一株植物乳杆菌体内降胆固醇的作用机制

目的:通过构建高胆固醇血症模型小鼠评价该菌株对小鼠体内胆固醇代谢及相关基因表达的影响。方法:以健康C57BL/6雄性小鼠为对象,设置空白组、模型组、低剂量组、高剂量组、普伐他汀对照组,分别以生理盐水、KLDS1.0386悬浊液和普伐他汀连续灌胃4周,检测小鼠血清胆固醇、甘油三酯、低密度脂蛋白和高密度脂蛋白水平;采用Western blotting法检测小鼠肝脏胆固醇几个关键基因(HMGCR,LDLR,SREBP2,CYP7A1,FXR)表达水平的变化。结果:灌胃KLDS1.0386后,高剂量组小鼠血清甘油三酯、总胆固醇和低密度脂蛋白水平明显降低(P<0.05);HMGCR和FXR的表达明显受到抑制(P<0.05),CYP7A1的表达量增加(P<0.05)。结论:获得一株在体内具有高效降胆固醇能力的植物乳杆菌KLDS1.0386,该菌可用作降胆固醇的益生菌。     

刺梨果酒改善2型糖尿病大鼠糖脂代谢紊乱的研究

为探究刺梨果酒对2型糖尿病大鼠糖脂代谢紊乱的影响及可能机制。采用高脂高糖膳食联合腹腔注射链佐霉素（Streptozocin,STZ）建立2型糖尿病大鼠模型,将造模成功的大鼠分为刺梨果酒高（8 mL/kg）、中（4 mL/kg）、低（2 mL/kg）剂量组和模型组,并设空白对照组,给药期间每2周测一次空腹血糖,实验时间28 d。实验结束后测量血清和肝脏中高密度脂蛋白胆固醇（High-density lipoprotein cholesterol,HDL-C）、果糖胺（fructosamine,FMN）、甘油三酯（Triglyceride,TG）、低密度脂蛋白胆固醇（Low-density lipoprotein cholesterol,LDL-C）、总胆固醇（Total cholesterol,TC）、肝糖原等含量;采用实时灾光定量PCR（real time polymerase chain reaction,RT-PCR）测定肝脏中腺苷酸活化蛋白激酶（AMP-activated protein kinase α,AMPK）、乙酰辅酶A羧化酶（Acetyl-CoA carboxylases alpha,ACACA）、β-羟-β-甲戊二酸单酰辅酶A还原酶（3-hydroxy-3-methylglutaryl coenzyme A reductase,HMG-CoA）、脂肪酸合成酶（fatty acid synthetase,FASN）、和葡萄糖转运载体2（Glucose Transporter 2,GLUT2）、胆固醇7α-羟化酶（Cholesterol 7α-hydroxylase,CYP7A1）等mRNA相对表达量。结果表明,与模型组相比,刺梨果酒可减缓2型糖尿病大鼠体重减轻和多饮、多食的症状;高、中剂量刺梨果酒降低实验大鼠空腹血糖和果糖胺的效果显著（P<0.05）;各剂量组均有降低实验大鼠血清和肝脏TC、TG、LDL-C的含量和升高HDL-C含量的作用,其中高、中剂量效果显著（P<0.05）;低、中、高刺梨果酒均可显著（P<0.05）上调AMPK、GLUT2和ACACA mRNA表达量,低、中、高刺梨果酒均可上调FASN mRNA表达量,其中高、中剂量组上调FASN mRNA表达量显著（P<0.05）;中、高剂量刺梨果酒可显著（P<0.05）下调G6Pase、PEPCK、HMG-COA和CYP7A1 mRNA表达量。结论:刺梨果酒改善2型糖尿病大鼠糖脂代谢紊乱的机制可能与通过抑制内源性胆固醇、增加脂肪的从头合成及提高葡萄糖跨膜转速率有关。     

p-辛弗林通过激活AMPK-FoxO1信号通路抑制肝细胞葡萄糖生成

目的：探讨p-辛弗林对肝细胞葡萄糖生成的影响及其作用机制。方法：采用MTS法检测p-辛弗林对HepG2肝细胞株的细胞活力的影响,确定受试物的作用浓度后,比色法测定葡萄糖的生成、葡萄糖-6-磷酸酶（glucose-6-phosphatase,G6Pase）和磷酸烯醇丙酮酸羧基激酶（phosphoenolpyruvate carboxykinase,PEPCK）活力,Western blot蛋白印迹法检测腺苷酸活化蛋白激酶（adenosine 5’-monophosphate-activated protein kinase,AMPK）、磷酸化AMPK（p-AMPK）、乙酰辅酶A羧化酶（acetyl coenzyme A synthetase,ACC）、磷酸化ACC（p-ACC）、叉头框转录因子1（forkhead box class O1,FoxO1）以及磷酸化FoxO1（p-FoxO1）的表达;利用AMPK选择性抑制剂Compound C和AMPK siRNA作用HepG2肝细胞株后,检测p-辛弗林对HepG2肝细胞株葡萄糖的生成、G6Pase和PEPCK活力的影响。结果：p-辛弗林能剂量依赖性地抑制肝细胞葡萄糖的生成,激活AMPK信号通路,促进p-AMPK、p-ACC和p-FoxO1水平增加,极显著抑制G6Pase和PEPCK的活性（P＜0.01）。p-辛弗林的这些影响部分地被Compound C和AMPK siRNA所抑制（P＜0.01）。结论：p-辛弗林能够通过激活AMPK-FoxO1信号通路抑制肝细胞葡萄糖生成。     

Effects of buckwheat sprouts on plasma and hepatic parameters in type 2 diabetic db/db mice

We examined the effects of buckwheat sprouts (BS) (Fagopyrum esculentum Moench) on lipid and carbohydrate metabolism and on in vivo oxidative stress in type 2 diabetic mice. Mice (C57BL/KsJ-lepr(db)/lepr(db), db/db) were fed a diet containing 0%, 5%, or 10% BS based on AIN-93G for 21 d. Plasma parameters, such as total cholesterol, arteriosclerotic index, thiobarbituric acid reactive substances (TBARS), and the HbA1c concentration of whole blood in the diabetic BS-fed groups were lower than those in the diabetic control (AIN-93G) group. Concentrations of hepatic parameters, such as lipids, total cholesterol, triglyceride, and TBARS levels in BS-fed groups, were lower than those in the diabetic control group. Although gene expressions of the hepatic lipid regulation enzymes such as 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoAR) and cholesterol 7α-hydroxylase (CYP7A1) in diabetic BS-fed groups were higher than in the diabetic control group, the elevation of mRNA level of CYP7A1 was greater than that of HMG-CoAR. In addition, concentration of bile acids in feces was higher in the diabetic BS-fed groups than in the diabetic control group. These results suggest that BS have various in vivo activities in relation to antidiabetic effects in type 2 diabetic mice, especially for improvement in lipid metabolism. It was deduced that excretion of bile acids in feces by feeding the BS diet would contribute to the suppression of the cholesterol concentration in the plasma and liver tissues of mice.     

Piperine reverses high fat diet-induced hepatic steatosis and insulin resistance in mice

This study examined the effect of piperine on hepatic steatosis and insulin resistance induced in mice by feeding a high-fat diet (HFD) for 13 weeks and elucidated potential underlying molecular mechanisms. Administration of piperine (50 mg/kg body weight) to mice with HFD-induced hepatic steatosis resulted in a significant increase in plasma adiponectin levels. Also, elevated plasma concentrations of insulin and glucose and hepatic lipid levels induced by feeding a HFD were reversed in mice when they were administered piperine. However, piperine did not reduce body weight and other biochemical markers to an extent where they became equal to the levels found in the CD-fed mice. Piperine reversed HFD-induced down-regulation of adiponecitn-AMP-activated protein kinase (AMPK) signalling molecules which play an important role in mediating lipogenesis, fatty acid oxidation and insulin signalling in the livers of mice. The expressions of lipogenic target genes were decreased, whereas the expression of carnitine palmitoyltransferase 1 (CPT1) gene involved in fatty acid oxidation was increased in the livers of the Pin50 group. Piperine significantly decreased the phosphorylation of insulin receptor substrate-1 (IRS-1) compared with the HFD-fed mice. Administration of piperine appeared to reverse preexisting HFD-induced hepatic steatosis and insulin resistance, probably by activation of adiponectin-AMPK signalling in mice.     

Mulberry extract inhibits oleic acid-induced lipid accumulation via reduction of lipogenesis and promotion of hepatic lipid clearance

BACKGROUND: Mulberries are a traditional edible food used to treat hepatic disease. The anti‐obesity and hypolipidemic effects of mulberry water extracts (MWE) have attracted increasing interest. In the present study, MWE were assessed for their hepatic lipid‐lowering potential when administered in fatty acid overload conditions in HepG2 cells. RESULTS: We found that MWE significantly reduced lipid accumulation, suppressed fatty acid synthesis, and stimulated fatty acid oxidation. Furthermore, MWE also inhibited acetyl coenzyme A carboxylase activities by stimulating adenosine monophosphate‐activated protein kinase (AMPK). MWE attenuated the expression of sterol regulatory element‐binding protein‐1 (SREBP‐1) and its target molecules, such as fatty acid synthase. Similar results were also measured in the expressions of enzymes involved in triglyceride and cholesterol biosyntheses including glycerol‐3‐phosphate acyltransferase, 3‐hydroxy‐3‐methylglutaryl‐CoA reductase, and SREBP‐2. In contrast, the lipolytic enzyme expression of peroxisome proliferator activated receptor α and carnitine palmitoyltransferase‐1 were increased. CONCLUSIONS: Our study suggests that the hypolipidemic effects of MWE occur via phosphorylation of AMPK and inhibition of lipid biosynthesis. Therefore, the mulberry extract may be active in the prevention of fatty liver. Copyright © 2011 Society of Chemical Industry     

Effect of curcumin supplementation on blood glucose, plasma insulin, and glucose homeostasis related enzyme activities in diabetic db/db mice

We investigated the effect of curcumin on insulin resistance and glucose homeostasis in male C57BL/KsJ-db/db mice and their age-matched lean non-diabetic db/+ mice. Both db/+ and db/db mice were fed with or without curcumin (0.02%, wt/wt) for 6 wks. Curcumin significantly lowered blood glucose and HbA 1c levels, and it suppressed body weight loss in db/db mice. Curcumin improved homeostasis model assessment of insulin resistance and glucose tolerance, and elevated the plasma insulin level in db/db mice. Hepatic glucokinase activity was significantly higher in the curcumin-supplemented db/db group than in the db/db group, whereas glucose-6-phosphatase and phosphoenolpyruvate carboxykinase activities were significantly lower. In db/db mice, curcumin significantly lowered the hepatic activities of fatty acid synthase, beta-oxidation, 3-hydroxy-3-methylglutaryl coenzyme reductase, and acyl-CoA: cholesterol acyltransferase. Curcumin significantly lowered plasma free fatty acid, cholesterol, and triglyceride concentrations and increased the hepatic glycogen and skeletal muscle lipoprotein lipase in db/db mice. Curcumin normalized erythrocyte and hepatic antioxidant enzyme activities (superoxide dismutase, catalase, gluthathione peroxidase) in db/db mice that resulted in a significant reduction in lipid peroxidation. However, curcumin showed no effect on the blood glucose, plasma insulin, and glucose regulating enzyme activities in db/+ mice. These results suggest that curcumin seemed to be a potential glucose-lowering agent and antioxidant in type 2 diabetic db/db mice, but had no affect in non-diabetic db/+ mice.     

Red yeast barley reduces plasma glucose levels and activates AMPK phosphorylation in <Emphasis Type="Italic">db/db</Emphasis> mice

Red yeast (Monascus purpureus) fermented over rice has a limited hypoglycemic activity. To enhance its glucose-lowering effect, we fermented red yeast over waxy barley, a hypoglycemic grain with high levels of fibers and β-glucans, and investigated the metabolic effects of red yeast barley (RYB) in high-fat-fed hyperglycemic db/db mice for 6 weeks. The fasting glucose levels were significantly reduced in the RYB group at 6 weeks by 25% (p<0.05), as was the glucose tolerance (−27% of area under the curve in RYB vs. controls, p<0.05). Plasma insulin levels and the expression of PPAR-γ were unaltered, however, the phosphorylation activation of hepatic AMP-activated protein kinase (AMPK) was increased significantly in RYB group compared with controls suggesting that hypoglycemic effect of RYB may be achieved by AMPK-dependent mechanism. RYB may be used as a hypoglycemic functional food modulating cellular AMPK activity.     

刺梨果酒对高脂诱导肥胖小鼠脂代谢的影响

目的:研究刺梨果酒对高脂诱导小鼠肥胖发生过程预防效果及其机理.方法:将50只小鼠随机分为空白组、模型组、刺梨果酒低剂量组(0.25 mL/80 g)、中剂量组(0.5 mL/80 g)和高剂量组(1 mL/80 g),每组10只,实验时间8周.实验结束后,测定小鼠脏器指数、血清及肝脏脂代谢相关生理生化指标;应用qRT-...     

Korean red ginseng attenuates hepatic lipid accumulation via AMPK activation in human hepatoma cells

In this study, we examined Korean red ginseng (KRG) extract affects on the lipid metabolism in HepG2 cells. Increase in AMP-activated protein kinase (AMPK) phosphorylation was observed when the cells were treated with KRG. Activation of AMPK was also demonstrated by measuring the phosphorylation of acetyl-CoA caboxylase (ACC), a substrate of AMPK. KRG down-regulated gene expressions of sterol regulatory element binding protein 1c (SREBP1c) and its target proteins, such as fatty acid synthase (FAS) and stearoyl-CoA desaturase (SCD1) in time- and dose-dependent fashions. In contrast, gene expressions of peroxisome proliferator-activated receptor α (PPARα) and CD36 were increased. These effects were reversed in the presence of compound C, an AMPK inhibitor. However, there were no differences in gene expressions of SREBP2, 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, and low-density-lipoprotein receptor (LDLR). Taken together, KRG induced supression of SREBP1c and activation of PPARα via AMPK and these effects seem to be one of anti-hyperlipidemic mechanism of KRG in HepG2 cells.     

牦牛酥油鞘磷脂对小鼠脂质代谢紊乱和肝脏组织炎症的调节作用

研究牦牛酥油鞘磷脂对高脂饮食小鼠脂质代谢紊乱和肝脏组织炎症的调节作用.选取30只C57BL/6J雄性小鼠随机分为5组,分别为低脂组、高脂组、鞘磷脂高剂量组(鞘磷脂添加量为1.20g/100g)、鞘磷脂中剂量组(鞘磷脂添加量为0.60g/100g)和鞘磷脂低剂量组(鞘磷脂添加量为0.30g/100g).采用酶联免疫和荧光...     

Xanthigen attenuates high-fat diet-induced obesity through down-regulation of PPARγ and activation of the AMPK pathway

Xanthigen, a mixture of brown seaweed and pomegranate seed extracts, has weight loss properties and lipid-lowering effects in mice and humans. This study elucidated the Xanthigen mechanism of an anti-obesity activity in high-fat diet (HFD)-fed mice. Xanthigen decreased expression of peroxisome proliferator-activated receptor γ (PPARγ) in the adipose tissue of HFD-fed mice. The serum leptin level and the adipose tissue leptin expression in mice fed HFD plus Xanthigen were significantly decreased, compared to HFD-fed mice. Phosphorylation of AMPactivated protein kinase (AMPK) α and β and acetyl-CoA carboxylase (ACC) in the adipose tissue of HFD plus Xanthigen-fed mice was elevated, and HMG-CoA reductase (HMGCR) expression was decreased. Xanthigen may have an anti-obesity activity by down-regulation of PPARγ and activation of the AMPK pathway.     

Antiobese and hypocholesterolaemic effects of an Adenophora triphylla extract in HepG2 cells and high fat diet-induced obese mice

The ethyl acetate extract from Adenophora triphylla root (ATea) had strong antioxidant effect. We hypothesised that a high fat (HF) diet might induce oxidative stress and so, dietary antioxidant may have beneficial effects on hypercholesterolaemia, but the underlying mechanisms involved are not fully understood. To test this hypothesis, C57BL/6 mice were fed with HF diet for 9 weeks. In the last 4 weeks, the HF diet was supplemented with 0, 25 or 75 mg/kg ATea. ATea decreased body weight gain and both ATea doses significantly reduced the plasma and hepatic cholesterol levels of the obese mice. Analysis of the hepatic expression of proteins known to play important roles in cholesterol metabolism indicated that ATea significantly enhanced low density lipoprotein receptor (LDL receptor) and cholesterol 7α-hydroxylase (CYP7A1) expression but inhibited the 3-hydroxy-3-methylglutaryl–CoA reductase (HMG–CoA reductase) expression in HepG2 cells and mice. No mutagenic activity was observed at high doses of ATea.     

Consumption of barley β‐glucan ameliorates fatty liver and insulin resistance in mice fed a high‐fat diet

Consumption of a diet high in barley β‐glucan (BG) has been shown to prevent insulin resistance. To investigate the mechanism for the effects of barley BG, three groups of male 7‐wk‐old C57BL/6J mice were fed high‐fat diets containing 0, 2, or 4% of barley BG for 12 wk. The 2% BG and 4% BG groups had significantly lower body weights compared with the 0% BG group. The 4% BG group demonstrated improved glucose tolerance and lower levels of insulin‐resistance index and glucose‐dependent insulinotropic polypeptide. Consumption of the BG diet decreased hepatic lipid content. Mice on the BG diet also demonstrated decreased fatty acid synthase and increased cholesterol 7α‐hydroxylase gene expression levels. The BG diet promoted hepatic insulin signaling by decreasing serine phosphorylation of insulin receptor substrate 1 and activating Akt, and it decreased mRNA levels of glucose‐6‐phosphatase and phosphoenolpyruvate carboxykinase. In summary, consumption of BG reduced weight gain, decreased hepatic lipid accumulation, and improved insulin sensitivity in mice fed a high‐fat diet. Insulin signaling enhanced due to the expression changes of glucose and lipid metabolism genes by BG consumption. Consumption of barley BG could be an effective strategy for preventing obesity, insulin resistance, and the metabolic syndrome.     

Metabolic response of soy pinitol on lipid‐lowering,antioxidant and hepatoprotective action in hamsters fed‐high fat and high cholesterol diet

This study was performed to investigate the lipid‐lowering, antioxidant, and hepato‐protective effects of pinitol in dose‐dependent manners in hamsters fed‐high fat and high cholesterol (HFHC) diet. Pinitol supplementation (0.05%, P‐I and 0.1% pinitol, P‐II) with an HFHC diet (10% coconut oil plus 0.2% cholesterol) for 10 wks significantly lowered the white adipose tissue weights, hepatic lipid droplets, plasma glucose, total‐cholesterol, nonHDL‐cholesterol, total‐cholesterol/HDL‐cholesterol ratio, and hepatic lipid levels. Whereas it significantly increased the brown adipose tissue weight, plasma HDL‐cholesterol, apolipoprotein A‐I (apo A‐I) concentrations, paraoxonase (PON) activity, and/or mRNA expression, compared to the HFHC control group. Plasma insulin and adiponectin levels were significantly lower and higher, respectively, in both P‐I and P‐II groups than the HFHC control group. Dietary pinitol significantly inhibited hepatic HMG‐CoA reductase, acyl‐CoA:cholesterol acyltransferase (ACAT), and cytochrome P4502E1 (CYP2E1) activities without altering their mRNA expressions compared to the control group. Pinitol significantly elevated the hepatic antioxidant enzyme activities, whereas it also significantly reduced the hepatic lipid peroxide and H₂O₂ production. Accordingly, these results indicate that both 0.05 and 0.1% pinitol supplementation may improve the lipid and antioxidant metabolism in HFHC diet‐fed hamsters. In particular, pinitol supplementation was very effective on the elevation of antiatherogenic factors, including plasma HDL‐cholesterol, apo A‐I, adiponectin, and PON.     

平卧菊三七对小鼠血糖及血脂的影响

高血糖和高血脂已严重威胁人类健康,本研究探讨平卧菊三七（GPM）对小鼠血糖和血脂的影响,并通过分子生物学手段阐明其作用机制。将40只昆明小鼠随机分成4组,即对照组、2%、4%和8% GPM,喂养小鼠12周,称量小鼠体重和脏器,测定血中的生化指标和肝脏及粪中脂类含量,用qRT-PCR及蛋白印迹等方法分析肝脏mRNA和蛋白表达的变化。结果显示GPM对小鼠体重增加和脏器重量没有明显变化。4%以上GPM与对照组相比显著降低血中的甘油三酯（TG）、总胆固醇、低密度脂蛋白的胆固醇和血糖及肝脏中TG的浓度。而粪中的TG却明显增加。8% GPM明显抑制羟甲基戊二酰CoA还原酶（HMGCR）的活力和mRNA及蛋白表达水平,而Glut4的mRNA和蛋白表达明显增加。以上结果表明GPM通过调节HMGCR和Glut4的mRNA及蛋白表达,和抑制肠道对TG吸收,达到降糖降脂作用。     

Anti-obesity and anti-diabetic effects of ethanol extract of Artemisia princeps in C57BL/6 mice fed a high-fat diet

Artemisia princeps is commonly used as a food ingredient and in traditional Asian medicine. In this study, we examined the effects of long-term administration of an ethanol extract of A. princeps (APE) on body weight, white adipose tissue, blood glucose, insulin, plasma and hepatic lipids, and adipocytokines in C57BL/6 mice fed a high-fat diet. Daily feeding of a 1% APE diet for 14 weeks normalized elevated body weight, white adipose tissue, and plasma glucose and insulin levels, and delayed impaired glucose tolerance in mice a fed high-fat diet. These events were not observed in mice fed a control diet containing 1% APE. Liver triglyceride and cholesterol levels were similar in mice fed a 1% APE-diet and those fed a control diet. In the high-fat diet groups, APE inhibited hepatic fatty acid synthase (FAS) and suppressed the elevation of plasma leptin, but had no effect on adiponectin levels. These findings suggest that the regulation of leptin secretion by APE may inhibit FAS activity with subsequent suppression of triglyceride accumulation in the liver and adipose tissues. Inhibition of lipid accumulation can, in turn, lead to improvements in impaired glucose tolerance.     

Effect of abomasal glucose infusion on plasma concentrations of gut peptides in periparturient dairy cows

Six Holstein cows fitted with ruminal cannulas and permanent indwelling catheters in the portal vein, hepatic vein, mesenteric vein, and an artery were used to study the effects of abomasal glucose infusion on splanchnic plasma concentrations of gut peptides. The experimental design was a randomized block design with repeated measurements. Cows were assigned to one of 2 treatments: control or infusion of 1,500 g of glucose/d into the abomasum from the day of parturition to 29 d in milk. Cows were sampled 12 ± 6 d prepartum and at 4, 15, and 29 d in milk. Concentrations of glucose-dependent insulinotropic polypeptide, glucagon-like peptide 1(7–36) amide, and oxyntomodulin were measured in pooled samples within cow and sampling day, whereas active ghrelin was measured in samples obtained 30 min before and after feeding at 0800 h. Postpartum, dry matter intake increased at a lower rate with infusion compared with the control. Arterial, portal venous, and hepatic venous plasma concentrations of the measured gut peptides were unaffected by abomasal glucose infusion. The arterial, portal venous, and hepatic venous plasma concentrations of glucose-dependent insulinotropic polypeptide and glucagon-like peptide 1(7–36) amide increased linearly from 12 d prepartum to 29 d postpartum. Plasma concentrations of oxyntomodulin were unaffected by day relative to parturition. Arterial and portal venous plasma concentrations of ghrelin were lower postfeeding compared with prefeeding concentrations. Arterial plasma concentrations of ghrelin were greatest prepartum and lowest at 4 d postpartum, giving a quadratic pattern of change over the transition period. Positive portal venous-arterial and hepatic venous–arterial concentration differences were observed for glucagon-like peptide 1(7–36) amide. A negative portal venous–arterial concentration difference was observed for ghrelin pre-feeding. The remaining portal venous–arterial and hepatic venous–arterial concentration differences of gut peptides did not differ from zero. In conclusion, increased postruminal glucose supply to postpartum transition dairy cows reduced feed intake relative to control cows, but did not affect arterial, portal venous, or hepatic venous plasma concentrations of gut peptide hormones. Instead, gut peptide plasma concentrations increased as lactation progressed. Thus, the lower feed intake of postpartum dairy cows receiving abomasal glucose infusion was not attributable to changes in gut peptide concentrations.     

D-Psicose,a Sweet Monosaccharide,Ameliorate Hyperglycemia,and Dyslipidemia in C57BL/6J db/db Mice

ABSTRACT: D-psicose has been implicated in glycemic control in recent animal and human studies. In this study, the effects of D-psicose on glycemic responses, insulin release, and lipid profiles were compared with those of D-glucose and D-fructose in a genetic diabetes model. C57BL/6J db/db mice were orally supplemented with 200 mg/kg BW of D-psicose, D-glucose, or D-fructose, respectively, while diabetes control or wild type mice were supplemented with water instead. D-psicose sustained weight gain by about 10% compared to other groups. The initial blood glucose level maintained from 276 to 305 mg/dL during 28 d in the D-psicose group, whereas a 2-fold increase was found in other groups (P < 0.05) among diabetic mice. D-psicose significantly improved glucose tolerance and the areas under the curve (AUC) for glucose among diabetes (P < 0.05), but had no effect on serum insulin concentration. The plasma lipid profile was not changed by supplemental monosacchrides, although the ratio of LDL-cholesterol/HDL-cholesterol was ameliorated by D-psicose. The administration of D-psicose reversed hepatic concentrations of triglyceride (TG) and total cholesterol (TC) by 37.88% and 62.89%, respectively, compared to the diabetes control (P < 0.05). The current findings suggest that D-psicose shows promise as an antidiabetic and may have antidyslipidemic effects in type 2 diabetes.