Effect of Roasting Degree, Extraction Time, and Temperature of Coffee Beans on Anti-Hyperglycaemic and Anti-Hyperlipidaemic Activities Using Ultrasound-Assisted Extraction.

Coffee consumption has been linked to a low risk of metabolic syndrome. However, evidence supporting its anti-hyperglycaemic and anti-hyperlipidaemic activities remain poorly defined. The ultrasound-assisted extraction (UAE) technique has been shown to achieve high yields of bioactive compounds in coffee, with preserved functionality. The goal of the present study was to determine the effect of various coffee roasting extracts using UAE on their anti-hyperglycaemic and anti-hyperlipidaemic properties. We examined α-amylase and α-glucosidase, micelle size, micelle solubility, and pancreatic lipase activities. Coffee roasting degrees were classified as light coffee (LC), medium coffee (MC), and dark coffee (DC). We showed that DC at 80°C for 10 min, 40°C for 20 min, and 20°C for 20 min has a high potency to inhibit α-amylase, α-glucosidase, and pancreatic lipase activities by 33.79±3.25%, 19.68±1.43%, and 36.63±1.58%, respectively. LC enhanced cholesterol micelle size and suppressed cholesterol micelle solubility, which suggests that coffee roasting may enhance anti-hyperglycaemic and anti-hyperlipidaemic activities.

Dried mulberry fruit ameliorates cardiovascular and liver histopathological changes in high-fat diet-induced hyperlipidemic mice.

BACKGROUND AND AIM: Metabolic disease encompasses most contemporary non-communicable diseases, especially cardiovascular and fatty liver disease. Mulberry fruits of Morus alba L. are a favoured food and a traditional medicine. While they are anti-atherosclerotic and reduce hyperlipidemic risk factors, studies need wider scope that include ameliorating cardiovascular and liver pathologies if they are to become clinically effective treatments. Therefore, the present study sought to show that freshly dried mulberry fruits (dMF) might counteract the metabolic/cardiovascular pathologies in mice made hyperlipidemic by high-fat diet (HF). EXPERIMENTAL PROCEDURE: C57BL/6J mice were fed for 3 months with either: i) control diet, ii) HF, iii) HF+100 mg/kg dMF, or iv) HF+300 mg/kg dMF. Body weight gain, food intake, visceral fat accumulation, fasting blood glucose, plasma lipids, and aortic, heart, and liver histopathologies were evaluated. Adipocyte lipid accumulation, autophagy, and bile acid binding were also investigated. RESULTS AND CONCLUSION: HF increased food intake, body weight, visceral fat, plasma total cholesterol (TC) and low-density lipoprotein (LDL), TC/HDL ratio, blood glucose, aortic collagen, arterial and cardiac wall thickness, and liver lipid. Both dMF doses prevented hyperphagia, body weight gain, and visceral fat accumulation, lowered blood glucose, plasma TG and unfavourable TC/HDL and elevated plasma HDL beyond baseline. Arterial and cardiac wall hypertrophy, aortic collagen fibre accumulation and liver lipid deposition ameliorated in dMF-fed mice. Clinical trials on dMF are worthwhile but outcomes should be holistic commensurate with the constellation of disease risks. Here, dMF should supplement the switch to nutrient-rich from current energy-dense diets that are progressively crippling national health systems.

Potential of Coffee Fruit Extract and Quinic Acid on Adipogenesis and Lipolysis in 3T3-L1 Adipocytes.

This study was to assess the impact of different colors of coffee fruit (green, yellow and red) on adipogenesis and/or lipolysis using 3T3-L1 adipocytes. Characterization of chemical constituents in different colors of coffee fruit extracts was determined by ESI-Q-TOF-MS. The cytotoxicity of the extracts in 3T3-L1 preadipocytes were evaluated by MTT assay. Oil-red O staining and amount of glycerol released in 3T3-L1 adipocytes were measured for lipid accumulation and lipolysis activity. All coffee fruit extracts displayed similar chromatographic profiles by chlorogenic acid > caffeoylquinic acid > caffeic acid. Different colors of raw coffee fruit possessed inhibitory adipogenesis activity in 3T3-L1 adipocytes, especially CRD decreased lipid accumulation approximately 47%. Furthermore, all extracts except CYF and their major compounds (malic, quinic, and chlorogenic acid) increased glycerol release. Our data suggest that different colors of coffee fruit extract have possessed anti-adipogenic and lipolytic properties and may contribute to the anti-obesity effects.

Spirogyra neglecta inhibits the absorption and synthesis of cholesterol in vitro.

BACKGROUND: Spirogyra neglecta (SN) has many nutritional benefits and it is commonly used to ameliorate different human conditions including inflammation, gastric ulcer, hyperglycemia, and hyperlipidemia. However, the mechanism of the hypocholesterolemic effect of SN still remains unclear. Therefore, the present study was aimed to evaluate the effect of SN extract particularly on cholesterol absorption and synthesis mechanisms. METHODS: For cholesterol absorption, the uptake of cholesterol was measured by using tritium radiolabeling of cholesterol in Caco-2 cells. Bile acid binding, micelles size, and cholesterol solubility were analyzed in in vitro assays, while cholesterol synthesis was evaluated by using a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase assay kit. RESULTS: SN extract was found to decrease cholesterol uptake in Caco-2 cells and decreased the solubility of cholesterol in micelles. The SN extract bound to taurocholate, taurodeoxycholate, and glycodeoxycholate bile acids, and increased micelles size. SN has also demonstrated an inhibitory effect on HMG-CoA reductase (HMGR) enzymatic activity. For further experimentation, the treatment combination of SN and ezetimibe (0.04 mg/mL) showed a greater significant reduction in cholesterol uptake than the extract alone. CONCLUSION: These observations suggested that inhibitory cholesterol absorption effects of SN could be mediated through the modulation of size and solubility of cholesterol micelles, resulting in interference of cholesterol uptake. In addition, SN inhibited the rate limiting step of cholesterol synthesis. This study provides supporting evidence for the potential usage of SN as a cholesterol lowering agent.

Sericin reduces serum cholesterol in rats and cholesterol uptake into Caco-2 cells.

A cholesterol lowering effect of sericin was investigated both in vivo and in vitro. Rats were dosed with cholesterol with and without sericin for 14 days. Non-high-density lipoprotein (HDL) and total serum cholesterols were reduced in rats fed high-cholesterol diet with all three tested doses of sericin (10, 100, and 1000 mg kg(-1) day(-1)). The potential mechanism of actions was determined by measuring the uptake of radiolabeled cholesterol into differentiated Caco-2 cells and cholesterol solubility in mixed lipid micelles. Concentration of sericin as low as 25 and 50 µg/mL inhibited 30% of cholesterol uptake into Caco-2 cells whereas no effect was found at higher concentration. Cholesterol micellar solubility was reduced in the presence of sericin. This study suggests the cholesterol lowering effect of sericin results from its inhibition of cholesterol absorption in intestinal cells and its reduction of cholesterol solubility in lipid micelles.