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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.

To investigate the association between pathological myopia (PM) and immunological/inflammatory markers and to identify the possible risk factors for the formation of myopic choroidal neovascularization (mCNV).One hundred fourteen unrelated subjects were recruited: 63 PM patients (PM group) with spherical equivalent of at least -8.00 diopters (range, -8.00 to -25.00) and axial length exceeding 26.5 mm, accompanied by characteristic pathologic changes, and 51 emmetropic age- and sex-matched individuals (control group) with spherical equivalent within ±1.0 diopter in both eyes. In the PM group, patients were assigned to two subgroups, mCNV group and no CNV group, according to the results of fluorescein angiography. Serum high-sensitivity C-reactive protein (hs-CRP) and complement profile (C3, C4, and CH50) were assayed. Statistical analysis was performed between the two groups. Binary logistic regression analysis was used to analyze the relative risk factors that were associated with the development of mCNV in the PM group patients.The range of axial length was 26.50 to 37.08 mm in the PM group and 22.32 to 24.56 mm in the control group. There were 24 patients in the mCNV group and 39 patients in the no CNV group. The PM group patients had significantly higher serum hs-CRP (p = 0.033), C3 (p = 0.004), and CH50 (p0.001) compared with the control group patients. There were no significant differences between the two groups for C4 level (p = 0.071). Binary logistic regression analysis, which included hs-CRP, C3, C4, CH50, age, and sex as covariates, showed that C3 (p = 0.03) and age (p = 0.01) were risk factors for mCNV, whereas serum hs-CRP, C4, CH50, and sex were not statistically significant predictors of mCNV in the PM group patients (p0.05).Our data support the hypothesis that immunological/inflammatory markers, namely hs-CRP, C3, and CH50 may play an important role in the development of PM, and that C3 level may be a predictive risk factor for mCNV formation.

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.

Background: Body energy homeostasis is largely regulated by the interactions between appetite-related brain regions and gut hormones. Objective: We hypothesized that the sensitivity of appetite-related brain regions [eg, hypothalamus, insula, thalamus, parahippocampal/ hippocampal cortex, caudate, putamen, amygdala, and orbitofrontal cortex (OFC)] varies for each macronutrient, and the differential sensitivity is associated with gut hormone concentrations in humans. Design: Brain activation responses to ingested fat, glucose, protein, and water in the above-mentioned 8 brain regions of 14 healthy men were investigated by using functional magnetic resonance imaging. Fasting and postprandial plasma glucose, insulin, ghrelin, cholecystokinin (CCK), and glucagon-like peptide 1 (GLP-1) concentrations were measured. The relation of the blood oxygen level–dependent (BOLD) signal with plasma glucose and hormone concentrations was assessed by using Pearson’s correlation analysis. Results: Ingested macronutrients similarly reduced the BOLD signal in the middle insula, thalamus, parahippocampal cortex, caudate, and lateral OFC. Protein ingestion reduced the BOLD signal in the amygdala more effectively than did fat and glucose ingestion. BOLD signal changes were positively correlated with circulating ghrelin concentrations and were negatively correlated with circulating insulin, CCK, and GLP-1 concentrations. The findings indicate variations in the correlation between brain activation and plasma hormone concentrations after ingestion of different macronutrients. Conclusions: The middle insula, thalamus, parahippocampal cortex, caudate, and lateral OFC, but not the amygdala, have sensitivities similar to those of isocaloric and isovolumetric macronutrient solutions. Differential correlations exist between BOLD signal changes in activated brain regions and postprandial changes in plasma concentrations of different gut hormones in response to the ingestion of different macronutrients. This trial was registered at chictr.org as ChiCTR-TRC-12001945. Am J Clin Nutr 2012; 96:275–82.

To investigate the effect of topical pranoprofen 0.1% on the clinical evaluation and conjunctival human leukocyte antigen II (HLA-DR) expression in dry eyes.Sixty patients with dry eyes were randomized to 2 groups. Patients in group 1 received topical pranoprofen 0.1% plus topical sodium hyaluronate 0.1%; and patients in group 2 received sodium hyaluronate without pranoprofen. Ocular surface disease index (OSDI), tearfilig;lm break-up time (TBUT), Schirmer I test, ocular surface staining (OSS), and conjunctival HLA-DR expression were evaluated before treatment and at 15 and 30 days after treatment.On day 15, patients in group 1 had significantly lower OSDI, OSS, and HLA-DR-positive cells compared with patients in group 2 (P0.01), and the TBUT was significantly longer in patients in group 1 than that of patients in group 2 (P0.01). On day 30, the difference between the 2 groups in OSS lost significance; however, there continued to be significant differences in the OSDI, TBUT, and HLA-DR expression between the 2 groups (P0.01). On days 15 and 30, the values in group 1 patients had significant improvement compared with their baseline values in terms of the above-mentioned parameters. The comparisons within group 2 did not reveal any significant differences. There was no significant effect in the Schirmer I test value in eyes of patients in group 1 or group 2 at days 15 or 30 (P0.05).Topical pranoprofen 0.1% has a beneficial effect in reducing the ocular signs and symptoms of dry eyes and decreasing the inflammatory markers of conjunctival epithelial cells.

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.