Dehulled Adlay (Coix lachryma-jobi L.) ameliorates hepatic gluconeogenesis and steatosis in streptozotocin/high-fat diet-induced diabetic rats.

Adlay (Coix lachryma-jobi L.) is a traditional Chinese herbal medicine with various biological activities. We investigated the anti-diabetic effects of different parts of adlay seeds, including polished adlay (PA), adlay bran (AB) and dehulled adlay (DA) in a streptozotocin (STZ)/high fat diet (HFD) diabetic rat model (DM). DM rats supplemented with or without PA (43%), AB (3%), or DA (46%) diet for 8 weeks. The plasma glucose and insulin levels and the insulin resistance index (HOMA-IR) were increased in DM group; among the three adlay diets, DA has the best effects attenuating all of these alterations in DM rats. Both AB and DA alleviated diabetes-impaired glucose tolerance. The increased hepatic phosphoenolpyruvate carboxykinase protein expression in DM group was improved by all of the three adlay diets. The increased ratio of glucose-6-phosphatase to glucokinase in DM group was suppressed by DA supplementation, further suggesting DA diet is most effective among the three diets. Both AB and DA diets had beneficial effects against hepatic steatosis, with better effects observed in DA group. These results suggest that the DA diet, composed of both polished adlay and adlay bran, possesses the best potential to improve glucose homeostasis, at least in part, by alleviating hepatic glucose metabolism and steatosis.

Improvement of Glycemic Control by a Functional Food Mixture Containing Maltodextrin, White Kidney Bean Extract, Mulberry Leaf Extract, and Niacin-Bound Chromium Complex in Obese Diabetic db/db Mice.

Steady-fiber granule (SFG) is a mixture containing maltodextrin, white kidney bean extract, mulberry leaf extract, and niacin-bound chromium complex. These active ingredients have been shown to be associated with improving either hyperglycemia or hyperlipidemia. This study was undertaken to evaluate the potential of SFG in the regulation of blood glucose homeostasis under obese diabetic conditions. Accordingly, db/db mice (8 weeks old) were administered with SFG at doses of 1.025, 2.05, or 5.125 g/kg BW daily via oral gavage for 4 weeks. No body weight loss was observed after SFG supplementation at all three doses during the experimental period. Supplementation of SFG at 2.05 g/kg BW decreased fasting blood glucose, blood fructosamine, and HbA1c levels in db/db mice. Insulin sensitivity was also improved, as indicated by HOMA-IR assessment and oral glucose tolerance test, although the fasting insulin levels were no different in db/db mice with or without SFG supplementation. Meanwhile, the plasma levels of triglyceride were reduced by SFG at all three doses. These findings suggest that SFG improves glycemic control and insulin sensitivity in db/db mice and can be available as an option for functional foods to aid in management of type 2 diabetes mellitus in daily life.

Fish Oil Enriched n-3 Polyunsaturated Fatty Acids Improve Ketogenic Low-Carbohydrate/High-Fat Diet-Caused Dyslipidemia, Excessive Fat Accumulation, and Weight Control in Rats.

Low-carbohydrate and high-fat diets have been used for body weight (BW) control, but their adverse effects on lipid profiles have raised concern. Fish oil (FO), rich in omega-3 polyunsaturated fatty acids, has profound effects on lipid metabolism. We hypothesized that FO supplementation might improve the lipid metabolic disturbance elicited by low-carbohydrate and high-fat diets. Male SD rats were randomized into normal control diet (NC), high-fat diet (HF), and low-carbohydrate/high-fat diet (LC) groups in experiment 1, and NC, LC, LC + 5% FO (5CF), and LC + 10% FO diet (10CF) groups in experiment 2. The experimental duration was 11 weeks. In the LC group, a ketotic state was induced, and food intake was decreased; however, it did not result in BW loss compared to either the HF or NC groups. In the 5CF group, rats lost significant BW. Dyslipidemia, perirenal and epididymal fat accumulation, hepatic steatosis, and increases in triglyceride and plasma leptin levels were observed in the LC group but were attenuated by FO supplementation. These findings suggest that a ketogenic low-carbohydrate/high-fat diet with no favorable effect on body weight causes visceral and liver lipid accumulation. FO supplementation not only aids in body weight control but also improves lipid metabolism in low-carbohydrate/high-fat diet-fed rats.

Effects of Chitosan Oligosaccharide on Plasma and Hepatic Lipid Metabolism and Liver Histomorphology in Normal Sprague-Dawley Rats.

Chitosan oligosaccharide is known to ameliorate hypercholesterolemia and diabetes. However, some studies found that chitosan oligosaccharide might induce mild to moderate hepatic damage in high-fat (HF) diet-induced obese rats or diabetic rats. Chitosan oligosaccharide can be as a dietary supplement, functional food, or drug. Its possible toxic effects to normal subjects need to be clarified. This study is designed to investigate the effects of chitosan oligosaccharide on plasma and hepatic lipid metabolism and liver histomorphology in normal Sprague-Dawley rats. Diets supplemented with 5% chitosan oligosaccharide have been found to induce liver damage in HF diet-fed rats. We therefore selected 5% chitosan oligosaccharide as an experimental object. Rats were divided into: a normal control diet group and a normal control diet +5% chitosan oligosaccharide group. The experimental period was 12 weeks. The results showed that supplementation of 5% chitosan oligosaccharide did not significantly change the body weight, food intake, liver/adipose tissue weights, plasma lipids, hepatic lipids, plasma levels of AST, ALT, and TNF-α/IL-6, hepatic lipid peroxidation and anti-oxidative enzyme activities, fecal lipids, and liver histomorphology in normal rats. These findings suggest that supplementation of 5% chitosan oligosaccharide for 12 weeks may not induce lipid metabolism disorder and liver toxicity in normal rats.

The Anti-Obesity Effect of Polysaccharide-Rich Red Algae (Gelidium amansii) Hot-Water Extracts in High-Fat Diet-Induced Obese Hamsters.

This study investigated the anti-obesity effect of a polysaccharide-rich red algae Gelidium amansii hot-water extract (GHE) in high-fat (HF) diet-induced obese hamsters. GHE contained 68.54% water-soluble indigestible carbohydrate polymers. Hamsters were fed with a HF diet for 5 weeks to induce obesity, and then randomly divided into: HF group, HF with 3% guar gum diet group, HF with 3% GHE diet group, and HF with orlistat (200 mg/kg diet) group for 9 weeks. The increased weights of body, liver, and adipose in the HF group were significantly reversed by GHE supplementation. Lower plasma leptin, tumor necrosis factor-α, and interleukin-6 levels were observed in the GHE+HF group compared to the HF group. GHE also increased the lipolysis rate and decreased the lipoprotein lipase activity in adipose tissues. GHE induced an increase in the phosphorylation of AMP-activated protein kinase (AMPK) and the protein expressions of peroxisome proliferator-activated receptor alpha (PPARα) and uncoupling protein (UCP)-2 in the livers. The decreased triglyceride and total cholesterol in the plasma and liver were also observed in obese hamsters fed a diet with GHE. These results suggest that GHE exerts a down-regulation effect on hepatic lipid metabolism through AMPK phosphorylation and up-regulation of PPARα and UCP-2 in HF-induced obese hamsters.

Omega-3 Fatty Acids-Enriched Fish Oil Activates AMPK/PGC-1α Signaling and Prevents Obesity-Related Skeletal Muscle Wasting.

Obesity is known to cause skeletal muscle wasting. This study investigated the effect and the possible mechanism of fish oil on skeletal muscle wasting in an obese rat model. High-fat (HF) diets were applied to induce the defects of lipid metabolism in male Sprague-Dawley rats with or without substitution of omega-3 fatty acids-enriched fish oil (FO, 5%) for eight weeks. Diets supplemented with 5% FO showed a significant decrease in the final body weight compared to HF diet-fed rats. The decreased soleus muscle weights in HF diet-fed rats could be improved by FO substitution. The decreased myosin heavy chain (a muscle thick filament protein) and increased FOXO3A and Atrogin-1 (muscle atrophy-related proteins) protein expressions in soleus muscles of HF diet-fed rats could also be reversed by FO substitution. FO substitution could also significantly activate adenosine monophosphate (AMP)-activated protein kinase (AMPK) phosphorylation, peroxisome-proliferator-activated receptor-γ (PPARγ) coactivator 1α (PGC-1α), and PPARγ protein expression and lipoprotein lipase (LPL) mRNA expression in soleus muscles of HF diet-fed rats. These results suggest that substitution of FO exerts a beneficial improvement in the imbalance of lipid and muscle metabolisms in obesity. AMPK/PGC-1α signaling may play an important role in FO-prevented obesity-induced muscle wasting.

Functional Comparison of High and Low Molecular Weight Chitosan on Lipid Metabolism and Signals in High-Fat Diet-Fed Rats.

The present study examined and compared the effects of low- and high-molecular weight (MW) chitosan, a nutraceutical, on lipid metabolism in the intestine and liver of high-fat (HF) diet-fed rats. High-MW chitosan as well as low-MW chitosan decreased liver weight, elongated the small intestine, improved the dysregulation of blood lipids and liver fat accumulation, and increased fecal lipid excretion in rats fed with HF diets. Supplementation of both high- and low-MW chitosan markedly inhibited the suppressed phosphorylated adenosine monophosphate (AMP)-activated protein kinase-α (AMPKα) and peroxisome proliferator-activated receptor-α (PPARα) protein expressions, and the increased lipogenesis/cholesterogenesis-associated protein expressions [peroxisome proliferator-activated receptor-γ (PPARγ), sterol regulatory element binding protein-1c and -2 (SREBP1c and SREBP2)] and the suppressed apolipoprotein E (ApoE) and microsomal triglyceride transfer protein (MTTP) protein expressions in the livers of rats fed with HF diets. Supplementation with both a low- and high-MW chitosan could also suppress the increased MTTP protein expression and the decreased angiopoietin-like protein-4 (Angptl4) expression in the intestines of rats fed with HF diets. In comparison between low- and high-MW chitosan, high-MW chitosan exhibits a higher efficiency than low-MW chitosan on the inhibition of intestinal lipid absorption and an increase of hepatic fatty acid oxidation, which can improve liver lipid biosynthesis and accumulation.

Red algae (Gelidium amansii) hot-water extract ameliorates lipid metabolism in hamsters fed a high-fat diet.

The purpose of this study was to investigate the effects of Gelidium amansii (GA) hot-water extracts (GHE) on lipid metabolism in hamsters. Six-week-old male Syrian hamsters were used as the experimental animals. Hamsters were divided into four groups: (1) control diet group (CON); (2) high-fat diet group (HF); (3) HF with GHE diet group (HF + GHE); (4) HF with probucol diet group (HF + PO). All groups were fed the experimental diets and drinking water ad libitum for 6 weeks. The results showed that GHE significantly decreased body weight, liver weight, and adipose tissue (perirenal and paraepididymal) weight. The HF diet induced an increase in plasma triacylglycerol (TG), total cholesterol (TC), low-density lipoprotein cholesterol and very-low-density lipoprotein cholesterol levels. However, GHE supplementation reversed the increase of plasma lipids caused by the HF diet. In addition, GHE increased fecal cholesterol, TG and bile acid excretion. Lower hepatic TC and TG levels were found with GHE treatment. GHE reduced hepatic sterol regulatory element-binding proteins (SREBP) including SREBP 1 and SREBP 2 protein expressions. The phosphorylation of adenosine monophosphate (AMP)-activated protein kinase (AMPK) protein expression in hamsters was decreased by the HF diet; however, GHE supplementation increased the phosphorylation of AMPK protein expression. Our results suggest that GHE may ameliorate lipid metabolism in hamsters fed a HF diet.

Long-Term Feeding of Chitosan Ameliorates Glucose and Lipid Metabolism in a High-Fructose-Diet-Impaired Rat Model of Glucose Tolerance.

This study was designed to investigate the effects of long-term feeding of chitosan on plasma glucose and lipids in rats fed a high-fructose (HF) diet (63.1%). Male Sprague-Dawley rats aged seven weeks were used as experimental animals. Rats were divided into three groups: (1) normal group (normal); (2) HF group; (3) chitosan + HF group (HF + C). The rats were fed the experimental diets and drinking water ad libitum for 21 weeks. The results showed that chitosan (average molecular weight was about 3.8 × 105 Dalton and degree of deacetylation was about 89.8%) significantly decreased body weight, paraepididymal fat mass, and retroperitoneal fat mass weight, but elevated the lipolysis rate in retroperitoneal fats of HF diet-fed rats. Supplementation of chitosan causes a decrease in plasma insulin, tumor necrosis factor (TNF)-α, Interleukin (IL)-6, and leptin, and an increase in plasma adiponectin. The HF diet increased hepatic lipids. However, intake of chitosan reduced the accumulation of hepatic lipids, including total cholesterol (TC) and triglyceride (TG) contents. In addition, chitosan elevated the excretion of fecal lipids in HF diet-fed rats. Furthermore, chitosan significantly decreased plasma TC, low-density lipoprotein cholesterol (LDL-C), very-low-density lipoprotein cholesterol (VLDL-C), the TC/high-density lipoprotein cholesterol (HDL-C) ratio, and increased the HDL-C/(LDL-C + VLDL-C) ratio, but elevated the plasma TG and free fatty acids concentrations in HF diet-fed rats. Plasma angiopoietin-like 4 (ANGPTL4) protein expression was not affected by the HF diet, but it was significantly increased in chitosan-supplemented, HF-diet-fed rats. The high-fructose diet induced an increase in plasma glucose and impaired glucose tolerance, but chitosan supplementation decreased plasma glucose and improved impairment of glucose tolerance and insulin tolerance. Taken together, these results indicate that supplementation with chitosan can improve the impairment of glucose and lipid metabolism in a HF-diet-fed rat model.

Supplementation of chitosan alleviates high-fat diet-enhanced lipogenesis in rats via adenosine monophosphate (AMP)-activated protein kinase activation and inhibition of lipogenesis-associated genes.

This study investigated the role of chitosan in lipogenesis in high-fat diet-induced obese rats. The lipogenesis-associated genes and their upstream regulatory proteins were explored. Diet supplementation of chitosan efficiently decreased the increased weights in body, livers, and adipose tissues in high-fat diet-fed rats. Chitosan supplementation significantly raised the lipolysis rate; attenuated the adipocyte hypertrophy, triglyceride accumulation, and lipoprotein lipase activity in epididymal adipose tissues; and decreased hepatic enzyme activities of lipid biosynthesis. Chitosan supplementation significantly activated adenosine monophosphate (AMP)-activated protein kinase (AMPK) phosphorylation and attenuated high-fat diet-induced protein expressions of lipogenic transcription factors (PPAR-γ and SREBP1c) in livers and adipose tissues. Moreover, chitosan supplementation significantly inhibited the expressions of downstream lipogenic genes (FAS, HMGCR, FATP1, and FABP4) in livers and adipose tissues of high-fat diet-fed rats. These results demonstrate for the first time that chitosan supplementation alleviates high-fat diet-enhanced lipogenesis in rats via AMPK activation and lipogenesis-associated gene inhibition.

Effects of long-term feeding of chitosan on postprandial lipid responses and lipid metabolism in a high-sucrose-diet-impaired glucose-tolerant rat model.

This study was designed to investigate the effects of long-term feeding of chitosan on postprandial lipid response and lipid metabolism in a high-sucrose (HS)-diet-impaired glucose-tolerant rat model. As the results, HS-diet-fed rats supplemented with 5 and 7% chitosan in diets for 9 weeks had lower postprandial plasma total cholesterol (TC) levels, but 7% chitosan in the diet had higher postprandial plasma triglyceride (TG) and TG-rich lipoprotein TG levels. Supplementation of chitosan significantly decreased the postprandial ratio of apolipoprotein B (apoB)48/apoB100 in TG-rich lipoprotein fractions of HS-diet-fed rats. Long-term supplementation of 5 and 7% chitosan in diets for 16 weeks had lower plasma TC, low-density lipoprotein cholesterol (LDL-C) + very low density lipoprotein cholesterol (VLDL-C), TC/high-density lipoprotein (HDL-C) ratio, leptin, and tumor necrosis factor-α (TNF-α) levels in HS-diet-fed rats. Moreover, it was noticed that the VLDL receptor (VLDLR) protein expression in skeletal muscles of HS-diet-fed rats was significantly decreased, which could be significantly reversed by supplementation of 5 and 7% chitosan. Rats supplemented with 7% chitosan in the diet significantly elevated the lipolysis rate and decreased the accumulation of TG in epididymal fat pads of HS-diet-fed rats. The plasma angiopoietin-like 4 (ANGPTL4) protein expression was not affected in HS-diet-fed rats, but it was significantly increased in 7% chitosan-supplemented HS-diet-fed rats. Taken together, these results indicate that supplementation of chitosan in the diet can improve the impairment of lipid metabolism in a HS-diet-fed rat model, but long-term high-dose chitosan feeding may enhance postprandial plasma TG and TG-rich lipoprotein TG levels in HS-diet-fed rats through an ANGPTL4-regulated pathway.

Chitosan reduces plasma adipocytokines and lipid accumulation in liver and adipose tissues and ameliorates insulin resistance in diabetic rats.

Chitosan is a natural product derived from chitin. To investigate the hypoglycemic and anti-obesity effects of chitosan, male Sprague-Dawley rats were divided into four groups: normal control, diabetic, and diabetic fed 5% or 7% chitosan. Diabetes was induced in rats by injecting streptozotocin/nicotinamide. After 10 weeks of feeding, the elevated plasma glucose, tumor necrosis factor-α, and interleukin-6 and lower adiponetin levels caused by diabetes were effectively reversed by chitosan treatment. In addition, 7% chitosan feeding also elevated plasma glucagon-like peptide-1 levels and lowered the insulin resistance index (homeostasis model assessment) in diabetic rats. Lower adipocyte granular intensities and higher lipolysis rates in adipose tissues were noted in the 7% chitosan group. Moreover, chitosan feeding reduced hepatic triglyceride and cholesterol contents and increased hepatic peroxisomal proliferator-activated receptor α expression in diabetic rats. Our results indicate that long-term administration of chitosan may reduce insulin resistance through suppression of lipid accumulation in liver and adipose tissues and amelioration of chronic inflammation in diabetic rats.

Suppressive effect of the ethanolic extract of adlay bran on cytochrome P-450 enzymes in rat liver and lungs.

Adlay ( Coix lachryma-jobi L. var. ma-yuen Stapf) is a grass crop and is reported to protect against various diseases such as cancer. To investigate the effect of the ethanolic extract of adlay bran (ABE) on drug-metabolizing enzymes and glutathione-related antioxidant enzymes in rats, three groups of eight male Sprague-Dawley rats each were fed a control diet or a diet containing 5 or 10% ABE for 4 weeks. Significant decreases in microsomal cytochrome P-450 (CYP) 1A1-catalyzed ethoxyresorufin O-deethylation, CYP2C-catalyzed diclofenac 4-hydroxylation, CYP2D-catalyzed dextromethorphan O-demethylation, and CYP3A-catalyzed testosterone 6ß-hydroxylation in the liver and CYP1A1-catalyzed ethoxyresorufin O-deethylation in the lungs of rats fed ABE were observed. Immunoblot analyses also showed decreases of CYP1A1, 1A2, 2C6, 2C11, 2D1, 2E1, 3A1, and 3A2 in the liver and CYP1A1 in the lungs. Furthermore, rats fed the 10% ABE diet had a higher glutathione content and glutathione peroxidase, glutathione reductase, and glutathione S-transferase activities in the lungs, but such an increase was not noted in the liver. Inhibition of various CYP-catalyzed enzyme reactions by ABE in rat and human liver microsomes had also been shown. The results of this study indicate that ABE feeding may suppress CYP enzyme activities and CYP protein expression in the liver and lungs of rats. Moreover, the increase of the antioxidant potential by ABE is tissue-specific.

Effect of taurine supplementation on cytochrome P450 2E1 and oxidative stress in the liver and kidneys of rats with streptozotocin-induced diabetes.

To investigate whether diabetes-induced alterations of CYP2E1 and oxidative stress can be modulated by dietary taurine supplementation, male Wistar rats were divided into non-diabetic, diabetic, and diabetic taurine-supplemented groups (administered at 2% in the drinking water). Increased levels of CYP2E1-catalyzed p-nitrophenol hydroxylation were found in liver and kidney microsomes of rats with STZ-induced diabetes compared to those of non-diabetic control rats. Immunoblot and RT-PCR analyses of CYP2E1 protein and mRNA levels in the liver and kidneys showed the same trend as with enzyme activities. Taurine supplementation significantly decreased the enzyme activity and expression (protein and mRNA) of CYP2E1 in diabetic rat kidneys. Plasma beta-hydroxybutyrate concentration was significantly reduced in taurine-treated diabetic rats. The induction of heme oxygenase-1 mRNA was suppressed by taurine treatment in diabetic rat kidneys. An increase in reduced glutathione (GSH) and a higher ratio of reduced to oxidized glutathione (GSH/GSSG) together with lower values of thiobarbituric acid-reactive substances (TBARS) were observed in the kidneys of taurine-treated diabetic rats. However, taurine supplementation caused only a slight or insignificant effect on these alternations in the liver of diabetic rats. Our results show dietary taurine may reduce CYP2E1 expression and activity, and oxidative stress in kidneys of diabetic rats.

Shengmai San reduces hepatic lipids and lipid peroxidation in rats fed on a high-cholesterol diet.

Shengmai San (SMS), which is comprised of the medicinal herbs of Panax ginseng C.A. Meyer, Schisandra chinensis Baill., and Ophiopogon japonicus Ker-Gawl (2:1:2)., is a traditional Chinese medicine being used for treating coronary heart disease. The aim of this study was to investigate the effects of SMS on the plasma and liver lipids, lipid peroxidation and antioxidant systems in liver and heart of cholesterol-fed rats. Rats were fed on a high-cholesterol (0.5%) diet (control group), high-cholesterol diet containing 2% SMS (2% SMS group) and 4% SMS (4% SMS group) for four weeks. The oxidative stress marker (thiobarbituric acid reactive substances, TBARS) and antioxidant defense systems including glutathione (GSH), glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST) and superoxide dismutase (SOD) activities in rat liver and heart were evaluated. Results showed that rats fed with SMS-containing diet had reduced the H(2)O(2)-induced erythrocytes susceptibility to hemolysis, and 4% SMS feeding rats had higher plasma GSH concentration compared to the animals fed with the control diet. However, SMS had no effect on plasma lipids (total cholesterol, triglyceride and high-density lipoprotein cholesterol) and TBARS concentration. On the other hand, rats fed with the 4% SMS diet reduced the hepatic cholesterol and triglyceride contents. Fecal bile acid excretion was significantly increased in rats fed with the SMS-containing diet. Higher hepatic GSH and lower TBARS concentrations were observed in rats fed with the 4% SMS diet compared with the rats fed with the control diet. No significant difference in activities of GSH-Px, GST and SOD was found in liver and heart after the SMS treatment. Results from this study indicate that the SMS may reduce hepatic lipids and lipid peroxidation in rats.

Effects of dehulled adlay on plasma glucose and lipid concentrations in streptozotocin-induced diabetic rats fed a diet enriched in cholesterol.

Adlay (Coix lachryma-jobi L. var. ma-yuen Stapf) is a cereal food for humans and has been also used as a superior medical herb substance and functional food for traditional treatment of diabetes in China. However, its scientific basis as a functional food is still unclear. The purpose of this study was to investigate the effect of dietary dehulled adlay on plasma lipid and glucose concentrations in diabetic rats. The diabetic male Sprague-Dawley (SD) rats, induced by injection of streptozotocin (60 mg/kg subcutaneously), were fed a cholesterol-rich diet (0.5% cholesterol) containing corn starch or dehulled adlay for four weeks. After completion of the experimental period, the abdominal adipose tissue and liver of rats were excised and weighed, and the plasma glucose, triglyceride, and lipoprotein cholesterol concentrations were assayed. The results showed that diabetic rats fed a dehulled adlay diet exhibited a greater adipose tissue weight (9.36 +/- 3.43 vs. 5.39 +/- 3.04 g, p < 0.05) and a reduced food intake (39.3 +/- 5.9 vs. 61.0 +/- 11.7 g/day, p < 0.05) when compared with animals fed a cornstarch diet. Significantly decreased plasma glucose (261.6 +/- 96.6 vs. 422.1 +/- 125.4 mg/dL, p < 0.05), total cholesterol (289.4 +/- 140.6 vs. 627.3 +/- 230.5 mg/dL, p < 0.05), and triglyceride (52.3 +/- 14.4 vs. 96.5 +/- 36.6 mg/dL, p < 0.05) levels were observed in rats fed the dehulled adlay diet. In addition, the ingestion of dehulled adlay appears to significantly decrease plasma low-density lipoprotein (LDL) plus very low-density lipoprotein (VLDL) cholesterol concentrations. Rats fed a dehulled adlay diet showed an increase in fecal weight and cholesterol contents of stools. Although a significantly decreased plasma thiobarbituric reactive substances (TBARS) value was observed in diabetic rats fed the dehulled adlay diet (6.2 +/- 3.4 vs. 11.0 +/- 3.8 nmol malondialdehyde (MDA)/mL, p < 0.05), no significant difference in the hepatic TBARS value was observed between the two dietary groups. Results from the present study suggest that dehulled adlay exhibited not only a hypolipidemic effect but also displayed a hypoglycemic ability in diabetic rats, indicating that dehulled adlay may play an important role in the regulation of plasma lipid and glucose metabolisms in diabetic rats induced by streptozotocin.