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Objective With the discovery of thermogenic adipocytes in humans, it has been hypothesized that enhancing adaptive thermogenesis may improve obesity. Although many studies have found that ginseng can improve obesity, the beneficial effects of ginsenoside Rd on obesity and its mechanisms have not been studied. Methods High-fat diet-induced obese mice were used as the study subjects, with intraperitoneal injection of Rd daily at a dose of 15 mg/kg. Body weight and energy metabolism were observed. The effects of Rd on glucose tolerance, insulin sensitivity, and cold tolerance were tested. The expression of genes associated with thermogenesis was analyzed. Finally, the mechanisms by which Rd regulates adaptive thermogenesis were studied. Results Rd ameliorated obesity and insulin resistance. Rd increased cold tolerance through enhancing thermogenic gene expression in brown adipose tissue and increased the browning of white adipose tissue induced by cold stress. Rd increased intracellular cyclic adenosine monophosphate (cAMP) content. Decreasing intracellular cAMP levels by an inhibitor of adenylyl cyclase SQ22536 abolished the promoting effects of Rd on the expression of thermogenic genes. Conclusions Rd improves obesity and insulin resistance. The upregulation of thermogenesis by Rd is dependent on the cAMP/protein kinase A signaling pathway.

Habitat is of great importance in determining the trophic transfer of pollutants in freshwater ecosystems; however, the major factors influencing chemical trophodynamics in pelagic and benthic food webs remain unclear. This study investigated the levels of p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE), polycyclic aromatic hydrocarbons (PAHs), and substituted PAHs (s-PAHs) in 2 plankton species, 6 invertebrate species, and 10 fish species collected from Lake Dianchi in southern China. Relatively high concentrations of PAHs and s-PAHs were detected with total concentrations of 11.4-1400 ng/g wet weight (ww) and 5.3-115 ng/g ww, respectively. Stable isotope analysis and stomach content analysis were applied to quantitatively determine the trophic level of individual organisms and discriminate between pelagic and benthic pathways, and the trophodynamics of the detected compounds in the two food webs were assessed. P,p'-DDE was found to exhibit relatively higher trophic magnification rate in the pelagic food web than in the benthic food web. In contrast, PAHs and s-PAHs exhibited greater dilution rates along the trophic levels in the pelagic food web. The lower species differences of pollutants accumulated in benthic organisms compared to pelagic organisms is attributable to extra uptake via ingested sediment in benthos. The average uptake proportions of PAHs and s-PAHs via ingested sediment in benthic biotas were estimated to be 31-77%, and that of p,p'-DDE was 46%. The uptake routes are of importance for assessing the trophic magnification potentials of organic pollutants, especially in eutrophic freshwater ecosystems.

To realize the oxidative damage of kidney mitochondrial complex in obese rats induced by high-fat diet and investigate the protective effects of sulforaphane against the damage.Eighty-eight adult male SD rats were used, after 1 week adaptability feeding, 8 rats were selected as control group and given low-fat diet. The other 80 rats were given high-fat diet. After 2 weeks, the 32 diet-induced obesity models were choosen whose weight gain was higher than 40%. The 32 rats were randomly divided into 4 groups, i.e. high fat group, high fat+sulforaphane low dose group, high fat+sulforaphane middle dose group and high fat+sulforaphane high dose group. The rats in the sulforaphane low, middle and high dose groups were orally administered with sulforaphane 5, 10 and 20 mg/kg, all the 4 groups were kept feeding high-fat diet for 5 weeks. All rats were sacrificed and their kidneys were removed to assay the index of oxidative damages.The content of ROS (0.26 ± 0.04) and MDA((0.87 ± 0.05) U/mg) in the hight-fat group were significantly higher than those in the control group((0.20 ± 0.02),(0.57 ± 0.08) U/mg)(t values were -3.02 and -4.72, P0.05). The activity of T-AOC((0.43 ± 0.04) U/mg) and MMP (12.09 ± 1.56) were lower than the control group ((0.48 ± 0.04 U/mg, (16.08 ± 3.12) )(t values were 2.06 and 2.28, P0.05). Gavage intervention with sulforaphane, the MDA amount ((0.67 ± 0.05), (0.55 ± 0.05), (0.56 ± 0.07) U/mg) in the sulforaphane low, middle and high dose groups were lower than the hight-fat group ((0.87 ± 0.05) U/mg (t values were 3.65, 5.71 and 5.60. P0.05). The activity of T-AOC ((0.49 ± 0.05), (0.55 ± 0.05), (0.54 ± 0.04) U/mg), T-SOD ((61.07 ± 2.79), (55.95 ± 2.39), (60.26 ± 6.02) U/mg) and the level of MMP ((17.17 ± 2.52), (18.24 ± 2.54), (18.21 ± 3.65)) were higher than in the high-fat group ((0.43 ± 0.04) U/mg,(47.22 ± 2.43) U/mg,(12.09 ± 1.56)) (tT-AOC values were -2.36, -4.83 and -4.30; tT-SOD values were -6.37, -4.71 and -5.99; tMMP values were -2.90, -3.52 and -3.50, P0.05). The activity of GSH-Px in the sulforaphane low and middle dose groups ((69.12 ± 8.63), (64.43 ± 6.58) U/mg) were higher than those in the high-fat group((53.03 ± 5.70) U/mg)(t values were -3.82 and -2.71, P0.05). But there were no significant difference between the high dose group ((60.02 ± 7.05) U/mg) and the high-fat group (t = -1.66, P0.05).High-fat diet can induce the mitochondrial oxidative dysfunction in kidney, and sulforaphane shows protective effect on the kidney mitochondrial complex from oxidative damage in obese rats induced by high-fat diet.

Gastrointestinal (GI) motility and gut hormones have been considered to be involved in the development and maintenance of obesity. Our aim was to assess the relationships between gastric emptying (GE), GI transit and gut hormones and leptin concentrations in diet-induced obese rat model. Male 6-week-old Sprague–Dawley rats were fed with a high-fat (HF) diet for 8 weeks to generate diet-induced obesity (DIO) and diet resistant (DR) rats. GE, GI transit and plasma ghrelin, cholecystokinin (CCK), PYY and leptin concentrations were determined in DIO, DR and control (CON) rats. The DIO rats had slower GE, higher plasma leptin and CCK concentrations, and lower plasma ghrelin concentration compared with CON and DR rats. GE was correlated with plasma ghrelin ( r = 0.402, P = 0.028), CCK ( r = − 0.518, P = 0.003) and leptin concentration ( r = − 0.514, P = 0.004). The slower GE, which can be considered as an adaptive response aimed at HF diet induced obesity, may be mediated by changes of plasma ghrelin, CCK and leptin concentrations.

To explore the gene expression of hormone sensitive lipase (HSL) and lipoprotein lipase (LPL) between obesity-prone (OP) and obesity-resistant (OR) rats induced by a high-fat diet.Eighty male Sprague-Dawley (SD) rats were fed with a high-fat diet for 5 weeks, then OP and OR rats were selected according to their body weight gain. All the rats were fed with basic diet for another 10 weeks, the rats were then sacrificed, and serum samples were collected. To discuss the function of HSL and LPL during the formation of obesity or obesity resistance, RT-PCR was used to compare the gene expression of HSL and LPL in white adipose tissue.At the end of the 5th week, when compared with OR rats, the gene expression of HSL in white adipose tissue was lower in OP rats, but the gene expression of LPL was higher in OP rats. After switched to basic diet for 10 weeks, HSL gene expression had no difference between OP and OR rats, but LPL gene was still highly expressed in OP rats.The formation of obesity prone rats may be associated with decreased HSL gene expression and increased LPL gene expression, which promote adipose synthesis and inhibit lipolysis. Highly expressed HSL gene may be associated with high fat diet, while increased LPL gene expression is the specific change of OP rats.

To study the blood hormone level between diet-induced obesity-resistant (DIO-R) rats and diet-induced obesity(DIO) rats in blood hormone.Fifty male Sprague-dawley (SD) rats were randomly divided into control group and high-fat group and they were fed with basic diet and high-fat diet respectively for 13 weeks. DIO-R and DIO rats were selected according to their body weight, then the intake of diet and body fat contents, the level of serum insulin, serum leptin and plasma NPY were determined by radioimmunoassay. The results showed that the weight, diet intake and body fat of DIO-R rats were significantly lower than those of DIO rats(P0.05). The level of serum insulin and plasma NPY of DIO-R rats were lower than those of DIO rats(P0.05). The level of serum leptin of rats in high-fat diet group was higher than that of the rat in basic diet group, but there was no significant difference between DIO-R and DIO rats(P0.05).High fat diets can induce SD rat to develop obesity and obesity-resistance. The balance of insulin-leptin-NPY feedback may play a partial of role in resisting diet-induced obesity of rats.

Obesity does great harm to people's health. In order to study the effects of chromium and fish oil on blood lipid and blood glucose in obese rats, 32 obese model rats were divided randomly into four groups: fish oil group(5 ml/kg BW), chromium group(3 mg/kg BW), fish oil + chromium group and high fat diet group. In the end of the experiment(6 weeks) fats around kidney and spermary were weighted and blood samples were collected to determine blood glucose and blood lipid. Result shows that blood glucose and blood lipid in experimental groups were lower than those in high fat diet group. The ratios of fats around kidney and/or around spermary to body weight in experimental groups were lower than those in high fat diet group.Chromium and fish oil decrease the risk of obese relative diseases.

In order to study the effect of iron on the expression of UCP2 in white fat and UCP3 in muscle in obese rats, a reverse transcription polymerase chain reaction (RT-PCR) technique is used to measure the expression of UCP2 and UCP3 mRNA. The results show: (1) Adequate iron improves the level of thyroid hormone in blood serum; (2) the body fat content of obese rat in 5, 10, and 20 times of iron supplement groups is lower than that of obese rats in normal iron supplement group; (3) the UCP2 and UCP3 mRNA expression of iron-deficient obese rats is low in iron-deficient obese rats; (4) iron supplement enhances the level of UCP3 mRNA expression in muscle and the level of UCP3 mRNA is the highest in the 5 times iron supplement group and about 2 times of that of basic diet group. However, there is no effect on the UCP2 mRNA expression induced by high energy diet. It suggested that adequate iron can improve the level of serum thyroid hormone, induce the UCP3 mRNA expression in muscle and mobilize fat to produce heat, but had no effect on UCP2 mRNA in white fat of obese rat.