice fed 0.4% and 0.8% puerarin diets. These results suggest that > 0.4% puerarin influenced the activity, mRNA and protein levels of hepatic lipid metabolism-related enzymes, decreasing serum and liver lipids, body weight gain and fat accumulation. Puerarin might be beneficial to prevent lifestyle-related diseases.

Deposition of amyloid‐β (Aβ) aggregates and formation of neurotoxic reactive oxygen species (ROS) are significant pathological signatures of Alzheimer's disease (AD). Resveratrol (Res) is an antioxidant with the potential to treat AD. However, the bioavailability and solubility of Res is very low and it cannot entirely inhibit Cu2+‐induced Aβ42 aggregation at low concentration. Herein, we combine the unique Aβ absorption property of selenium nanoparticles with the natural antioxidant agent Res to form Res@SeNPs. Our in vitro biological evaluation revealed that modification of Res with SeNPs provides a synergistic effect on Cu2+‐induced Aβ42 aggregation, ROS generation and, more importantly, protects PC12 cells from Aβ42–Cu2+ complexes‐induced cell death. It is believed that SeNPs can improve the application of Res in AD treatment as Res@SeNPs is more efficient than Res in reducing Aβ42 toxicity in long‐term use. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A: 3034–3041, 2018.

The deposition of amyloid-β (Aβ) plaques and formation of neurotoxic reactive oxygen species (ROS) is a significant pathological signature of Alzheimer’s disease (AD). Herein, a novel strategy is reported for combining the unique Aβ absorption property of selenium nanoparticles with the natural antioxidant agent chlorogenic acid (CGA) to form CGA@SeNPs. The in vitro biological evaluation revealed that CGA could clear the ROS induced by Aβ40 aggregates, but it did not inhibit the Aβ40 aggregation and cell membrane damage which were also caused by Aβ40 aggregates. Interestingly, CGA@SeNPs show an enhanced inhibition effect on Aβ40 aggregation and, more importantly, protect PC12 cells from Aβ aggregation-induced cell death. It is believed that CGA@SeNPs are more efficient than CGA in reducing Aβ40 toxic in long-term use.Electronic supplementary materialThe online version of this article (10.1186/s11671-018-2720-1) contains supplementary material, which is available to authorized users.

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To clarify the details of the anti-obesity effect of theanine, g -glutamylethylamide, female ICR mice were fed diets containing theanine at the concentrations of 0.01, 0.02, 0.04, 0.08 and 0.16% for 16 weeks. Bodyweight and food intake in the mice were measured every 4 weeks, and several organs and intraperitoneal adipose tissues (IPAT) were weighed after the feeding. In addition, lipid levels in the serum and liver were analyzed. As a result, the bodyweight increase and weight of IPAT were significantly reduced in mice fed 0.04% theanine compared with controls, but not in mice fed other diets. The levels of triglycerides (TG) and non-esterified fatty acids in the serum and TG level in the liver in mice fed the 0.04% theanine diet were remarkably decreased. These results indicated that bodyweight increase and fat accumulation were suppressed by a limited concentration of 0.04% theanine in mice.