Dietary resistant starch improves selected brain and behavioral functions in adult and aged rodents

Resistant starch (RS) is a dietary fiber that exerts multiple beneficial effects. The current study explored the effects of dietary RS on selected brain and behavioral functions in adult and aged rodents. Because glucokinase (GK) expression in hypothalamic arcuate nucleus and area postrema of the brainstem is important for brain glucose sensing, GK mRNA was measured by brain nuclei microdissection and PCR. Adult RS‐fed rats had a higher GK mRNA than controls in both brain nuclei, an indicator of improved brain glucose sensing. Next, we tested whether dietary RS improve selected behaviors in aged mice. RS‐fed aged mice exhibited (i) an increased eating responses to fasting, a behavioral indicator of improvement in aged brain glucose sensing; (ii) a longer latency to fall from an accelerating rotarod, a behavioral indicator of improved motor coordination; and (iii) a higher serum active glucagon‐like peptide‐1 (GLP‐1). Then, GLP‐1 receptor null (GLP‐1RKO) mice were used to test the role of GLP‐1 in brain glucose sensing, and they exhibited impaired eating responses to fasting. We conclude that in rodents (i) dietary RS improves two important indicators of brain function: glucose sensing and motor coordination, and (ii) GLP‐1 is important in the optimal feeding response to a fast.     

Dietary-resistant starch improves maternal glycemic control in Goto-Kakizaki rat

Scope: Dietary prebiotics show potential in anti‐diabetes. Dietary resistant starch (RS) has a favorable impact on gut hormone profiles, including glucagon‐like peptide‐1 (GLP‐1) consistently released, a potent anti‐diabetic incretin. Also RS reduced body fat and improved glucose tolerance in rats and mice. In the current project, we hypothesize that dietary‐resistant starch can improve insulin sensitivity and pancreatic β cell mass in a type 2 diabetic rat model. Altered gut fermentation and microbiota are the initial mechanisms, and enhancement in serum GLP‐1 is the secondary mechanism. Methods and results: In this study, GK rats were fed an RS diet with 30% RS and an energy control diet. After 10 wk, these rats were mated and went through pregnancy and lactation. At the end of the study, pancreatic β cell mass, insulin sensitivity, pancreatic insulin content, total GLP‐1 levels, cecal short‐chain fatty acid concentrations and butyrate producing bacteria in cecal contents were greatly improved by RS feeding. The offspring of RS‐fed dams showed improved fasting glucose levels and normal growth curves. Conclusion: Dietary RS is potentially of great therapeutic importance in the treatment of diabetes and improvement in outcomes of pregnancy complicated by diabetes.     

Tolerance, fermentation, and cytokine expression in healthy aged male C57BL/6J mice fed resistant starch

Health benefits of resistant starch (RS), a dietary fermentable fiber, have been well documented in young, but not in old populations. As the essential step of more comprehensive evaluations of RS on healthy aging, we examined the effects of dietary RS on tolerance, colonic fermentation, and cytokine expression in aged mice. Healthy older (18-20 months) C57BL/6J male mice were fed control, 18% RS, or 36% RS diets for 10 weeks. Body weight gain, body composition, and fat pad weights did not differ among the three groups after 10 weeks, indicating good tolerance of the RS diet. Fermentation indicators (cecum weights, and cecal proglucagon and PYY mRNA expression) were enhanced in an RS dose-dependent manner (p<0.01). Serum concentrations of soluble cytokine receptors (sTNF-Rb, sIL-4R, sIL-2Rα, sVEGFR1, and sRAGE) and TNFα expression (gene and protein) in visceral fat did not differ significantly among groups. Adiponectin protein concentrations, but not gene expression, were greater in epididymal fat of the 36% RS versus control groups (p<0.05). As a conclusion in aged mice, dietary RS is well tolerated, fermented in the colon, and stimulates colonic expression of proglucagon and PYY mRNA, and adiponectin protein in visceral fat.     

Chronic dietary intake of quercetin alleviates hepatic fat accumulation associated with consumption of a Western-style diet in C57/BL6J mice

Scope: To determine the effect of consumption of a quercetin‐rich diet on obesity and dysregulated hepatic gene expression. Methods and results: C56BL/6J mice were fed for 20 wk on AIN93G (control) or a Western diet high in fat, cholesterol and sucrose, both with or without 0.05% quercetin. Triglyceride levels in plasma, thiobarbituric acid‐reactive substances (oxidative stress marker) and glutathione levels and peroxisome proliferator‐activated receptor α expression in livers of mice fed with the Western diet were all improved after 8 wk feeding with quercetin. After 20 wk, further reductions of visceral and liver fat accumulation and improved hyperglycemia, hyperinsulinemia, dyslipidemia and plasma adiponectin and TNFα levels in these mice fed with quercetin were observed. The expression of hepatic genes related to steatosis, such as peroxisome proliferator‐activated receptor γ and sterol regulatory element‐binding protein‐1c was also normalized by quercetin. In mice fed with the control diet, quercetin did not affect body weight but reduces the plasma TNFα and hepatic thiobarbituric acid‐reactive substance levels. Conclusion: In mice fed with a Western diet, chronic dietary intake of quercetin reduces liver fat accumulation and improves systemic parameters related to metabolic syndrome, probably mainly through decreasing oxidative stress and reducing PPARα expression, and the subsequent reduced expression in the liver of genes related to steatosis.     

The effect of chemically‐modified resistant starch,RS type‐4, on body weight and blood lipid profiles of high fat diet‐induced obese mice

This study was conducted to investigate the effects of feeding chemically‐modified resistant starch type‐4 (RS4) of normal (NCS) and high‐amylose corn starch (HACS) on weight gain and plasma and liver lipid profiles of mice fed a high‐fat diet (HFD). The experimental four groups were, respectively, fed following diets: A 40% HFD with NCS, HACS, NCS‐ and HACS‐RS4. A normal diet (ND) group of mice fed the standard diet was also used as control. In order to produce RS4 by chemical modification, corn starches were treated with STMP/STPP. Total RS (TRS) and total dietary fiber (TDF) levels of chemically‐modified NCS were 26.4 and 44.0%, respectively, while TRS and TDF levels in chemically‐modified HACS were 78.1 and 78.5%, respectively. Onset gelatinization temperatures of both modified corn starches clearly shifted to higher temperatures after STMP/STPP treatment. At the end of the diet trial, the mice on the HACS diet decreased body weight gain compared to the NCS‐fed mice. Adding NCS‐ and HACS‐RS4 to the diet significantly reduced the weight gain relative to NCS and HACS groups. Both RS4 diets were effective in improving the lipid profile compared to their respective controls. They significantly reduced the level of total lipid and total cholesterol.     

Vitamin D3 regulation of body fat,cytokines, and calpain gene expression

BACKGROUND: We conducted an in vivo experiment to determine whether vitamin D₃ acts as a fat synthesizer and/or meat tenderizer in mice. At 6 weeks of age, 20 male C57BL/6 wild‐type mice were randomly divided into two groups (10 mice per group) and fed a modified AIN93G diet with (vitamin D₃ diet) or without (basal diet) 10 IU 25‐OH‐cholecalciferol kg^?3 for 3 weeks. RESULTS: When vitamin D₃ was fed to mice for 3 weeks, body fat was significantly increased compared to mice fed a basal diet. There was, however, no difference in body weight between the two groups. Vitamin D₃ increased the gene expressions of pro‐inflammatory cytokines and peroxisome proliferator‐activated receptor gamma, but decreased interleukin‐15 in adipose tissue through nuclear vitamin D receptor and uncoupling protein‐2 signals. The muscle inducible nitrate oxide synthase content of mice fed vitamin D₃ was higher than those fed a basal diet, while muscle arginase l showed a reverse phenomenon. longissimuss dorsi muscle of vitamin D₃‐fed mice showed more severe fat deposition than those fed a basal diet. Vitamin D₃ amplified muscle u‐ and m‐calpain protein content and suppressed muscle calpastatin protein content. CONCLUSION: These findings suggest that vitamin D₃ can be used as a fat synthesizer and meat tenderizer in meat‐producing animals. Copyright © 2011 Society of Chemical Industry     

Long-term high animal protein diet reduces body weight gain and insulin secretion in diet-induced obese rats

BACKGROUND: The effects of a high protein diet on insulin secretion and glucose metabolism have been quite controversial. The aim of this study was to evaluate the effects of long‐term isocaloric high animal protein intake on insulin secretion in diet‐induced obese rats. RESULTS: After the experimental period (24 weeks), the high‐fat diet‐induced obese rats that were fed isocaloric high‐protein diets (HP) had lower body weight gain (P < 0.01) and lower visceral fat (P < 0.05) than normal protein (NP) rats. Fasting plasma glucagon‐like peptide‐1 (GLP‐1) was also reduced significantly (P < 0.05), as well as serum insulin levels at 5 min and 10 min by intravenous insulin releasing test. In addition, insulin mRNA and pancreatic duodenal homeodomain‐1 (PDX‐1), GLP‐1 protein expression were both markedly lower in HP rats (P < 0.05), while PDX‐1 mRNA in HP rats had no difference from NP rats. CONCLUSION: These results suggest that long‐term isocaloric high animal protein intake reduces the acute insulin response in obese rats and the decrease of insulin is associated with both reduced weight gain and inhibition of PDX‐1 expression. GLP‐1 might be a negative feedback for the balance of energy metabolism secondary to changes of body weight and visceral fat. Copyright © 2012 Society of Chemical Industry     

RS4型抗性淀粉对高脂诱导肥胖小鼠脂质代谢相关基因表达的影响

目的：观察不同RS4型抗性淀粉对小鼠脂质代谢及相关基因表达的影响,探讨抗性淀粉干预脂质代谢的机制。方法：选用年龄和体质量合适的雄性C57BL/6J小鼠,分别饲喂含有羟丙基交联、交联酯化、柠檬酸乙酰化甘薯淀粉3 种RS4型抗性淀粉和甘薯原淀粉的高脂饲料12 周。12 周后,测定小鼠血清指标、体质量及观察小鼠肝脏组织形态变化;并采用实时荧光定量聚合酶链式反应技术检测各组小鼠肝组织中脂肪酸合成酶（fatty acid synthese,FAS）、固醇调节元件结合蛋白-1c（sterol regulatory element binding protein-1c,SREBP-1c）、3-羟基-3-甲基戊二酰辅酶A还原酶（3-hydroxy-3-methylglutary coenzyme a reductase,HMGCR）的mRNA表达水平。结果：饲喂添加3 种RS4型抗性淀粉的高脂饲料后,高脂诱导雄性C57BL/6J肥胖小鼠体质量、血清甘油三酯水平明显降低,肝细胞脂肪变性程度明显减轻、肝脏组织中SREBP-1c mRNA表达水平明显下调;添加柠檬酸乙酰化甘薯淀粉对FAS、SREBP-1c、HMGCR 的mRNA表达水平均有不同程度的下调。结论：柠檬酸乙酰化甘薯淀粉等RS4型抗性淀粉可对高脂诱导雄性C57BL/6J肥胖小鼠的脂质代谢起到一定的干预作用,并可下调其肝脏组织中SREBP-1c mRNA等基因的表达。     

Possible abilities of dietary factors to prevent and treat diabetes via the stimulation of glucagon‐like peptide‐1 secretion

There is a pressing need for countermeasures against diabetes, which has increased in incidence, becoming a global issue. Glucagon‐like peptide‐1 (GLP‐1), a molecule secreted in enteroendocrine L cells in the lower small and large intestines, is thought to be one of the most important molecular targets for the prevention and treatment of diabetes. There has been increasing interest in the possible ability of dietary factors to treat diabetes via modulating GLP‐1 secretion. There is thought to be a close relationship between incretin and diet, and the purported best approach for using dietary factors to increase GLP‐1 activity is promotion of secretion of endogenous GLP‐1. It have been reported that nutrients as well as various non‐nutrient dietary factors can function as GLP‐1 secretogogues. Here, we present our findings on the GLP‐1 secretion‐stimulating functions of two dietary factors, curcumin and extract of edible sweet potato leaves, which contain caffeoylquinic acid derivatives. However, it is necessary to reveal in greater detail the stimulation of GLP‐1 secretion by dietary factors for preventing and treating diabetes. It is desirable to clarify the exact GLP‐1 secretory pathway, the effect of metabolites derived from dietary factors in gut lumen, and the relationship between incretin and meal.     

Fat digestion and absorption in spice‐pretreated rats

BACKGROUND: A few common spices are known to stimulate secretion of bile with higher amount of bile acids which play a major role in digestion and absorption of dietary lipids. It would be appropriate to verify if these spices enable efficient digestion and absorption during high‐fat intake. In this context, dietary ginger (0.05%), piperine (0.02%), capsaicin (0.015%), and curcumin (0.5%) were examined for their influence on bile secretion, digestive enzymes of pancreas and absorption of dietary fat in high‐fat (30%) fed Wistar rats for 8 weeks. RESULTS: These spices enhanced the activity of pancreatic lipase, amylase, trypsin and chymotrypsin by 22‐57%, 32‐51%, 63‐81% and 12‐38%, respectively. Dietary intake of spices along with high‐fat enhanced fat absorption. These dietary spices increased bile secretion with higher bile acid content. Stimulation of lipid mobilisation from adipose tissue was suggested by the decrease in perirenal adipose tissue weight by dietary capsaicin and piperine. This was also accompanied by prevention of the accumulation of triglyceride in liver and serum in high‐fat fed rats. Activities of key lipogenic enzymes in liver were reduced which was accompanied by an increased activity of hormone‐sensitive lipase. CONCLUSION: Thus, dietary ginger and other spice compounds enhance fat digestion and absorption in high‐fat fed situation through enhanced secretion of bile salts and a stimulation of the activity pancreatic lipase. At the same time, the energy expenditure is facilitated by these spices to prevent the accumulation of absorbed fat. Copyright © 2011 Society of Chemical Industry     

Body composition and hormonal effects following exposure to mycotoxin deoxynivalenol in the high-fat diet-induced obese mouse

Scope: To characterize the effects of ingesting the common foodborne mycotoxin deoxynivalenol (DON) on body weight and composition in the high‐fat (HF) diet‐induced obese mice, a model of human obesity. Methods and results: Female B6C3F1 mice were initially fed HF diets containing 45% kcal (HF45) or 60% kcal (HF60) as fat for 94 days to induce obesity. Half of each group was either continued on unamended HF diets or fed HF diets containing 10 mg/kg DON (DON‐HF45 or DON‐HF60) for another 54 days. Additional control mice were fed a low‐fat (LF) diet containing 10% kcal as fat for the entire 148‐day period. DON induced rapid decreases in body weights and fat mass, which stabilized to those of the LF control within 11 days. These effects corresponded closely to a robust transient decrease in food consumption. While lean body mass did not decline in DON‐fed groups, further increases were suppressed. DON exposure reduced plasma insulin, leptin, insulin‐like growth factor 1, and insulin‐like growth factor acid labile subunit as well as increased hypothalamic mRNA level of the orexigenic agouti‐related protein. Conclusion: DON‐mediated effects on body weight, fat mass, food intake, and hormonal levels in obese mice were consistent with a state of chronic energy restriction.     

Lemon balm extract causes potent antihyperglycemic and antihyperlipidemic effects in insulin‐resistant obese mice

Over the last decades polyetiological metabolic diseases such as obesity and type 2 diabetes have emerged as a global epidemic. Efficient strategies for prevention and treatment include dietary intervention and the development of validated nutraceuticals. Safe extracts of edible plants provide a resource of structurally diverse molecules that can effectively interfere with multifactorial diseases. In this study, we describe the application of ethanolic lemon balm (Melissa officinalis) leaves extract for the treatment of insulin‐resistance and dyslipidemia in mice. We show that lemon balm extract (LBE) activates the peroxisome proliferator‐activated receptors (PPARs), which have key roles in the regulation of whole body glucose and lipid metabolism. Application of LBE (0.6 mg/mL) to human primary adipocytes resulted in specific peroxisome proliferator‐activated receptor target gene expression. LBE treatment of insulin‐resistant high‐fat diet‐fed C57BL/6 mice (200 mg/kg/day) for 6 weeks considerably reduced hyperglycemia and insulin resistance, plasma triacylglycerol, nonesterified fatty acids and LDL/VLDL cholesterol levels. Taken together, ethanolic lemon balm extract can potentially be used to prevent or concomitantly treat type 2 diabetes and associated disorders such as dyslipidemia and hypercholesterolemia.     

Addition of sucralose enhances the release of satiety hormones in combination with pea protein

Scope Exposing the intestine to proteins or tastants, particularly sweet, affects satiety hormone release. There are indications that each sweetener has different effects on this release, and that combining sweeteners with other nutrients might exert synergistic effects on hormone release. Methods and results STC‐1 cells were incubated with acesulfame‐K, aspartame, saccharine, sucralose, sucrose, pea, and pea with each sweetener. After a 2‐h incubation period, cholecystokinin(CCK) and glucagon‐like peptide 1 (GLP‐1) concentrations were measured. Using Ussing chamber technology, the mucosal side of human duodenal biopsies was exposed to sucrose, sucralose, pea, and pea with each sweetener. CCK and GLP‐1 levels were measured in basolateral secretions. In STC‐1 cells, exposure to aspartame, sucralose, sucrose, pea, and pea with sucralose increased CCK levels, whereas GLP‐1 levels increased after addition of all test products. Addition of sucrose and sucralose to human duodenal biopsies did not affect CCK and GLP‐1 release; addition of pea stimulated CCK and GLP‐1 secretion. Conclusion Combining pea with sucrose and sucralose induced even higher levels of CCK and GLP‐1. Synchronous addition of pea and sucralose to enteroendocrine cells induced higher levels of CCK and GLP‐1 than addition of each compound alone. This study shows that combinations of dietary compounds synergize to enhance satiety hormone release.     

Voluntary exercise and green tea enhance the expression of genes related to energy utilization and attenuate metabolic syndrome in high fat fed mice

Obesity and metabolic syndrome are growing public health problems. We investigated the effects of decaffeinated green tea extract (GTE) and voluntary running exercise (Ex) alone or in combination against obesity and metabolic syndrome in high fat (HF) fed C57BL/6J mice. After 16 wk, GTE + Ex treatment reduced final body mass (27.1% decrease) and total visceral fat mass (36.6% decrease) compared to HF‐fed mice. GTE + Ex reduced fasting blood glucose (17% decrease), plasma insulin (65% decrease), and insulin resistance (65% decrease) compared to HF‐fed mice. GTE or Ex alone had less significant effects. In the skeletal muscle, the combination of Ex and GTE increased the expression of peroxisome proliferator‐activated receptor‐γ coactivator‐1α (Ppargc1a), mitochondrial NADH dehydrogenase 5 (mt‐Nd5), mitochondrial cytochrome b (mt‐Cytb), and mitochondrial cytochrome c oxidase III (mt‐Co3). An increase in hepatic expression of peroxisome proliferator‐activated receptor‐α (Ppara) and liver carnitine palmitoyl transferase‐1α (Cpt1a) and a decrease in hepatic expression of stearoyl‐CoA desaturase 1 (Scd1) mRNA was observed in GTE + Ex mice. GTE + Ex was more effective than either treatment alone in reducing diet‐induced obesity. These effects are due in part to modulation of genes related to energy metabolism and de novo lipogenesis.     

Protective Effect of Dietary Ghrelin‐Containing Salmon Stomach Extract on Mortality and Cardiotoxicity in Doxorubicin‐Induced Mouse Model of Heart Failure

Ghrelin exhibits a cardioprotective effect. We examined whether orally administered ghrelin‐containing salmon stomach extract (sSE) instead of chemically synthesized ghrelin protects against doxorubicin (DOX)‐induced cardiotoxicity in mice. Mice were divided into four groups: (i) the control, (ii) DOX groups were fed a control diet (AIN‐93G), (iii) the sSE, and (iv) DOX + sSE groups were fed a 10% sSE diet (AIN‐93G + 10% sSE). After a 4‐week pretreatment of sSE, DOX or saline was administered to the corresponding groups by intraperitoneal injection. The groups fed the 10% sSE diet consumed significantly more food than the groups fed the control diet before the DOX injection. No mortality was observed in the DOX + sSE group, whereas 40% (2 of 5) mortality was observed in the DOX group. Compared with the DOX group, levels of ascites and plasma cardiac troponin I improved in the DOX + sSE group. Significantly lesser DOX‐induced collagen accumulation was observed in the left heart ventricle of the DOX group than in that of the DOX + sSE group. These results suggest that the dietary ghrelin contained in sSE mimics synthetic ghrelin in cardioprotective effect. Ghrelin in sSE (45 pmol/g) and the food intake‐stimulating effect of sSE may explain, at least in part, the protective effect of orally administered teleost ghrelin.     

味觉感知的人体肠-脑轴信号传导机制研究进展

味觉是人类感知生物摄取能的重要环节,胃肠道亦存在味觉感知现象。本文从胃肠道味觉受体、胃肠道味觉感知通路及肠-脑轴味觉信号传导机制等方面进行了分析,胃肠道中味觉感知表明胃肠道中存在味觉受体第一家族亚型（taste receptor type 1 member,T1R）1、T1R2、T1R3、味觉受体第二家族亚型（taste receptors type 2,T2Rs）等味觉受体,且肠道味觉物质刺激肠内分泌细胞分泌胆囊收缩素（cholecystokinin,CCK）、肽YY（peptide YY,PYY）等脑肠肽激素,与味觉信号在神经元的传递有关;肠道中鲜味物质谷氨酸钠显著激活大脑缰核、杏仁核和下丘脑亚核的神经网络,表明肠-脑轴味觉感知是基于胃肠道受体及脑肠肽、神经元和大脑中枢神经系统之间的共同调控,从而提出肠-脑轴味觉信号传导机制假说,认为甜味受体T1R2/T1R3和鲜味受体T1R1/T1R3具有相似的信号传导通路,味觉物质作用于肠道后,与肠道中相应的味觉受体结合,激活磷脂酶-β2（phospholipase C-β2,PLC-β2）,释放Ca2＋,引起肠道内环境的变化,刺激肠内分泌细胞分泌PYY、CCK等激素,被肠神经元突触特异性识别,将味觉信号传导至大脑神经中枢;而谷氨酸代谢型受体4（metabotropic glutamate receptor 4,mGluR4）和苦味受体T2Rs信号传导通路则是通过激活磷酸二酯酶（phosphodiesterase,PDE）,使细胞质内3’,5’-环腺苷酸（3’,5’-cyclic adenylic acid,cAMP）浓度降低,从而解除环核苷酸（cyclic nucleotide,cNMP）的抑制作用,从而释放Ca2＋。基于肠-脑轴味觉偏好,为味觉发生改变的患者开发治疗新药物、寻找新的药物靶点提供了新的方向。对肠-脑轴味觉信号传导机制的研究将为胃肠道生理的神经控制提供分子框架、精准控制人体对味觉营养物质的生理反应,并对味觉物质在肠-脑轴中的摄入、代谢、调节等及开发新的味觉感知途径提供新的理论依据。     

Conjugated linoleic acid (CLA) prevents body fat accumulation and weight gain in an animal model

ABSTRACT:  Conjugated linoleic acid (CLA) has been shown to reduce body fat and increase lean body mass in mice, rats, and pigs. A recent human trial indicated that CLA may work more effectively if used for prevention of body fat deposition and weight gain. To test this hypothesis, we conducted 2 experiments using relatively old mice (older than 6 mo): experiment 1, supplementation of CLA during dietary restriction and experiment 2, supplementation during ad libitum feeding followed by restriction. In experiment 1, there were significant effects of diet restriction and CLA supplementation on body composition, while CLA decreased body fat content in ad libitum diet but not significantly during diet restriction. In experiment 2, CLA fed animals had body weights similar to restricted animals and CLA significantly reduced body fat (significantly lower than prior to and post restriction, or pair fed). This suggests that CLA exerted modulation of body fat independent of reduced food intake. Based on these results, we concluded that CLA may be more effective at protecting against fat mass regain following weight loss than as a weight loss treatment.     

Purified berry anthocyanins but not whole berries normalize lipid parameters in mice fed an obesogenic high fat diet

Male C57BL/6 mice received diets with either 10% of kcal from fat, or a high fat diet [45% (HF45) or 60% (HF60) kcal from fat]. Diets were prepared with or without freeze‐dried powders (10%) from whole blueberries (BB), strawberries (SB), Concord grape or black raspberry. In the 2nd study, purified anthocyanins (ACNs) from SB or BB were added to the drinking water of the treatments fed the HF60 diet. In Study 1, serum triglycerides were increased by feeding the HF45 diet but were elevated further when black raspberry or BB was included in the HF45 diet. Liver total lipids and triglycerides were increased in mice fed HF45 diet and inclusion of any of the berry powders in the HF45 diet did not alter concentrations compared to HF45 controls. In the 2nd study, mice fed the HF60 diet plus purified ACNs from BB in the water had lower body weight gains and body fat than the HF60 fed. Serum cholesterol and triglyceride levels were elevated with the HF60 diet and decreased to control levels when ACNs from either SB or BB were included in the drinking water. Serum leptin levels were consistently decreased to control low fat levels in those ACN treatments in which measures of body fat were decreased. Administering purified ACNs from BB and strawberry via drinking water prevented the development of dyslipidemia and obesity in mice, but feeding diets containing whole berries or purple corn (PC) ACNs did not alter the development of obesity.