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* Bio Research Corporation of Yokohama, 1-1-1 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan and Yokohama City University School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan
3 To whom correspondence should be addressed. E-mail: eri.k{at}ensuiko.co.jp.
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ABSTRACT |
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 TOP ABSTRACT MATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • cyclodextrin • high-fat diet • mice and rats • Salacia reticulata • visceral fat mass.
Obesity is a medical condition involving an excess accumulation of body fat; it is one of the fastest growing major disorders throughout the industrialized world (1–4). It is often accompanied by metabolic syndrome, which is a cluster of interrelated common clinical disorders, including insulin resistance, glucose intolerance, hypertension, and dyslipidemia. The primary defects in energy balance that produce obesity, and visceral adiposity in particular, are sufficient to cause all aspects of metabolic syndrome. Furthermore, in obese individuals, the accumulation of adipose tissue predominantly in the visceral cavity plays a major role in the development of metabolic syndrome. Increased visceral fat accumulation is also a risk factor for type 2 diabetes mellitus, which is associated with insulin resistance. An increase in the prevalence of type 2 diabetes has been reported worldwide (5).
Various animal models that simulate obesity in humans have been used to search for effective antiobesity treatments. For example, in certain rodents, the intake of a high-fat (HF)4 diet generally causes obesity (6); impaired glucose tolerance and increased visceral fat mass promote the metabolic syndrome in the presence or absence of excessive energy intake (EI) (7–10).
A common strategy for reducing obesity is energy restriction, combined with adequate exercise, and this strategy has been shown consistently to reduce obesity in large, randomized, controlled studies. However, it is very difficult for most people to follow such recommendations over the long term. Thus, additional, drug-based measures are required to prevent obesity and the accumulation of body fat, especially visceral fat mass. Obesity therapies include the reduction of nutrient absorption and the administration of anorectic drugs, thermogenic drugs, or drugs that affect lipid mobilization and utilization. However, due to the adverse side effects associated with many of the antiobesity drugs, more recent drug trials have focused on screening the herbal medicines that were reported to have antiobesity activity because these types of preparations generally have only minimal side effects. Many studies showed that herbal products and plant extracts have antiobesity effects in mice and rats with HF diet–induced obesity (11–15).
Salacia reticulata (family Hippocrateaceae; commonly known as Kotala himbutu) is the most popular herbal resource in Sri Lanka (16), where many people use a water extract of its stems or roots as an herbal therapy for diabetes mellitus. Recent reports showed that a water extract of S. reticulata contains 
-glucosidase inhibitors (17–19) and that its polyphenolic constituents have lipase-inhibitory activity. In addition, female Zucker fatty rats fed an extract of the S. reticulata had a slight reduction in body weight (20). We prepared a mixture of S. reticulata aqueous extract and cyclodextrin (SRCD) that could be consumed as a foodstuff. Mixing the extract with cyclodextrin masked its undesirable wood smell and improved its solubility. Subsequent studies in humans (21) and rats (22) showed that SRCD inhibited the elevation of blood glucose level in an oral sucrose tolerance test. Nonetheless, although there is compelling evidence that SRCD affects glucose and lipid metabolism, there is a lack of information in the literature on the effect of SRCD in rodent models of HF diet–induced obesity.
The present study was conducted to test our hypothesis that SRCD-induced substrate and metabolic changes are associated with a reduction in HF diet–induced adiposity, especially visceral fat mass, in mice and rats. The first experiment examined the effects of SRCD on the elevation of plasma triacylglycerol levels induced in male rats by oral administration of a HF liquid diet. The second experiment investigated the effect of SRCD in female mice that consumed HF diets ad libitum. The third experiment examined whether SRCD also has an antiobesity effect in male rats restricted in EI to that of rats fed a normal (not HF) diet.
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MATERIALS AND METHODS |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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The dried stems of S. reticulata (5 kg) from Sri Lanka were washed thoroughly with water, crushed, and extracted (95°C, 1 h) with 10 volumes of boiled water (50 L). Then, an amount of cyclodextrin (250 g) equal to the weight of the solvent (250 g) was added and mixed. The solvent was evaporated at <40°C, and the remaining solution was spray-dried to obtain SRCD (500 g). The SRCD consisted of 2.8% moisture, 1.3% protein, 83.7% carbohydrate, 0.3% fat, 6.8% ash, and 5.1% dietary fiber. The polyphenol content, determined by the colorimetric method (Folin-Ciocalteu method), was 6.8%. The mangiferin content was 0.65% as determined by HPLC using a Wakosil-II 5C18AR column (Wako Pure Chemical) with methanol:1% acetic acid (10:90) as the mobile phase, detection at a wavelength of 360 nm, a column temperature of 35°C, and a flow rate of 1 mL/min.
Animals
Female C57BL/6J mice (6 wk old) and 6- and 7-wk-old male Sprague-Dawley rats were obtained from Japan SLC. The mice were housed in aluminum cages, and the rats were housed individually in stainless steel metabolic cages. The mice and rats were kept in a temperature-controlled room at 22 ± 1°C and 50–60% humidity with a 12-h light cycle (lights on at 0700). The mice and rats had free access to tap water and laboratory food (MF, Oriental Yeast) until they were assigned to individual groups. This study was approved by the Laboratory Animal Care Committee of Yokohama City University; the mice and rats were maintained in accordance with the Guidelines for the Care and Use of Laboratory Animals of Yokohama City University.
Experimental diet
The HF liquid diet, which was an emulsion prepared as described by Warwick and Synowski (23), contained 6.5% energy (%E) as protein, 33.4%E carbohydrate, and 60.1%E fat. The composition of the HF liquid diet was 54 g evaporated milk, 11.2 g soybean oil, 1 g sodium taurocholate, and 14 g sucrose, with the volume adjusted to 100 mL with water. The 4 diets, i.e., normal diet, HF diet, HF diet + 0.2% SRCD, and HF diet + 0.5% SRCD, were prepared in pellet form by Research Diets. The diet compositions are shown in Table 1. The normal diet was based on the AIN-93G recommendation (24) and contained 20%E protein, 64%E carbohydrate, and 16%E fat. The HF diet contained 20%E protein, 35%E carbohydrate, and 45%E fat, which consisted of soybean oil and lard. The SRCD (0.2 or 0.5%) was added at the expense of cornstarch in the HF diet.
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Experiment 2: Effects of dietary SRCD in female mice that consumed a HF diet ad libitum. Mice (n = 39) were divided into 4 groups. After a 1-wk adaptation period, each group was fed one of the following diets: normal diet (n = 10), HF diet (n = 10), 0.2% SRCD diet (n = 10), and 0.5% SRCD diet (n = 9). The mice had free access to food and tap water for 8 wk and were weighed weekly. Food intake was monitored twice each week. At the end of wk 8, the mice were killed between 0900–1200 (postprandial condition). Blood was collected from an eye wound into chilled test tubes and was centrifuged at 2000 x g at 4°C for 10 min. Plasma glucose, triacylglycerol, total cholesterol, HDL cholesterol, and free fatty acid (FFA) concentrations were measured immediately. The remaining plasma was stored at –80°C until further use. The liver, kidneys, and visceral (intra-abdominal) fat mass, including mesenteric, perirenal, and perimetrial fat, were excised and weighed.
Experiment 3: Effects of dietary SRCD in energy-restricted male rats that consumed a HF diet. The rats were provided with an amount of food containing the energy normally consumed in 1 d. To determine the amount of energy required by the rats, the amount of food consumed by 7- to 10-wk-old rats fed a normal (not HF) diet (monitor rats; not a test group) was measured. Their food intake increased over 9 wk. We determined their required energy level to be 401.3 kJ/(rat·d), and this amount was provided in the HF diet. We set the energy provided in the HF diet at 100% of the ad libitum intake of rats fed a normal diet to prevent the excessive EI that occurs in rats fed a HF diet (6,9). Male 7-wk-old rats (n = 14) were divided into 2 groups (n = 7) and given free access to the HF diet and tap water for 4 d to adapt to this diet; we measured the energy consumed by the rats during this period. The energy restriction started on d 5 at 257.7 kJ/(rat·d), because this was the least amount of energy consumed during the adaptation period. We increased the amount of energy offered to the rats each day for 4 d (257.7, 322.1, and 386.4 kJ/d) and then maintained it at 401.3kJ/(rat·d) from d 17 through 40. The actual food intake was determined by measuring daily the amount of food left in the cages. The rats were weighed every other day. From d 13 to 39, 1 mL of SRCD solution, representing 0.2% of the diet, was given orally once daily to each rat in the treated group. Feces from each of the rats were collected for a 48-h period on d 34 and 35. At the end of the experiment, the rats were deprived of food for 18 h and were then anesthetized. They were killed by cardiac puncture, and tissues were collected as in Expt. 2. Blood was centrifuged at 2000 x g at 4°C for 10 min. Plasma glucose, triacylglycerol, total cholesterol HDL cholesterol, and FFA concentrations were measured immediately. The remaining plasma was stored at –80°C. The liver, kidneys, cecum, and visceral fat (mesenteric, perirenal, and epididymal fat) were excised and weighed.
Oral glucose tolerance test
In Expt. 2, the mice were administered an oral glucose tolerance test (OGTT) after 7 wk of consuming the experimental diet. On the day of the test, the mice were deprived of food for 12 h and weighed, and a blood sample was removed from the tail vein. The mice were then administered a glucose solution by gavage (1 g/kg), and tail blood was collected 30, 60, and 120 min later. The area under the curve for glucose (AUCglucose) was calculated using the trapezoidal rule.
Assays
The blood glucose levels during the OGTT were assayed immediately using an Antsense II system (Horiba). The collected feces were dried and weighed. Total fat was determined by the method of Folch et al. (25). Apparent fat absorption was calculated using the formula: [(fat intake – fecal fat)/fat intake] x 100. Plasma glucose, triacylglycerol, total cholesterol, and HDL cholesterol concentrations were assayed using a multilayer film analytical element (Drichem-5500, Fuji Film Medical). The plasma FFA concentration was determined by an enzymatic colorimetric assay (NEFA C-test kit, Wako Pure Chemical). To measure plasma insulin concentrations, a mouse insulin ELISA kit (RID) and an ultrasensitive rat insulin ELISA kit (Morinaga) were used in Expts. 2 and 3, respectively. For the plasma leptin measurements, a RayBio mouse leptin ELISA kit (RayBiotech) and a rat leptin ELISA kit (Wako Pure Chemical) were used in Expts. 2 and 3, respectively. Plasma adiponectin concentration was determined using a mouse or rat adiponectin ELISA kit (Otsuka Pharmaceutical) in Expt. 2 or 3, respectively.
Statistical analysis
The data are expressed as means ± SD. All statistical analyses were performed using StatView version 5.0 (SAS Institute). When variances associated with each experimental mean were unequal, the data were log-transformed before analysis. Changes in plasma triacylglycerol concentration (Expt. 1) and body weight (Expt. 3) were analyzed by repeated-measures ANOVA, and significant differences between groups were analyzed by Dunnett's test. In Expt. 2, changes in body weight were analyzed by repeated-measures ANOVA, and other data were analyzed by one-way ANOVA. The differences among the HF, 0.2% SRCD, and 0.5% SRCD groups were analyzed using the Tukey-Kramer test. Data of mice fed the normal diet were not included in the statistical analysis. Except for body weight, the groups were compared by one-way ANOVA in Expt. 3. Differences with P < 0.05 were considered significant.
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RESULTS |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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22% greater than in the mice fed the normal diet, but the HF-fed groups did not differ from one another. The energy efficiency (EE) of the 0.5% SRCD group was lower than that of the HF-diet and 0.2% SRCD groups (P < 0.05). The weight gain, EI, and EE of the 0.2% SRCD group did not differ from those of the HF-diet group.
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The addition of SRCD to the HF diet improved oral glucose tolerance. The glucose concentration in food-deprived mice did not differ among the 3 groups (6.89 ± 0.84, 5.96 ± 1.1, 5.70 ± 1.1, and 5.02 ± 1.3 mmol/L in the normal, HF-diet, 0.2% SRCD, and 0.5% SRCD groups, respectively). The AUCglucose was less for the 0.5% SRCD group (843 ± 111 mmol x min/L) than for the HF-diet group (1011 ± 142 mmol x min/L, P < 0.05), and intermediate in the 0.2% SRCD group (949 ± 129 mmol x min/L). The AUC in the mice fed the normal diet was 872 ± 47 mmol x min/L. Visceral fat mass was positively correlated with the AUCglucose among all of the mice (r = 0.609, P < 0.0001).
Experiment 3. The body weight of the SRCD group on d 21, d 9 of SRCD administration, was lower than that of the HF-diet group (P < 0.05, Fig. 3). The SRCD group gained less weight (P < 0.05) and had lower EI (P < 0.05), EE (P < 0.05), and fecal fat than rats fed the HF diet only (Table 4). Apparent fat absorption was higher in the SRCD group than in the HF-diet group (P < 0.05).
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Relations between visceral fat mass and EE, EI, liver weight, and kidney weight. In Expt. 1, visceral fat mass was correlated with EI (r = 0.695, P < 0.001), EE (r = 0.905, P < 0.0001), and liver weight (r = 0.630, P < 0.0001) in all of the mice. In Expt. 2, visceral fat mass was correlated with EI (r = 0.779, P < 0.001) and liver weight (r = 0.689, P < 0.001) in all of the rats; EE tended to correlate with visceral fat mass (r = 0.454, P = 0.10).
Relations between visceral fat mass and metabolic variables. In Expt. 1, the visceral fat mass was correlated with plasma triacylglycerol (r = 0.433, P < 0.01), insulin (r = 0.545, P < 0.001), leptin (r = 0.798, P < 0.0001), and adiponectin (r = 0.413, P < 0.01) concentrations in all of the mice. In Expt. 2, visceral fat mass was correlated with plasma triacylglycerol (r = 0.530, P < 0.05) and leptin (r = 0.635, P < 0.05) concentrations in all of the rats.
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DISCUSSION |
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TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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-glucosidase inhibitors, which affect carbohydrate absorption (17–19), and various polyphenols, including mangiferin, catechins, and tannins, which inhibit lipid-metabolizing enzymes (20). We speculated that a decrease in fat absorption may be a mechanism by which SRCD exerts its antiobesity effect. Therefore, we examined the effects of SRCD on elevated plasma triacylglycerol levels induced by oral administration of a HF liquid diet in rats. The results suggested that SRCD has antiobesity activity mediated by delayed intestinal absorption of dietary fat. The experiments clearly showed that the consumption of SRCD suppresses 2 types of HF diet–induced obesity and especially the accumulation of visceral fat mass. The lower body weight gain in mice and rats fed a SRCD-supplemented diet was associated with lower EE. Given that the EI of the mice fed the 0.2% and 0.5% SRCD diets was not altered in Expt. 2, in which there was free access to food, the lower weight gain in the 0.5% SRCD group suggests that the metabolic processes were less efficient in this group. In the energy-restricted rats in Expt. 3, 0.2% SRCD clearly reduced weight gain, EE, EI, and adiposity in those fed the HF diet. The dose of SRCD selected for use in Expts. 2 and 3 was based on other reports in rats (17,20,22). The difference in the effective dose of SRCD between Expts. 2 and 3 was probably the result of variations in the method of preparation, differences between animal species (mouse vs. rat), and/or differences in the dosing scheme (addition to the diet vs. gavage). The decrease in EI in energy-restricted rats was unexpected. There are reports of declines in food intake and decreases in body weight in mice and rats fed a HF diet with herb or plant extracts, and it was suggested that metabolic changes (15), the expression of appetite-related peptides (26), or altered energy expenditure (12) are produced by the treatment. It is thought that animals generally prefer diets that are sweet and avoid those that are bitter. It is possible that the bitter taste of compounds such as the polyphenols in SRCD affected the appetite of the rats. However, we administrated the SRCD solution orally to the rats in Expt. 3. This suggests that a metabolic change or influence on appetite occurred in rats fed a HF diet with SRCD. Murase et al. (27) reported that 0.5% tea catechins in a HF diet reduced obesity and EI, and did not increase the fecal excretion of fat in mice. They postulated that the antiobesity effect of tea catechins was due not only to the decrease in EI but was also related to energy expenditure. The amount of fecal fat in the SRCD group was significantly lower, but the apparent fat absorption was significantly higher than that of the HF-diet group in Expt. 3. This result indicates that the energy consumed by the rats fed the SRCD was used by the body, and it may have been that energy expenditure was stimulated in the SRCD group. However, the cecal weight and amount of N excreted via feces (data not shown) were greater in the SRCD group in Expt. 3, indicating that intestinal bacterial fermentation occurred; thus, the energy from the diet may have been utilized by intestinal bacteria. In addition, there was a report that intestinal Clostridium perfingens, a bile salt hydrolase-active bacteria, and bile acid influenced lipid metabolism in broilers (28). Lipid metabolism may have been influenced by the intestinal bacteria in rats fed SRCD. However, variables related to energy expenditure or bacterial fermentation were not measured in our study; thus, further study is warranted to clarify the precise mechanism of this phenomenon.
Of the various body fat depots, the amount of visceral fat is correlated best with insulin sensitivity in animal models and humans. (8,29) Insulin action is markedly impaired in individuals with visceral obesity (30), and the removal of visceral fat prevents the insulin resistance and glucose intolerance associated with aging (31). In the present study, the impaired oral glucose tolerance that accompanied the consumption of a HF diet was returned to normal by SRCD supplementation. Visceral fat mass correlated positively with AUCglucose in all of the mice (r = 0.609, P < 0.0001). We hypothesize that the hypoglycemic effect of SRCD is secondary to the metabolic changes associated with reduced adiposity. Our results provide useful information regarding the use of SRCD as a dietary adjunct for the management of body weight and glucose intolerance induced by a HF diet. The plasma glucose concentration was significantly greater in the 0.5% SRCD group than in 0.2% SRCD group in Expt. 2. We postulate that this may have been attributable to the postprandial condition in which the mice were sampled because the glucose level did not differ among the three groups in the OGTT when rats had been deprived of food for 12 h.
Leptin is a fat-derived key regulator of appetite and energy expenditure, and leptin concentration is usually positively correlated with general adiposity (32). In our study, mice fed a HF diet containing 0.5% SRCD had plasma leptin concentrations comparable to those of the normal diet group in Expt. 2, and there was a correlation between leptin concentration and visceral fat mass in mice and rats in Expts. 2 and 3.
Adiponectin is secreted by fat cells and circulates in the blood. The hormone has antiatherosclerotic and insulin-sensitizing properties that suppress hepatic glucose production and enhance glucose uptake into skeletal muscle. Plasma levels of adiponectin are negatively correlated with total body fat (33) and with visceral fat mass in women (34). In contrast to these reports, Baratta et al. (35) reported that the plasma adiponectin level was statistically independent of body fat mass in nondiabetic and diabetic patients. In our study, adiponectin correlated positively with visceral fat mass. Given that the regulation of adiponectin expression and secretion is most prominent in visceral adipose tissue (33,36), the decrease in plasma adiponectin may have been caused by decreased visceral fat mass. Furthermore, SRCD may first alter the accumulation of visceral fat mass, followed by the regulation of leptin and adiponectin secretion by adipose cells.
In summary, SRCD suppresses the increases in plasma triacylglycerol, total cholesterol, FFA, leptin, adiponectin, and visceral fat that occur with HF diet–induced obesity in the absence of excessive EI. These data suggest that SRCD alters the body's energy balance through its effects on glucose and fat metabolism. It also suppresses both the accumulation of visceral fat and glucose intolerance. The observed effects are likely to be caused by more than one bioactive compound present in SRCD. Dietary SRCD supplementation offers an alternate approach for studying the complex relations between energy balance, adiposity, and endocrine function, and SRCD may be effective in managing body weight in humans who consume a diet rich in fats.
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FOOTNOTES |
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2 Supported by the Bio Research Corporation of Yokohama.
4 Abbreviations used: AUC, area under the curve; %E, % energy; EE, energy efficiency; EI, energy intake; FFA, free fatty acids; OGTT, oral glucose tolerance test; HF, high fat; SRCD, mixture of Salacia reticulata aqueous extract and cyclodextrin.
Manuscript received 3 October 2005. Initial review completed 2 November 2005. Revision accepted 27 November 2005.
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