Hepatic steatosis by dietary-conjugated linoleic acid is accompanied by accumulation of diacylglycerol and increased membrane-associated protein kinase C ε in mice

Scope : Conjugated linoleic acid reduces weight gain and adipose mass while inducing liver enlargement, hepatic steatosis, and insulin resistance in mice. The objective of this study was to determine if hepatic steatosis induced by conjugated linoleic acid would predict for hepatic diacylglycerol accumulation, increased membrane‐associated protein kinase C ε, and hyperglycemia. Methods and results : Six‐wk‐old C57Bl/6 male mice were fed a high‐saturated fat diet for 3 wk and were then randomized to high‐saturated fat diet with or without conjugated linoleic acid (1.5% wt). Following a 6‐wk intervention, hepatic triacylglycerol, diacylglycerol, membrane‐associated protein kinase C ε, and gluconeogenic gene expression were determined. Fasting glucose was determined at baseline and at the end of the study. Conjugated linoleic acid increased hepatic triacylglycerol and diacylglycerol concentration in association with increased membrane‐associated protein kinase C ε. Diacylglycerol concentration proved to be a better predictor than triacylglycerol concentration for the change from baseline in fasting glucose concentration and final insulin concentration. The increase in diacylglycerol concentration was also associated with increased hepatic gluconeogenic gene expression in conjugated linoleic acid‐treated animals. Conclusion : Our data suggest that conjugated linoleic acid can initiate the pathophysiology responsible for hepatic insulin resistance. Additional studies are needed to determine if the accumulation of hepatic diacylglycerol by conjugated linoleic acid leads to hepatic insulin resistance.     

Dill seed extract improves abnormalities in lipid metabolism through peroxisome proliferator‐activated receptor‐α (PPAR‐α) activation in diabetic obese mice

Dill, a small annual herb, is widely used as a flavoring agent in dishes including salads. It has been demonstrated that dill extract and its essential oil show hypolipidemic effects in rats. However, the mechanism of these effects has not been elucidated yet. We found that dill seed extract (DSE) activated peroxisome proliferator‐activated receptor‐α (PPAR‐α), an indispensable regulator for hepatic lipid metabolism, by luciferase assay. Thus, we performed DSE feeding experiments using diabetic obese model KK‐Ay mice to examine the effects of DSE on PPAR‐α activation in vivo. A 4‐week feeding of DSE contained in a high‐fat diet decreased plasma triacylglyceride and glucose levels and increased the mRNA expression levels of fatty acid oxidation‐related genes in the liver. In addition, the DSE feeding as well as bezafibrate (a PPAR‐α potent agonist) feeding increased oxygen consumption rate and rectal temperature. These results indicate that DSE suppresses high‐fat diet‐induced hyperlipidemia through hepatic PPAR‐α activation.     

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.     

Modulatory effects of yerba maté (Ilex paraguariensis) on the PI3K‐AKT signaling pathway

The aim of this study was to evaluate the effects of yerba maté (YM) extract on the phosphatidylinositol 3‐kinase (PI3K)‐AKT signaling pathway in vivo. The mice were introduced to either standard‐ or high‐fat diet (HFD). After 8 weeks on an HFD, mice were randomly assigned to one of the two treatment conditions, water or yerba maté extract at 1.0 g/kg. After treatment, glucose blood level and hepatic insulin response were evaluated. Liver tissue was examined to determine the mRNA levels using the PI3K‐AKT PCR array. The nuclear translocation of forkhead box O1 (FOXO1) was determined by an electrophoretic mobility‐shift assay. Our data demonstrated that yerba maté extract significantly decreased the final body weight, glucose blood levels, and insulin resistance of mice. Molecular analysis demonstrated that an HFD downregulated Akt2, Irs1, Irs2, Pi3kca, Pi3kcg, and Pdk1; after yerba maté treatment, the levels of those genes returned to baseline. In addition, an HFD upregulated Pepck and G6pc and increased FOXO1 nuclear translocation. The intervention downregulated these genes by decreasing FOXO1 nuclear translocation. The results obtained demonstrate for the first time the specific action of yerba maté on the PI3K‐AKT pathway, which contributed to the observed improvement in hepatic insulin signaling.     

石榴皮提取物改善肥胖大鼠糖、脂代谢紊乱的分子机制

目的:探讨高脂饮食诱发的大鼠肥胖对肝脏糖代谢的影响,揭示石榴皮提取物(EPP)改善肥胖大鼠糖、脂代谢紊乱的分子机制.方法:应用高脂饲料(D12451)和对照饲料(D12450H)分别饲养大鼠16周,复制肥胖动物模型.在造模的同时,灌胃大鼠3个剂量的EPP(50,100,200 mg/kg)进行干预.结果:高脂饲料喂养1...     

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.     

乳酸菌发酵大麦提取物对胰岛素抵抗的干预作用

研究乳酸菌发酵大麦提取物(LFBE)对饮食诱导的肥胖大鼠胰岛素抵抗的干预作用及其机制。通过饲喂高脂饲料的方法建立营养型肥胖模型大鼠,在饲喂模型大鼠高脂饲料的同时,分别灌胃LFBE(1 000 mg/kg bw)和水(4 mL/kg bw) 8周后,测定其体重、血脂、炎症因子等指标。结果显示,与模型对照组相比,LFBE能显著降低营养型肥胖大鼠的体重、血脂和胰岛素水平,提高糖耐量,说明LFBE可以减缓肥胖大鼠体重的增加,改善糖代谢紊乱和胰岛素抵抗症状。同时,LFBE可抑制促炎因子的表达,抑制NF-B和c-Jun氨基末端激酶(JNK)/p38介导的丝裂原活化蛋白激酶(MAPK)信号通路,从而改善胰岛素抵抗症状。研究结果表明,LFBE具有干预胰岛素抵抗的作用,其作用机制主要与抑制MAPK(JNK、p38)的磷酸化以及NF-B活性有关。     

Effects of the Polysaccharide from the Sporophyll of Brown Alga Undaria Pinnatifida on Serum Lipid Profile and Fat Tissue Accumulation in Rats Fed a High‐Fat Diet

We investigated the effects of the polysaccharide from the sporophyll of a selected brown alga Undaria pinnatifida on serum lipid profile, fat tissue accumulation, and gastrointestinal transit time in rats fed a high‐fat diet. The algal polysaccharide (AP) was prepared by the treatment of multiple cellulase‐producing fungi Trichoderma reesei and obtained from the sporophyll with a yield of 38.7% (dry basis). The AP was mostly composed of alginate and fucoidan (up to 89%) in a ratio of 3.75:1. The AP was added to the high‐fat diet in concentrations of 0.6% and 1.7% and was given to male Sprague–Dawley rats (5‐wk‐old) for 5 wk. The 1.7% AP addition notably reduced body weight gain and fat tissue accumulation, and it improved the serum lipid profile, including triglycerides, total cholesterol, and very low‐density lipoprotein‐cholesterol. The effects were associated with increased feces weight and shortened gastrointestinal transit time. In addition, the lipid peroxidation of the liver was decreased in both groups.     

Chinese Cabbage (Brassica campestris L.) does not Improve Glucose Tolerance,Serum Insulin,or Blood Lipid Profiles in a Rat Model of Type‐2 Diabetes

ABSTRACT: The present study was conducted to investigate the effects of a low (0.5%) and a high (2.0%) dietary dose of freeze‐dried Chinese cabbage (CC) (Brassica campestris L.) powder in a type‐2 diabetes (T2D) model of rats. Five‐week‐old male Sprague–Dawley rats were fed a high fat (HF)‐containing diet for 2 wk then randomly divided into 4 groups of 8 animals, namely: normal control (NC), diabetic control (DBC), Chinese cabbage low (CCL, 0.5%), and Chinese cabbage high (CCH, 2.0%) groups. Diabetes was induced by an intraperitoneal injection of streptozotocin (STZ; 40 mg/kg body weight) in all groups except the NC group. After 4 wk feeding of experimental diets, although food intake was not different among the DBC, CCL, and CCH groups, body weight gain was significantly (P < 0.05) higher in the CCH group compared to the DBC group. Relatively higher serum insulin concentrations and better glucose tolerance were observed in the CC‐fed groups compared to the DBC group; however, the results were not significantly different. Fasting blood glucose, blood glycated hemoglobin (HbA1c), liver weight, and liver glycogen levels were not influenced by the CC‐containing diets. Additionally, hypertriglyceridemic tendencies were observed in the CC‐fed groups compared to the NC and DBC groups, while difference observed for total‐, HDL‐, and LDL‐cholesterols between the groups were negligible. Results of this study suggest that up to 2% dietary dose of freeze‐dried CC is not significantly effective to reduce diabetes‐related symptoms in an HF diet‐fed STZ‐induced T2D model of rats.     

Jaboticaba berry peel intake prevents insulin‐resistance‐induced tau phosphorylation in mice

The hyperphosphorylation of microtubule‐associated protein tau (tau) in the hippocampus can be caused by central and peripheral insulin resistance and these alterations are related to the development of tauopathies, such as Alzheimer's disease. In this study, we used a high‐fat diet to induce obesity and insulin resistance in adult Swiss mice and checked whether supplementation with Myrciaria jaboticaba berry peel for 10 weeks could improve insulin sensitivity, learning/memory performance, and prevent tau phosphorylation in the hippocampus. Furthermore, adipocytokines, inflammatory markers, and oxidative stress were assessed. Myrciaria jaboticaba peel has phenolic compounds (e.g., cyanidin, ellagic acid), dietary fiber and carotenoids, which contribute to great antioxidant capacity. Supplementation of the high‐fat diet with 4% M. jaboticaba peel prevented fat weight gain and reduced peripheral insulin resistance. The treated group also showed lower tau phosphorylation in the hippocampus corroborating better learning/memory performance in the Morris water maze test. Maintenance of neuronal viability, lower levels of hippocampal inflammatory markers, and improved brain antioxidant defenses were also related to the consumption of M. jaboticaba peel. These findings contribute to a better understanding of how a high‐fat diet supplemented with jaboticaba berry peel counteracts the impairment of cognitive functions caused by high‐fat diet intake and diet‐induced insulin resistance.     

Comparison of the Effects of Roasted and Boiled Red Kidney Beans (Phaseolus vulgaris L.) on Glucose/Lipid Metabolism and Intestinal Immunity in a High‐Fat Diet‐Induced Murine Obesity Model

Consumption of the common bean (Phaseolus vulgaris L.) is associated with beneficial effects on lipid and glucose metabolism; however, the influence of the bean processing method on these health benefits is not well understood. To investigate this, we processed red kidney beans (RKBs), a variety of the common bean, by roasting and boiling and compared the physiological effects of the two preparations in male C57BL/6N mice fed a high‐fat diet (HFD). The two RKB preparations differed mainly in their resistant starch content (roasted, 24.5%; boiled, 3.1%). Four groups of mice were fed for 12 weeks on a normal diet or a HFD (45 kcal% fat) supplemented with 10% control chow (HFD control group), 10% roasted RKB, or 10% freeze‐dried boiled RKB. We found that intake of roasted RKBs prevented hypercholesterolemia and increased fecal IgA and mucin content compared with the HFD control group, while intake of boiled RKBs improved glucose tolerance. Both RKB preparations suppressed the HFD‐associated increase in plasma aspartate aminotransferase and alanine aminotransferase levels, which are markers of liver injury. Mice fed roasted RKBs showed significantly increased hepatic expression of cholesterol 7‐alpha‐monooxygenase mRNA, suggesting that cholesterol suppression may be due to enhanced bile acid biosynthesis. In contrast, mice fed boiled RKBs showed significantly increased cecal content of n‐butyric acid, which may be related to the improved glucose tolerance in this group. These results indicate that the method by which RKBs are processed can profoundly affect their health benefits.     

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.     

Production and metabolic responses of periparturient Holstein cows to dietary conjugated linoleic acid and trans-octadecenoic acids

Thirty-eight multiparous Holstein cows were utilized in a completely randomized design to examine the effect of feeding calcium salts of conjugated linoleic acid (CLA) and trans-octadecenoic acids (trans-C18:1) on animal performance and lipid and glucose metabolism during the transition to lactation. Dietary treatments were initiated approximately 28 d prior to expected calving dates and continued through d 49 postpartum. Prepartum treatments consisted of 1) a basal diet (Control), 2) basal diet + 150 g/d of CLA mix (CLA), and 3) basal diet + 150 g/d of trans-C18:1 mix (TRANS). Amounts of calcium salts of CLA and trans-C18:1 mixes were adjusted to 225 g/d during the 49-d postpartum treatment period. All diets were offered as a total mixed ration. Prepartum fat supplementation had no detectable effects on dry matter intake, body weight, or body condition score. After parturition, cows in the TRANS group consumed less dry matter at wk 4, 5, and 6 of lactation than did cows in the control group. Cows fed the trans-C18:1 supplement were in a more severe negative energy balance than those fed the control diet at 1 wk of lactation. Periparturient fat supplementation had no detectable effects on milk yield during wk 1 to 7 of lactation. Milk fat was not affected during wk 1 to 4, but was reduced after wk 4 of lactation by dietary CLA. Feeding calcium salts of CLA decreased short- to medium-chain fatty acid (C4 to C14) concentrations and increased both linoleic and linolenic acid concentrations in milk fat. Concentrations of nonesterified fatty acids and beta-hydroxybutyric acid in blood were greater in cows fed the CLA-supplemented diet than in those fed the control diet at 1 wk of lactation. In spite of small numerical tendencies, hepatic lipid and triacylglycerol concentrations did not vary significantly among dietary treatments. Periparturient fat supplementation had no detectable effects on plasma glucose and insulin concentrations. Steady-state concentrations of hepatic mRNA encoding pyruvate carboxylase and phosphoenolpyruvate carboxykinase were greater for the TRANS treatment group than the control and CLA groups. Results indicate that dietary CLA and trans-C18:1 fatty acids may affect lipid and glucose metabolism in early postpartum Holstein cows through distinct mechanisms.     

普洱茶提取物及其复合配方改善糖尿病大鼠的糖脂代谢紊乱

本文观察了普洱茶提取物、玉米须提取物、低聚果糖及其复合配方对糖尿病模型大鼠糖脂代谢及胰岛素敏感性的影响。80只健康成年雄性SD大鼠随机分为8组:正常对照组给予普通饲料,模型对照组、普洱茶组、低聚果糖组、玉米须组以及低、中、高剂量复合配方组给予高脂饲料,受试物组经口灌胃给予6种受试物4周后,腹腔注射链脲佐菌素造模,继续给予受试物至实验结束。实验前后分别进行葡萄糖耐量试验,实验结束后测定各项指标。与模型对照组比较,普洱茶组大鼠体重、血清甘油三酯、肝脏胆固醇、肝脏甘油三酯、腹壁脂肪含量、脏体比、胰岛素抵抗指数分别降低了14.87%、77.59%、40.18%、39.18%、63.06%、55.81%和79.88%,但血糖和葡萄糖耐量无明显变化;低聚果糖组大鼠腹壁脂肪重量、脏体比、胰岛素抵抗指数分别降低了30.99%、29.46%和57.09%;玉米须组大鼠仅肝脏甘油三酯降低了36.06%;而三者复合配方能够显著降低大鼠的体重、体脂、血脂和肝脂水平,有效改善糖脂代谢紊乱和胰岛素抵抗。     

Fucosylated Chondroitin Sulfate from Sea Cucumber Improves Insulin Sensitivity via Activation of PI3K/PKB Pathway

This study was to investigate the effects of fucosylated chondroitin sulfate (CHS) from sea cucumber on insulin sensitivity in skeletal muscle of type 2 diabetic mice induced by a high‐fat high‐sucrose diet (HFSD). CHS supplementation for 19 wk significantly improved insulin sensitivity by 20%, and reduced blood glucose and insulin levels. Western blotting assay showed that CHS significantly increased insulin‐stimulated glucose transporter 4 (GLUT4) translocation to 1.7‐fold, phosphorylation of phosphoinositide 3‐kinase (PI3K) at p85 to 5.0‐fold, protein kinase B (PKB) at Ser473 to 1.5‐fold, and Thr308 to 1.6‐fold in skeletal muscle. However, PI3K, PKB, and GLUT4 total proteins expression were unchangeable. In addition, qRT‐PCR analysis proved that the insulin signaling was activated by CHS treatment, showing the increased mRNA expressions of glucose uptake‐related key genes. It indicated that CHS improved insulin sensitivity by activation of PI3K/PKB signaling in skeletal muscle of type 2 diabetic mice. Identification of potential mechanism by which CHS increased insulin sensitivity might provide a new functional food or pharmaceutical application of sea cucumber.     

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.     

Chromium dinicocysteinate supplementation can lower blood glucose,CRP, MCP‐1, ICAM‐1, creatinine,apparently mediated by elevated blood vitamin C and adiponectin and inhibition of NFκB,Akt, and Glut‐2 in livers of zucker diabetic fatty rats

Chromium and cysteine supplementation can improve glucose metabolism in animal studies. This study examined the hypothesis that a cysteinate complex of chromium is significantly beneficial than either of them in lowering blood glucose and vascular inflammation markers in Zucker diabetic fatty (ZDF) rats. Starting at the age of 6 wk, ZDF rats were supplemented orally (daily gavages for 8 more weeks) with saline‐placebo (D) or chromium (400 μg Cr/Kg body weight) as chromium dinicocysteinate (CDNC), chromium dinicotinate (CDN) or chromium picolinate (CP) or equimolar L ‐cysteine (LC, img/Kg body weight), and fed Purina 5008 diet for 8 wk. ZDF rats of 6 wk age before any supplementations and onset of diabetes were considered as baseline. D rats showed elevated levels of fasting blood glucose, HbA₁, CRP, MCP‐1, ICAM‐1 and oxidative stress (lipid peroxidation) and lower adiponectin and vitamin C, when compared with baseline rats. In comparison to D group, CDNC group had significantly lower blood glucose, HbA₁, CRP, MCP‐1, ICAM‐1 and lipid peroxidation and increased vitamin C and adiponectin levels. CDN, CP or LC showed significantly less or no effect on these biomarkers. Only CDNC lowered blood creatinine levels in comparison to D. While CDN and CP had no effect, activation of NFκB, Akt and glucose transporter‐2 levels were decreased, insulin receptor substrate 1 (IRS‐1) activation increased in livers of CDNC‐rats. CDNC effect on glycemia, NFκB, Akt and IRS‐1 in liver was significantly greater compared with LC. Blood chromium levels did not differ between Cr‐groups. Exogenous vitamin C supplementation significantly inhibited MCP‐1 secretion in U937 monocytes cultured in high‐glucose‐medium. CDNC is a potent hypoglycemic compound with anti‐inflammatory activity apparently mediated by elevated blood vitamin C and adiponectin and inhibition of NFκB, Akt, and Glut‐2 and increased IRS‐1 activation in livers of type 2 diabetic rats.     

Limonia fruit as a food supplement to regulate fluoride‐induced hyperglycaemia and hyperlipidaemia

BACKGROUND: Limonia fruit pulp is edible and used in a number of food preparations. This fruit is also used as a folk medicine to treat various ailments and reportedly possesses antihyperglycaemic and antihyperlipidaemic activities. The purpose of the present study was to examine the potential of Limonia acidissima L. (LA) fruit pulp in regulating the carbohydrate and lipid profiles in fluoride‐exposed rats. RESULTS: Exposure to fluoride (100 mg l^?1 NaF) resulted in significant increases in plasma and hepatic carbohydrate and lipid profiles. Administration of LA fruit powder (2.5, 5 and 10 g kg^?1) in the diet for 4 weeks resulted in significant decreases in plasma glucose and lipid profiles and hepatic glucose‐6‐phosphatase activity and significant increases in hepatic glycogen content and hexokinase activity and plasma high‐density lipoprotein cholesterol. Phytochemical analysis of the LA fruit pulp revealed the presence of fibres, phytosterols, saponins, polyphenols, flavonoids and ascorbic acid. CONCLUSION: Consumption of LA fruit pulp is beneficial in controlling hyperglycaemia and hyperlipidaemia in fluoride‐induced toxicity. Since fibres, phytosterols, saponins, polyphenols, flavonoids and total ascorbic acid are known to influence both carbohydrate and lipid metabolisms, the decline in carbohydrate and lipid levels in LA‐administered fluoride‐exposed rats could be attributed to the phytoconstituents of the fruit. Copyright © 2012 Society of Chemical Industry     

Diet‐induced obesity regulates the galanin‐mediated signaling cascade in the adipose tissue of mice

Galanin is a neuropeptide that regulates the food intake, neurogenesis, memory, and gut secretion. This study was conducted to evaluate the high‐fat diet (HFD)‐induced regulation of the galanin receptors (GalRs) and the associated signaling molecules in the adipose tissues of mice. Twenty C57BL/6J mice were given either an HFD or a normal diet for 12 wk. The results of the semiquantitative RT‐PCR analyses indicated that the HFD upregulated the expression of GalR1, GalR2, GalR3, resistance to audiogenic seizures, peroxisome proliferator‐activated receptorγ2, adipocyte protein 2, and protein kinase Cδ and downregulated the expression of peroxisome proliferative activated receptor γ coactivator 1α and uncoupling protein 1 in the adipose tissues. The immunoblot results showed that the protein levels of peroxisome proliferator‐activated receptorγ2 and adipocyte protein 2, and the phosphorylation of c‐Raf and extracellular signal‐regulated kinase 1/2 were increased, while the phosphorylation of cyclic adenosine monophosphate‐responsive element‐binding protein, which regulates peroxisome proliferative activated receptor γ coactivator 1α and uncoupling protein 1, was decreased in the epididymal adipose tissues of the HFD‐fed mice. These results suggest the possible association of the galanin‐mediated signaling pathways in the manifestation of the HFD‐induced activation of adipogenesis along with the suppression of thermogenesis in the adipose tissues of mice.