ABSTRACT
Raspberry ketones have important therapeutic properties such as anti-influenza and prevention of diabetes. In order to obtain raspberry ketone from Chlamydomonas reinhardtii, two enzymes catalyzing the last two steps of raspberry ketone synthesis, i.e. 4-coumaryl-CoA ligase (4CL) and polyketide synthase (PKS1), were fused using a glycine-serine-glycine (GSG) tripeptide linker to construct an expression vector pChla-4CL-PKS1. The fusion gene 4CL-PKS1 driven by a PSAD promoter was transformed into a wild-type (CC125) and a cell wall-deficient C. reinhardtii (CC425) by electroporation. The results showed the recombinant C. reinhardtii strain CC125 and CC425 with 4CL-PKS1 produced raspberry ketone at a level of 6.7 μg/g (fresh weight) and 5.9 μg/g (fresh weight), respectively, both were higher than that of the native raspberry ketone producing plants (2-4 μg/g).
Subject(s)
Acyl Coenzyme A , Butanones , Chlamydomonas reinhardtii/genetics , Ligases , Polyketide SynthasesABSTRACT
To investigate the molecular mechanisms of the antiobese effect of raspberry ketone against high-fat diet fed rats. Methods: Fifty adult male rats were randomly assigned to receive a standard diet, a high fat diet, and the high-fat diet and 0.5%, 1% or 2% raspberry ketone. Body weight, biochemical parameters and gene expression of CCAAT enhancer-binding protein (C/EBP)-d, fatty acid synthase (FAS), acetyl CoA carboxylase (ACC), peroxisome proliferator-activated receptor alpha (PPAR-a), hormone-sensitive lipase (HSL) and hepatic carnitine palmitoyltransferase 1 A (CPT1A) were investigated. Results: Body weight, blood glucose, insulin, total lipids, triacylglycerols, total cholesterol and low-density lipoprotein cholesterol were increased in high-fat diet fed rats. These high fat diet-induced changes were attenuated by treatment with raspberry ketone. High-density lipoprotein cholesterol was decreased in highfat diet fed rats but increased in rats treated with raspberry ketone. Molecular investigations showed induction of gene expression of C/EBP-d , FAS, ACC, CPT1A and inhibition of gene expression of PPAR-a and HSL in high-fat diet fed rats as compared with control. Raspberry ketone treament reversed these changes except CPT1A. Conclusions: Raspberry ketone can prevent obesity induced by a high-fat diet in rats by induction of the expression of enzymes, controlling lipolysis and fatty acids b oxidation as well as inhibition of gene expressions of adipogenic factors.
ABSTRACT
Objective: To investigate the molecular mechanisms of the anti-obese effect of raspberry ketone against high-fat diet fed rats. Methods: Fifty adult male rats were randomly assigned to receive a standard diet, a high fat diet, and the high-fat diet and 0.5％, 1％or 2％ raspberry ketone. Body weight, biochemical parameters and gene expression of CCAAT enhancer-binding protein (C/EBP)-δ, fatty acid synthase (FAS), acetyl CoA carboxylase (ACC), peroxisome proliferator-activated receptor alpha (PPAR-α), hormone-sensitive lipase (HSL) and hepatic carnitine palmitoyltransferase 1 A (CPT1A) were investigated. Results: Body weight, blood glucose, insulin, total lipids, triacylglycerols, total cholesterol and low-density lipoprotein cholesterol were increased in high-fat diet fed rats. These high fat diet-induced changes were attenuated by treatment with raspberry ketone. High-density lipoprotein cholesterol was decreased in high-fat diet fed rats but increased in rats treated with raspberry ketone. Molecular investigations showed induction of gene expression of C/EBP-δ, FAS, ACC, CPT1A and inhibition of gene expression of PPAR-α and HSL in high-fat diet fed rats as compared with control. Raspberry ketone treament reversed these changes except CPT1A. Conclusions: Raspberry ketone can prevent obesity induced by a high-fat diet in rats by induction of the expression of enzymes, controlling lipolysis and fatty acids β oxidation as well as inhibition of gene expressions of adipogenic factors.
ABSTRACT
Objective: To study the chemical constituents of Artemisia argyi. Methods: The chemical constituents were isolated by silica gel column chromatography and HPLC, and its structure were identified by their spectral data and physicochemical properties analysis. Results: Thirty-four compounds were isolated from A. argyi with the structures identified as 5-hydroxy-6,7,3’,4’- tetramethoxyflavone (1), eupatorin (2), p-hydroxy-acetophenone (3), raspberry ketone (4), zingiberone (5), 7-hydroxycoumarin (6), p-hydroxybenzoic acid (7), desacetoxymatricarin (8), 3α-hydroxy-1(10),4,11(13)-triene-12,6α-olide (9), jaceosidin (10), 7-hydrxyterpineol (11), cis-2,8-dihydroxy-p-mentha-1(7)-en (12), trans-2,8-dihydroxy-p-mentha-1(7)-en (13), artemisetin (14), scopoletin (15), arteminolide C (16), desacetylmatricarin (17), artecalin (18), 11,13-dehydrodesacetylmatricarin (19), 1,9-azelaic acid (20), 3-methoxy-tanapartholide (21), phaseic acid (22), seco-guaiaretic acid (23), 5,3’,4’-trihydroxy-6,7-dimethoxy-flavone (24), 1,7-pimelic acid (25), 10-epi-ajafinin (26), 3-epi-iso-seco-tanapartholide (27), austroyunnane C (28), artanomaloide (29), ligustolide A (30), seco-tanapartholide B (31), 3-dehydroxy-iso-seco-tanapartholide (32), 3α-hydroxyreynosin (33), dihydrophaseic acid (34). Conclusion: Compounds 4, 22, 25, 30, 33, 34 are separated from the Artemisia for the first time. Compounds 5, 7, 8, 11-13, 21, 23, 24, 26-28 are isolated from A. argyi for the first time.
ABSTRACT
OBJECTIVE: To observe the hypoglycemic effect of raspberry ketone and its mechanism on diabetic model mice induced by alloxan. METHODS: Healthy male KM mice were used to establish diabetic models by injecting alloxan via tail vein, and then randomly divided into model control group, metformin group (90 mg · kg-1), and raspberry ketone low, middle and high (200, 400, 800 mg · kg-1) dose groups. Normal control group was set. All groups had been treated for 20 d. Fasting blood glucose (FBG) was measured on 0, 7 and 14 d. After 20 d, glucose tolerance test was carried out. Fast insulin (FINS) of the mice were measured, and the insulin sensitivity index(ISI) was calculated by determining the contents of FBG and FINS. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malonaldehyde (MDA) in serum were measured. Pathological changes of pancreas and insulin expression were examined. RESULTS: Raspberry ketone could effectively control the increase of fasting plasma glucose (P < 0.05) and reduce the role of the area under the glucose curve. Compared with the model group, the levels of FINS, SOD and GSH-Px activity were significantly improved (P < 0.05), and MDA content was decreased (P < 0.05) in the high dose raspberry ketone group. The pathological symptoms of pancreas were relieved in the high dose group. CONCLUSION: Raspberry ketone can effectively control blood glucose, protect pancreatic islet β cells, and improve insulin secretion in diabetic mice by effectively inhibiting the oxidative stress.
ABSTRACT
To investigate the scientific grounds for the effect of raspberry ketone bathing that is claimed to increase energy consumption by stimulating metabolism, a bathing experiment was conducted in 10 normal healthy adults.<br>As a result, no appreciable difference was detected among tap water, CO<sub>2</sub>-enriched water and raspberry water in respect to blood pressure, pulse rate and depth thermometer readings, which suggested that bathing in warm raspberry water was safe, producing no marked load on the cardiovascular system. Changes in the skin surface temperature indicated slow elevation of body temperature, from which bathing in warm raspberry water was considered to produce no marked load on the body even if bathing lasted relatively long as compared with bathing in warm tap water or CO<sub>2</sub>-enriched warm water. From the skin tissue blood flow data, it seemed likely that the increase in blood flow caused by bathing in warm raspberry water was produced, not by vasodilatation as in CO<sub>2</sub>-enriched warm water bathing, but by such mechanisms as acceleration of metabolism. Data on insulin suggested that bathing in warm raspberry water affected the carbohydrate metabolism as compared with that in warm tap water or CO<sub>2</sub>-enriched warm water. Since there was no difference among warm water groups in changes in the adrenocortical hormone “cortisol”, raspberry ketone bathing was considered not to have specific activity. Data on NK cell activity showed that bathing in warm raspberry water produced no appreciable effect on the immune system. It was suggested that measurement of β-endorphin should be performed after adjustment of psychological environments.<br>The results of expiration air analysis also indicated that, while bathing in CO<sub>2</sub>-enriched warm water was related to changes in the cardiovascular system, bathing in warm raspberry ketone water produced no appreciable load on the cardiovascular system but consumed energy through acceleration of metabolic activities.