- Open Access
Antiobesity and lipid-lowering effects of Bifidobacterium spp. in high fat diet-induced obese rats
© An et al; licensee BioMed Central Ltd. 2011
Received: 20 May 2011
Accepted: 12 July 2011
Published: 12 July 2011
Recent studies have reported the preventive effects of probiotics on obesity. Among commensal bacteria, bifidobacteria is one of the most numerous probiotics in the mammalian gut and are a type of lactic acid bacteria. The aim of this study was to assess the antiobesity and lipid-lowering effects of Bifidobacterium spp. isolated from healthy Korean on high fat diet-induced obese rats.
Thirty-six male Sprague-Dawley rats were divided into three groups as follows: (1) SD group, fed standard diet; (2) HFD group, fed high fat diet; and (3) HFD-LAB group, fed high fat diet supplemented with LAB supplement (B. pseudocatenulatum SPM 1204, B. longum SPM 1205, and B. longum SPM 1207; 108 ~ 109 CFU). After 7 weeks, the body, organ, and fat weights, food intake, blood serum levels, fecal LAB counts, and harmful enzyme activities were measured.
Administration of LAB reduced body and fat weights, blood serum levels (TC, HDL-C, LDL-C, triglyceride, glucose, leptin, AST, ALT, and lipase levels), and harmful enzyme activities (β-glucosidase, β-glucuronidase, and tryptophanase), and significantly increased fecal LAB counts.
These data suggest that Bifidobacterium spp. used in this study may have beneficial antiobesity effects.
Obesity, a condition in which an abnormally large amount of fat is stored in the adipose tissue, resulting in an increase in body weight, is one of the major public health problems in the United States and other developed countries. In general, it is accepted that obesity results from disequilibrium between energy intake and expenditure , and this condition has a great impact on several metabolic and chronic ailments including heart disease, cancer, arthritis, obstructive sleep apnea, hypertension, hyperlipidemia, and type 2 diabetes associated with insulin resistance . To date, pharmacological treatments do not appear to be effective in producing sustained long-term weight loss . Therefore, further research is needed to discover new drug therapies that can be used to reduce the prevalence of obesity.
Probiotics are defined as viable microbial dietary supplements that exert beneficial effects on host health . Probiotics have attracted public attention because of their potential effectiveness for both the prevention and the treatment of immune diseases . In addition, recent experimental studies have demonstrated the preventive effects of some bacterial strains on obesity. Among commensal bacteria, bifidobacteria are one of the most numerous probiotics in the mammalian gut and are a type of lactic acid bacteria. Bifidobacteria are widely used and well tolerated. In one study, a strain of Bifidobacterium longum exhibited a more significant effect in lowering serum total cholesterol than a mixed culture of Streptococcus thermophilus and Lactobacillus delbrueckii subspecies bulgaricus (SL) both in rats and humans . Another study found that in probiotic treated-mice, Bifidobacterium spp. significantly and positively correlated with improved glucose-tolerance, glucose-induced insulin-secretion, and normalized inflammatory tone (decreased endotoxemia, plasma and adipose tissue pro-inflammatory cytokine) . Finally, VSL no. 3, a mixture of viable lyophilized bifidobacteria, lactobacilli and Streptococcus thermophilus, improved diet-induced obesity and its related hepatic steatosis and insulin resistance by increasing hepatic natural killer T-cells and reducing inflammatory signaling in mice . These data suggest that some specific strains of bifidobacteria related to lipid metabolism and body weight may be potential therapeutic candidates for management of obesity.
In the present study, we used a LAB supplement of Bifidobacterium pseudocatenulatum SPM 1204 (immuno-enhancement and anti-microbial effects) , Bifidobacterium longum SPM 1205 (inhibitory effect on harmful enzyme activities of intestinal microflora) , and Bifidobacterium longum SPM 1207 (hypocholesteremia effect) , and investigated the antiobesity and lipid-lowering effects of Bifidobacterium spp. on high fat diet-induced obese rats.
Materials and methods
Bacterial strains used in this study
Culture media and methods
Main enumerated microorganisms
Incubation time (day)
BL agar mediumb
GAM agar mediumc
Animals and treatment
Feeding schedules used in the present study
Treatment (oral administration for 5 weeks)
0.2 ml of sterilized PBS
40% High Fat Diet
0.2 ml of sterilized PBS
40% High Fat Diet
0.2 ml of LAB (108 ~109 CFU) in sterilized PBS
Compositions of experimental diet
High Fat Diet
(AIN-76A diet #100000)
(AIN-76A diet #101556)
Analysis of blood serum and organ weight
At the end of the 7-week experimental period, blood samples from each rat were collected into tubes using cardiac puncture. The serum was separated from the blood by centrifugation at 3,500 rpm for 10 min. The total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), triglyceride, glucose, leptin, alanine aminotransferase (AST), aspartate aminotransferase (ALT) levels in the serum were analyzed by Korea Animal Medical Science Institute (Korea). Also, the fat (epididymal and retroperitoneal), liver, spleen and kidney were removed immediately after the sacrifice and weighed.
Measurement of α-amylase and lipase activities
The activities of α-amylase and lipase were measured with the α-Amylase Assay Kit (BioAssay Systems, USA) and Lipase Assay Kit (BioAssay Systems, USA), respectively.
Fecal sampling and bacteriological analysis
Fecal samples were collected from the rats weekly to determine the total LAB counts and harmful enzyme activities. Fecal samples were taken directly from the rectum by rectal stimulation and immediately transferred into sterile tubes and stored at 4°C.
Fecal samples (0.1 g) were suspended in 0.9 ml of 0.1 M phosphate buffer (pH 6.8 containing 0.5% cysteine) by vortexing, and 0.1 ml was then serially diluted 10-fold from 10-1 to 10-7. 1 ml was then poured into selective General Anaerobic Medium (GAM) agar medium (Table 1). After 48 h of incubation under anaerobic conditions, colonies were counted as Bifidobacterium spp. . The numbers of colony forming units (CFU) are expressed as log10 CFU per gram.
Harmful enzyme activities of intestinal microflora
The harmful activities of enzymes such as β-glucosidase, β-glucuronidase, tryptophanase, and urease of intestinal microflora related to colon cancer were tested in fecal samples of rats as previously described [14–16].
Assay of β-glucosidase activity
β-glucosidase activity was assayed in a 2-ml reaction mixture containing 0.8 ml of 2 mM p-nitrophenyl-β-D-glucopyranoside and 0.2 ml of enzyme solution (suspended fecal sample). The reaction was incubated for 30 min at 37°C and then stopped by adding 1 ml of 0.5 N NaOH. The reaction mixture was then centrifuged at 3,000 rpm for 10 min. Enzyme activity was measured by monitoring absorbance at 405 nm.
Assay of β-glucuronidase activity
β-glucuronidase activity was assayed in a 2-ml reaction mixture consisting of 0.8 ml of 2 mM p-nitrophenyl-β-D-glucuronide and 0.2 ml of the enzyme solution. The reaction was incubated for 30 min at 37°C and then stopped by adding 1 ml of 0.5 N NaOH. The reaction mixture was centrifuged at 3,000 rpm for 10 min. Enzyme activity was measured by monitoring absorbance at 405 nm.
Assay of tryptophanase activity
Tryptophanase activity was assayed in a 2.5-ml reaction mixture consisting of 0.2 ml of complete reagent solution (2.75 mg of pyridoxal phosphate, 19.6 mg of disodium EDTA dihydrate, and 10 mg of bovine serum albumin in 100 ml of 0.05 M potassium phosphate buffer, pH 7.5), 0.2 ml of 20 mM tryptophan, and 0.1 ml of the enzyme solution. The reaction was incubated for 1 h at 37°C and then stopped by adding 2 ml of color reagent solution (14.7 g p-dimethylaminobenzaldehyde in 52 ml H2SO4 and 948 ml 95% ethanol). The reaction mixture was then centrifuged at 3,000 rpm for 10 min. Enzyme activity was measured by monitoring absorbance at 550 nm.
Assay of urease activity
Urease activity was assayed in a 0.5-ml reaction mixture consisting of 0.3 ml of urea substrate solution (4 mM urea in 20 mM sodium phosphate buffer, pH 7.0) and 0.1 ml of the enzyme solution. The reaction was incubated for 30 min at 37°C and then stopped by adding 0.1 ml of 1 N (NH4)2SO4. Phenolnitroprusside reagent (1 ml) and alkaline hypochlorite reagent (NaClO, 1 ml) were added to the stopped reaction mixture and incubated for 20 min at 65°C. The reaction mixture was centrifuged at 3,000 rpm for 10 min. Enzyme activity was measured by monitoring absorbance at 603 nm.
Results were expressed as mean ± standard deviation. Significant differences among groups were determined using Duncan's Multiple Range Test (SAS ver. 8.1, SAS Institute Inc., Cary, NC, USA). Values of P < 0.05 were considered significant.
Body weight, organ weight, fat weight, and food intake
Weights of body, fat, spleen, kidney, and liver
Body weight (g)
381.00 ± 11.95B
413.86 ± 30.28A
402.20 ± 29.23AB
Fat weight (g) (epididymal + retroperitoneal)
13.94 ± 2.66B
20.94 ± 4.08A
18.47 ± 2.02A
Fat pad weight (g/100 g body weight)
3.63 ± 0.65B
5.11 ± 0.60A
4.83 ± 0.40A
0.66 ± 0.03
0.60 ± 0.07
0.64 ± 0.10
2.59 ± 0.15
2.60 ± 0.18
2.61 ± 0.08
18.47 ± 1.95AB
20.04 ± 2.27A
17.59 ± 2.33B
Analysis of blood serum levels
Serum levels of cholesterol, triglyceride, glucose, leptin, AST, and ALT
88.20 ± 12.24
92.20 ± 11.02
89.70 ± 17.33
54.40 ± 9.25A
47.40 ± 7.55AB
46.09 ± 7.25B
19.15 ± 2.96A
16.75 ± 3.27AB
15.22 ± 4.40B
146.18 ± 33.76B
262.40 ± 110.75A
246.70 ± 74.18A
230.40 ± 41.31AB
236.50 ± 35.53A
200.36 ± 37.09B
433.88 ± 117.15B
575.68 ± 149.86A
538.08 ± 158.12AB
98.50 ± 33.78AB
111.00 ± 13.39A
84.45 ± 13.77B
38.00 ± 5.25B
65.00 ± 8.16A
62.70 ± 4.35A
Serum levels of α-amylase and lipase
182.36 ± 10.73
172.33 ± 12.51
191.57 ± 16.16
91.10 ± 21.38B
224.25 ± 33.21A
216.52 ± 22.52A
Fecal total LAB counts
Harmful enzyme activities of intestinal microflora
Many studies have reported antiobesity effects of some bacterial strains such as Lactobacillus spp. and Bifidobacterium spp. [17–19, 8]. In the present study, we observed that feeding of a high fat diet for 5 weeks produced significant increases in body weight, and administration of LAB reduced body weight gain and fat weight. However, there was no significant difference in spleen, kidney, and liver weights.
Our results demonstrated that the TC, HDL-C, and LDL-C levels in serum were decreased in the HFD-LAB group. The reduction of TC or LDL in serum is reported to lower the risk of coronary heart disease . Recent studies showed that probiotics, including Bifidobacterium longum , Lactobacillus acidophilus , had hypocholesteremic effects in both rat and human. The mechanisms involved may be as follows [22–27]: (1) fermentation products of lactic acid bacteria inhibit cholesterol synthesis enzymes and thus reduce cholesterol production; (2) the bacteria facilitate the elimination of cholesterol in feces; (3) the bacteria inhibit the absorption of cholesterol back into the body by binding with cholesterol; (4) the bacteria interfere with the recycling of bile salt (a metabolic product of cholesterol) and facilitate its elimination, which raises the demand for bile salt made from cholesterol and thus results in body cholesterol consumption; and (5) the assimilation of lactic acid. In addition, we found that levels of triglyceride, glucose, AST, and ALT in serum were reduced in HFD-LAB group. Similar results have been observed with some specific probiotics strains [19, 8, 17].
Leptin has been identified as an antiobesity hormone that regulates body weight by controlling food intake and energy expenditure via the hypothalamic-pituitary-gonadal axis [28–30]. It appears that leptin may be an important factor in obesity management. Leptin is a 16 KDa secreted protein produced by the ob gene. Adipose tissue produces leptin and releases it into the bloodstream. As fat deposits grow, blood leptin levels tend to increase. Thus, leptin levels are closely related to the percentage of body fat; markedly higher serum leptin levels have been found in obese individuals compared with non-obese individuals [31, 32]. In contrast, leptin levels are severely reduced in underweight individuals compared with normal weight individuals [33, 34]. In the present study, leptin levels were higher in the HFD-fed groups than in the SD group, but were lower in the HFD-LAB group than in the HFD group. Similar effects have been observed in other studies using mouse  and human . The results of these studies suggest that reductions in fat mass and body weight are associated with a reduction in leptin.
α-Amylase, a digestive enzyme secreted from the pancreas and salivary gland, is involved in important biological processes such as digestion of carbohydrates. Many crude drugs inhibit α-amylase activity . Natural α-amylase inhibitors are beneficial in reducing post-prandial hyperglycemia by slowing down the digestion of carbohydrates and, consequently, the absorption of glucose. Reducing post-prandial hyperglycemia prevent glucose uptake into adipose tissue to inhibit synthesis and accumulation of triacylglycerol . On the other hand, it is well known that dietary lipid is not directly absorbed from the intestine unless it has been subjected to the action of pancreatic lipase. The two main products formed by the hydrolysis of pancreatic lipase are fatty acid and 2-monoacylglycerol. Inhibition of these digestive enzymes is therefore beneficial in the treatment of obesity . Our results showed that lipase levels were slightly decreased in the HFD-LAB group, whereas α-amylase levels were increased. That is, LAB had an inhibitory effect on lipase.
In our study, fecal LAB counts were obviously decreased in the HFD-fed groups compared with those in the SD group. Similarly, Cani et al.  demonstrated that a high fat diet changed the intestinal microbiota composition; in particular, the number of Bifidobacterium spp. was reduced. Kalliomaki et al.  also observed that fecal Bifidobacterium spp. counts were higher in children who remained at normal weight at the age of seven, while this was not the case in overweight children. After treatment with LAB, we found that the LAB counts in the HFD-LAB group were significantly increased compared with those in the HFD group. This result means that LAB survive passage through the upper-gastrointestinal tract after oral feeding, and ingested LAB affect the intestinal environment to favor LAB colonization .
Several studies have shown that these specific bacteria reduce the intestinal endotoxin levels and improve mucosal barrier function [41–43]. Furthermore, LAB have anti-tumor effects and block harmful intestinal enzyme activities, a recognized risk factor for colon cancer [44, 45]. The results of the present study showed the harmful enzyme activities of intestinal microflora in the HFD-LAB group were clearly decreased compared with those in the other groups; in particular, the activities of β-glucosidase, β-glucuronidase, and tryptophanase were significantly decreased.
In conclusion, we suggest that the LAB supplement (B. pseudocatenulatum SPM 1204, B. longum SPM 1205, B. longum SPM 1207) used in this study may have beneficial antiobesity effects. Further clinical trials to confirm these effects should therefore be conducted.
This study was supported by the Sahmyook University Research Fund in 2010. The authors are grateful to the Department of Pharmacy of Sahmyook University and for the financial support provided by the Sahmyook University Research Fund.
- Wood SC, Seeley RJ, Porte JD, Schwarts MW: Signal that regulate food intake and energy homeostasis. Sci. 1998, 280: 1378-1383. 10.1126/science.280.5368.1378.View ArticleGoogle Scholar
- Wickelgren I: Obesity; how big a problem?. Sci. 1998, 280: 1364-1367. 10.1126/science.280.5368.1364.View ArticleGoogle Scholar
- Glenny AM, OĭMeara S, Melville A, Sheldon TA, Wilson C: The treatment and prevention of obesity; a systematic review of the literature. Int J Obes. 1997, 21: 715-737. 10.1038/sj.ijo.0800495.View ArticleGoogle Scholar
- Fuller R: Probiotics in man and animals. J Appl Bacteriol. 1989, 66: 365-378.View ArticlePubMedGoogle Scholar
- Borchers AT, Selmi C, Meyers FJ, Keen CL, Gershwin ME: Probiotics and immunity. J Gastroenterol. 2009, 44: 26-46. 10.1007/s00535-008-2296-0View ArticlePubMedGoogle Scholar
- Xiao JZ, Kondo S, Takahashi N, Miyaji K, Oshida K, Hiramatsu A, Iwatsuki K, Kokubo S, Hosono A: Effects of milk products fermented by Bifidobacterium longum on blood lipids in rats and healthy adult male volunteers. J Dairy Sci. 2003, 86: 2452-2461. 10.3168/jds.S0022-0302(03)73839-9View ArticlePubMedGoogle Scholar
- Cani PD, Neyrinck AM, Fava F, Knauf K, Burcelin RG, Tuohy KM: Selective increases of bifidobacteria in gut microflora improves high-fat diet induced diabetes in mice through a mechanism associated with endotoxemia. Diabetologia. 2007, 50: 2374-2383. 10.1007/s00125-007-0791-0View ArticlePubMedGoogle Scholar
- Ma X, Hua J, Li Z: Probiotics improve high fat diet induced hepatic steatosis and insulin resistance by increasing hepatic NKT cells. J Hepatol. 2008, 49: 821-830. 10.1016/j.jhep.2008.05.025PubMed CentralView ArticlePubMedGoogle Scholar
- Han SH, Cho KH, Lee CK, Song YC, Park SH, Ha NJ, Kim KJ: Enhancement of antigen presentation capability of dendritic cells and activation of macrophages by the components of Bifidobacterium pseudocatenulatum SPM 1204. J Appl Pharm. 2005, 13: 174-180.Google Scholar
- Choi SS, Kang BY, Chung MJ, Kim SD, Park SH, Kim JS, Kang CY, Ha NJ: Safety assessment of potential lactic acid bacteria Bifidobacterium longum SPM 1205 isolated from healthy Koreans. J Microbiol. 2005, 43: 493-498.PubMedGoogle Scholar
- Lee DK, Jang S, Baek EH, Kim MJ, Lee KS, Shin HS, Chung MJ, Kim JE, Lee KO, Ha NJ: Lactic acid bacteria affect serum cholesterol levels, harmful fecal enzyme activity, and fecal water content. Lipids Health Dis. 2009, 8: 21-28. 10.1186/1476-511X-8-21PubMed CentralView ArticlePubMedGoogle Scholar
- Scardovi V: Genus Bifidobacterium. Bergey's Manual of Systemic Bacteriology. Edited by: Krieg NR, Holt JG. 1986, 2: 1418-1434. Williams & Willikins, MD,Google Scholar
- Ahn JB: Isolation and characterization of Bifidobacterium producing exopolysaccharide. Food Eng Prog. 2005, 9: 291-296.Google Scholar
- Gutmann I, Bergmeyer HU: Urea. In methods of enzymatic analysis. Edited by: Bergmeyer HU. 1974, 1791-1794. New York: Academic Press,View ArticleGoogle Scholar
- Kim DH, Kang HJ, Kim SW, Kobayashi K: pH-inducible β-glucuronidase and β-glucosidase of intestinal bacteria. Chem Pharm Bull. 1992, 40: 1967-1969.Google Scholar
- Kim DH, Lee JH, Bae EA, Han MJ: Induction and inhibition of indole of intestinal bacteria. Arch Pharm Res. 1995, 18: 351-533. 10.1007/BF02976331.View ArticleGoogle Scholar
- Lee HY, Park JH, Seok SH, Baek MW, Kim DJ, Lee KE, Paek KS, Lee YH, Park JH: Human originated bacteria, Lactobacillus rhamnosus PL60, produce conjugated linoleic acid and show anti-obesity effects in diet-induced obese mice. Biochim Biophys Acta. 2006, 1761: 736-744.View ArticlePubMedGoogle Scholar
- Takemura N, Okubo T, Sonoyama K: Lactobacillus plantarum strain No. 14 reduces adipocyte size in mice fed high fat diet. Exp Biol Med. 2010, 235: 849-856. 10.1258/ebm.2010.009377.View ArticleGoogle Scholar
- Yin YN, Yu QF, Fu N, Liu XW, Lu FG: Effects of four Bifidobacteria on obesity in high fat diet induced rats. World J Gastroenterol. 2010, 16: 3394-3401. 10.3748/wjg.v16.i27.3394PubMed CentralView ArticlePubMedGoogle Scholar
- Taylor GRJ, Williams CM: Effects of probiotics and prebiotics on blood lipids. Br J Nutr. 1998, 80: S225-230.PubMedGoogle Scholar
- Park YH, Kim JG, Shin YW, Kim SH, Whang KY: Effect of dietary inclusion of Lactobacillus acidophilus ATCC 43121 on cholesterol metabolism in rats. J Microbiol Biotechnol. 2007, 17: 655-662.PubMedGoogle Scholar
- Beena A, Prasad V: Effect of yogurt and bifidus yogurt fortified with skim milk powder, condensed whey and lactosehydrolysed condensed whey on serum cholesterol and triacylglycerol levels in rats. J Dairy Res. 1997, 64: 453-457. 10.1017/S0022029997002252View ArticlePubMedGoogle Scholar
- Fukushima M, Nakao M: The effect of a probiotic on faecal and liver lipid classes in rats. Br J Nutr. 1995, 73: 701-710. 10.1079/BJN19950074View ArticlePubMedGoogle Scholar
- Grunewald KK: Serum cholesterol levels in rats fed skim milk fermented by Lactobacillus acidophilus. J Food Sci. 1982, 47: 2078-2079. 10.1111/j.1365-2621.1982.tb12955.x.View ArticleGoogle Scholar
- Hashimoto H, Yamazaki K, Arai Y, Kawase M, He F, Hosoda M, Hosono A: Effect of lactic acid bacteria on serum cholesterol level in rats fed cholesterol diet. Anim Sci Technol. 1998, 69: 702-707.Google Scholar
- Rao DR, Chawan CB, Pulusani SR: Influence of milk and Thermophilus milk on plasma cholesterol levels and hepatic cholesterogenesis in rats. J Food Sci. 1981, 46: 1339-1341. 10.1111/j.1365-2621.1981.tb04168.x.View ArticleGoogle Scholar
- Suzuki Y, Kaizu H, Yamauchi Y: Effect of cultured milk on serum cholesterol concentrations in rats which fed high cholesterol diets. Anim Sci Technol. 1991, 62: 565-571.Google Scholar
- Jéquier E: Leptin signaling, adiposity, and energy balance. Ann N Y Acad Sci. 2002, 967: 379-388.View ArticlePubMedGoogle Scholar
- Frederich RC, Hamann A, Anderson S: Leptin levels reflect body lipid content in mice; Evidence for diet-induced resistance to leptin action. Nat Med. 1995, 1: 1311-1314. 10.1038/nm1295-1311View ArticlePubMedGoogle Scholar
- Friedman JM: The function of leptin in nutrition, weight, and physiology. Nutr Rev. 2002, 60: S1-S14.View ArticlePubMedGoogle Scholar
- Hamilton BS, Paglia D, Kwan AY, Deitel M: Increased obese mRNA expression in omental fat cells from massively obese humans. Nat Med. 1995, 1: 953-956. 10.1038/nm0995-953View ArticlePubMedGoogle Scholar
- Considine RV, Shinha MK, Heiman ML: Serum immunoreactive leptin concentrations in normal weight and obese humans. N Engl J Med. 1996, 334: 292-295. 10.1056/NEJM199602013340503View ArticlePubMedGoogle Scholar
- Grinspoon S, Gulick T, Askari H: Serum leptin levels in women with anorexia nervosa. J Clin Endocrinol Metab. 1996, 81: 3861-3863. 10.1210/jc.81.11.3861PubMedGoogle Scholar
- Ferron F, Considine RV, Peino R: Serum leptin concentrations in patients with anorexia nervosa, bulimia nervosa and non-specific eating disorders correlate with the body mass index but are independent of the respective disease. Clin Endocrinol. 1997, 46: 289-293. 10.1046/j.1365-2265.1997.1260938.x.View ArticleGoogle Scholar
- Kobayashi K, Saito Y, Nakazawa I, Yoshizaki F: Screening of crude drugs for influence on amylase activity and postprandial blood glucose in mouse plasma. Biol Pharm Bull. 2000, 23: 1250-1253.View ArticlePubMedGoogle Scholar
- Maury J, Issad T, Perdereau D, Gouhot B, Ferre P, Girard J: Effect of acarbose on glucose homeostasis, lipogenesis and lipogenic enzyme gene expression in adipose tissue of weaned rats. Diabetologia. 1993, 36: 503-509. 10.1007/BF02743265View ArticlePubMedGoogle Scholar
- Ono Y, Hattori E, Fukaya Y, Imai S, Ohizumi Y: Anti-obesity effect of Nelumbo nucifera leaves extract in mice and rats. J Ethnopharmacol. 2006, 106: 238-244. 10.1016/j.jep.2005.12.036View ArticlePubMedGoogle Scholar
- Cani PD, Delzenne NM, Amar J, Burcelin R: Role of gut microflora in the development of obesity and insulin resistance following high-fat diet feeding. Pathol Biol. 2008, 56: 305-309. 10.1016/j.patbio.2007.09.008View ArticlePubMedGoogle Scholar
- Kalliomaki M, Collado MC, Salminen S, Isolauri E: Early differences in fecal microbiota composition in children may predict overweight. Am J Clin Nutr. 2008, 87: 534-538.PubMedGoogle Scholar
- Pochart P, Marteau P, Bouhnik Y, Goderel I, Bourlioux P, Rambaud JC: Survival of bifidobacteria ingested via fermented milk during their passage through the human small intestine: and in vivo study using intestinal perfusion. Am J Clin Nutr. 1992, 55: 78-80.PubMedGoogle Scholar
- Griffiths EA, Duffy LC, Schanbacher FL, Qiao H, Dryja D, Leavens A: In vivo effects of bifidobacteria and lactoferrin on gut endotoxin concentration and mucosal immunity in Balb/c mice. Dig Dis Sci Apr. 2004, 49: 579-589.View ArticleGoogle Scholar
- Wang Z, Xiao G, Yao Y, Guo S, Lu K, Sheng Z: The role of bifidobacteria in gut barrier function after thermal injury in rats. J Trauma Sep. 2006, 61: 650-657.View ArticleGoogle Scholar
- Wang ZT, Yao YM, Xiao GX, Sheng ZY: Risk factors of development of gut-derived bacterial translocation in thermally injured rats. World J Gastroenterol Jun. 2004, 10: 1619-1624.View ArticleGoogle Scholar
- Lee DK, Jang S, Kim MJ, Kim JH, Chung MJ, Kim KJ, Ha NJ: Anti-proliferative effects of Bifidobacterium adolescentis SPM 0212 extract on human colon cancer cell lines. BMC Cancer. 2008, 8: 310- 10.1186/1471-2407-8-310PubMed CentralView ArticleGoogle Scholar
- Goldin BR, Gualtieri LJ, Moore RP: The effect of Lactobacillus GG on the initiation and promotion of DMH-induced intestinal tumors in the rat. Nutr Cancer. 1996, 25: 197-204. 10.1080/01635589609514442View ArticlePubMedGoogle Scholar
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.