Fecal Lipid Excretion Research Articles

Jaboticaba (Myrciaria cauliflora) Peel Supplementation Prevents Hepatic Steatosis Through Hypolipidemic Effects and Cholesterol Metabolism Modulation in Diet-Induced Nonalcoholic Fatty Liver Disease Rat Model.

Jaboticaba (Myrciaria cauliflora), a Brazilian fruit, is a good source of dietary fiber and phenolic compounds, which are concentrated mainly in the peel. These compounds have been considered promising in prevention and treatment of hypercholesterolemia and hepatic steatosis. In this study, we investigated the effects of 4% jaboticaba peel powder (JPP) supplementation on cholesterol metabolism and hepatic steatosis in livers of rats fed a high-fat (HF) diet. The rats were fed a standard AIN-93M (control) diet or an HF diet containing 32% lard and 1% cholesterol, both with and without 4% JPP. The M. cauliflora peel composition revealed a low-lipid high-fiber content and phenolic compounds. The phenolic compounds in JPP, tentatively identified by high-performance liquid chromatography and mass spectrometry (HPLC-MS/MS) analysis, were confirmed to contain phenolic acids, flavonoids, and anthocyanins. Moreover, JPP presented significant antioxidant activity in vitro and was not cytotoxic to HepG2 cells, as determined by the lactate dehydrogenase (LDH) assay. After 6 weeks of treatment, our results showed that JPP supplementation increased lipid excretion in feces, reduced serum levels of total cholesterol and nonhigh-density lipoprotein cholesterol, decreased serum aspartate aminotransferase (AST) activity, and attenuated hepatic steatosis severity in rats fed the HF diet. Furthermore, JPP treatment downregulated expression of ACAT-1, LXR-α, CYP7A1, and ABCG5 genes. Therefore, jaboticaba peel may represent a viable dietary strategy to prevent nonalcoholic fatty liver disease as the JPP treatment alleviated hepatic steatosis through improvement of serum lipid profiles and modulation of mRNA expression of genes involved in cholesterol metabolism.

Celastrol inhibits intestinal lipid absorption by reprofiling the gut microbiota to attenuate high-fat diet-induced obesity

SummaryCelastrol, a compound extracted from traditional Chinese medicine, has been reported as a potent anti-obesity agent with controversial mechanisms. Here both C57BL/6J and leptin-deficient (ob/ob) mice fed a high-fat diet (HFD) displayed body weight loss after celastrol therapy, opposing the previous viewpoint that celastrol improves obesity by sensitizing leptin signaling. More importantly, celastrol downregulated lipid transporters in the intestine, increased lipid excretion in feces, and reduced body weight gain in HFD mice. Meanwhile, analysis of gut microbiota revealed that celastrol altered the gut microbiota composition in HFD-fed mice, and modulating gut microbiota by antibiotics or fecal microbiota transplantation blocked the celastrol effect on intestinal lipid transport and body weight gain, suggesting a critical role of the gut microbiota composition in mediating the anti-obesity role of celastrol under HFD. Together, the findings revealed that celastrol reduces intestinal lipid absorption to antagonize obesity by resetting the gut microbiota profile under HFD feeding.

Sar1b mutant mice recapitulate gastrointestinal abnormalities associated with chylomicron retention disease

Chylomicron retention disease (CRD) is an autosomal recessive disorder associated with biallelic Sar1b mutations leading to defects in intracellular chylomicron (CM) trafficking and secretion. To date, a direct cause-effect relationship between CRD and Sar1b mutation has not been established, but genetically modified animal models provide an opportunity to elucidate unrecognized aspects of these mutations. To examine the physiological role and molecular mechanisms of Sar1b function, we generated mice expressing either a targeted deletion or mutation of human Sar1b using the CRISPR-Cas9 system. We found that deletion or mutation of Sar1b in mice resulted in late-gestation lethality of homozygous embryos. Moreover, compared with WT mice, heterozygotes carrying a single disrupted Sar1b allele displayed lower plasma levels of triglycerides, total cholesterol, and HDL-cholesterol, along with reduced CM secretion following gastric lipid gavage. Similarly, decreased expression of apolipoprotein B and microsomal triglyceride transfer protein was observed in correlation with the accumulation of mucosal lipids. Inefficient fat absorption in heterozygotes was confirmed via an increase in fecal lipid excretion. Furthermore, genetically modified Sar1b affected intestinal lipid homeostasis as demonstrated by enhanced fatty acid β-oxidation and diminished lipogenesis through the modulation of transcription factors. This is the first reported mammalian animal model with human Sar1b genetic defects, which reproduces some of the characteristic CRD features and provides a direct cause-effect demonstration.

Berberine alleviates lipid metabolism disorders via inhibition of mitochondrial complex I in gut and liver.

This study is to investigate the relationship between berberine (BBR) and mitochondrial complex I in lipid metabolism. BBR reversed high-fat diet-induced obesity, hepatic steatosis, hyperlipidemia and insulin resistance in mice. Fatty acid consumption, β-oxidation and lipogenesis were attenuated in liver after BBR treatment which may be through reduction in SCD1, FABP1, CD36 and CPT1A. BBR promoted fecal lipid excretion, which may result from the reduction in intestinal CD36 and SCD1. Moreover, BBR inhibited mitochondrial complex I-dependent oxygen consumption and ATP synthesis of liver and gut, but no impact on activities of complex II, III and IV. BBR ameliorated mitochondrial swelling, facilitated mitochondrial fusion, and reduced mtDNA and citrate synthase activity. BBR decreased the abundance and diversity of gut microbiome. However, no change in metabolism of recipient mice was observed after fecal microbiota transplantation from BBR treated mice. In primary hepatocytes, BBR and AMPK activator A769662 normalized oleic acid-induced lipid deposition. Although both the agents activated AMPK, BBR decreased oxygen consumption whereas A769662 increased it. Collectively, these findings indicated that BBR repressed complex I in gut and liver and consequently inhibited lipid metabolism which led to alleviation of obesity and fatty liver. This process was independent of intestinal bacteria.

High-phosphorus diets reduce aortic lesions and cardiomyocyte size and modify lipid metabolism in Ldl receptor knockout mice

The consumption of phosphorus in Western populations largely exceeds the recommended intake, while vitamin D supply is often insufficient. Both situations are linked to an increased cardiovascular risk. A 17-week two-factorial study with Ldl receptor-/- mice was conducted to investigate the cardiovascular impact of dietary phosphorus [adequate (0.3%; P0.3) vs. high (1.5%; P1.5)] in combination with a low (50 IU/kg; D50) or adequate vitamin D diet (1000 IU/kg; D1000). The data demonstrate that mice fed the P1.5 vs. P0.3 diets developed smaller vascular lesions (p = 0.013) and cardiac hypotrophy (p = 0.011), which were accompanied by diminished IGF1 and insulin signalling activity in their hearts. Vitamin D showed no independent effect on atherogenesis and heart morphology. Feeding P1.5 vs. P0.3 diets resulted in markedly reduced serum triacylglycerols (p < 0.0001) and cholesterol (p < 0.0001), higher faecal lipid excretion (p < 0.0001) and a reduced mRNA abundance of hepatic sterol exporters and lipoprotein receptors. Minor hypocholesterolaemic and hypotriglyceridaemic effects were also found in mice fed the D1000 vs. D50 diets (p = 0.048, p = 0.026). To conclude, a high phosphorus intake strongly affected the formation of vascular lesions, cardiac morphology, and lipid metabolism, although these changes are not indicative of an increased cardiovascular risk.

Health Benefits of Green Tea in Obesity

Adipocytes play a central role in maintaining lipid homeostasis and energy balance by storing triacylglycerols (TAGs) or releasing free fatty acids in response to changes in energy requirements. Obesity is a major risk factor for many diseases, including diabetes, hypertension, and cardiovascular disease. Besides, morbidity and mortality associated with being overweight and obese are on the rise. The development of obesity is characterized by an increase in lipid cells due to mitogenesis and differentiation, which are regulated by genetic, endocrine, metabolic, neurological, pharmacological, environmental, and nutritional factors. Therefore, understanding the mechanism by which a given nutrient affects the mitogenesis of preadipocytes and their differentiation into adipocytes could help prevent the onset and progression of obesity, along with all its consequences in humans. It has been shown that nutraceuticals such as tea catechins and BCAAs (leucine, isoleucine, and valine) could be effective in preventing obesity. Green tea catechins (CTGs) are polyphenolic flavonoids, which were previously called vitamin P. CTGs, especially EGCGs, have been shown to reduce body weight and body fat. In support of its anti-obesity effect, some in vivo data have shown that EGCG or green tea extract containing EGCG reduces the absorption of food, lipids, TAGs, cholesterol, and leptins. Furthermore, it stimulates energy expenditure and fat oxidation, and ultimately increases the level of high-density lipoproteins and fecal excretion of lipids. EGCG regulates various enzymes linked to anabolism and lipid catabolism, such as acetyl-CoA carboxylase (ACC), fatty acid synthase, pancreatic lipase, gastric lipase, and lipoxygenase; it also reduces the increase in insulin (INS) and TAG during the differentiation period of nine days. Taken together, these observations, in vivo and in vitro, suggest that the EGCG contained in green tea can modulate the mitogenic, endocrine, and metabolic functions of fat cells. In this study, we report the biochemical and biological evidence indicating the benefits of green tea in obesity.

Administration of indigenous probiotics modulate high-fat diet-induced metabolic syndrome in Sprague Dawley rats.

Modulation of the gut microbiota by probiotics, is emerging as a promising approach for the management of metabolic diseases but due to their species and strain specific response, isolation of new probiotic strains is gaining importance. The present study was designed to assess the effect of isolated and well characterised indigenous probiotics, Lactobacillus pentosus GSSK2, Lactobacillus fermentum PUM and Lactobacillus plantarum GS26A in high fat diet (HFD) induced metabolic syndrome. It was observed that though supplementation of all three probiotics for 12weeks to Sprague Dawley rats fed with HFD, ameliorated the anthropometric parameters, but L. pentosus GSSK2 showed maximum reduction in weight gain while maximum decrease in abdominal circumference, Lee's index, BMI and visceral fat deposition was observed in L. plantarum GS26A compared with HFD animals. Further, administration of L. plantarum GS26A to HFD animals led to significant increase in lactic acid bacteria count and lipid excretion in feces followed by L. pentosus GSSK2 and L. fermentum PUM compared with counter controls. Additionally, both L. pentosus GSSK2 and L. plantarum GS26A exhibited improved glucose tolerance, liver biomarkers, alleviated oxidative stress and restored the histoarchitechture of adipose tissue, colon and liver compared with HFD animals. The study highlights the prophylactic potential of isolated probiotics in experimental metabolic syndrome model and revealed that amongst all three probiotics, L. pentosus GSSK2 and L. plantarum GS26A were equally effective and more promising than L. fermentum PUM in improving metabolic dysfunctions and may be employed as functional foods but needs to be correlated clinically.

Supplementation with Sea Vegetables Palmaria mollis and Undaria pinnatifida Exerts Metabolic Benefits in Diet-Induced Obesity in Mice.

ABSTRACTBackgroundSea vegetables are rich sources of nutrients as well as bioactive components that are linked to metabolic health improvement. Algal polysaccharides improve satiety and modulate gut microbiota while proteins, peptides, and phenolic fractions exert anti-inflammatory, antioxidant, and antidiabetic effects.ObjectiveWe tested the hypothesis that dietary supplementation with either Pacific dulse (Palmaria mollis, red algae) or wakame (Undaria pinnatifida, brown algae) could remediate metabolic complications in high-fat diet-induced obesity.MethodsIndividually caged C57BL/6J mice (n = 8) were fed ad libitum with either a low-fat diet (LFD), 10% kcal fat; high-fat diet (HFD), 60% kcal fat; HFD + 5% (wt:wt) dulse (HFD + D); or HFD + 5% (wt:wt) wakame (HFD + W) for 8 weeks. Food intake and weight gain were monitored weekly. Glucose tolerance, hepatic lipids, fecal lipids, and plasma markers were evaluated, and the gut microbiome composition was assessed.ResultsDespite the tendency of higher food and caloric intake than the HFD (P = 0.04) group, the HFD + D group mice did not exhibit higher body weight, indicating lower food and caloric efficiency (P < 0.001). Sea vegetable supplementation reduced plasma monocyte chemotactic protein (MCP-1) (P < 0.001) and increased fecal lipid excretion (P < 0.001). Gut microbiome analysis showed that the HFD + D group had higher alpha-diversity than the HFD or LFD group, whereas beta-diversity analyses indicated that sea vegetable–supplemented HFD-fed mice (HFD + D and HFD + W groups) developed microbiome compositions more similar to those of the LFD-fed mice than those of the HFD-fed mice.ConclusionSea vegetable supplementation showed protective effects against obesity-associated metabolic complications in C57BL/6J male mice by increasing lipid excretion, reducing systemic inflammatory marker, and mitigating gut microbiome alteration. While the obese phenotype development was not prevented, metabolic issues related to lipid absorption, inflammation, and gut microbial balance were improved, showing therapeutic promise and warranting eventual mechanistic elucidations.

Eriocitrin Improves Adiposity and Related Metabolic Disorders in High-Fat Diet-Induced Obese Mice

Eriocitrin (EC) is an abundant flavonoid in lemons, which is known as a strong antioxidant agent. This study investigated the biological and molecular mechanisms underlying the anti-obesity effect of EC in high-fat diet (HFD)-fed obese mice. C57BL/6N mice were fed an HFD (40 kcal% fat) with or without 0.005% (w/w) EC for 16 weeks. Dietary EC improved adiposity by increasing adipocyte fatty acid (FA) oxidation, energy expenditure, and mRNA expression of thermogenesis-related genes in brown adipose tissue (BAT) and skeletal muscle, whereas it also decreased lipogenesis-related gene expression in white adipose tissue. In addition to adiposity, EC prevented hepatic steatosis by diminishing lipogenesis while enhancing FA oxidation in the liver and fecal lipid excretion, which was linked to attenuation of hyperlipidemia. Moreover, EC improved insulin sensitivity by decreasing hepatic gluconeogenesis and proinflammatory responses. These findings indicate that EC may protect against diet-induced adiposity and related metabolic disorders by controlling thermogenesis of BAT and skeletal muscle, FA oxidation, lipogenesis, fecal lipid excretion, glucose utilization, and gluconeogenesis.

Effect of arrowroot (Maranta sp.) Food Products Supplementation in Diet Induced Hypercholesterolemic Mice

Food enriched with dietary fiber content has been associated to lower blood lipid profile. In this study, the flour, starch, and cookies from locally grown arrowroot plant, which is known to contain dietary fiber, were investigated for anti-lipidemic activity. Six groups of male ICR mice were fed with a high cholesterol diet for six weeks. At the end of six-week cholesterol induction, Group 1 received distilled water (dH20), Group 2 was fed with arrowroot starch (ARS), Group 3 with arrowroot starch cookies (ARSC), Group 4 with arrowroot flour (ARF), Group 5 with arrowroot flour cookies (ARFC), and Group 6 received simvastatin (SIM) for two weeks. Body weights were recorded before and after cholesterol induction and after arrowroot treatments. Lipid profile (total cholesterol, HDL, LDL, VDLD, triglycerides) of serum was measured at the end of the experiment. Also, livers were dissected, weighed, and evaluated for ballooning of hepatocytes, lipid inclusion (steatosis), and portal inflammation. After two weeks of treatment with arrowroot food products, a significant reduction of body weights on hypercholesterolemic mice were observed but the reduction was comparable with the group that received only distilled water. However, treatment with arrowroot starch significantly reduced the blood total cholesterol and the histological changes induced by a high cholesterol diet. Treatment with arrowroot starch and starch cookies significantly decreased steatosis, ballooning of hepatocytes, and resulted in the absence of portal inflammation in the liver—suggesting its hypolipidemic activity. Liver lipid profile and fecal lipid excretion analysis should be conducted to further support the result of this study.

Plasma triacylglycerol-reducing activity of ergosterol linolenate is associated with inhibition of intestinal lipid absorption

Abstract This study investigated the role of ergosterol linolenate in the alleviation of hyperlipidemia induced by a high-fat diet and further explored the expression of key genes involved in lipid absorption and metabolism in mice. Twenty-four male C57BL/6J mice were divided into three groups and fed one of three experimental diets: a high-fat diet (HF), or a HF diet with either ergosterol (ER) or ergosterol linolenate (EL), respectively, for 6 weeks. The results demonstrate that EL significantly reduced plasma triacylglycerol (TG) levels by 20%, weight gain by 50% and relative perirenal and epididymal fat by 23.6%. This was accompanied by a significant decrease in liver cholesterol, liver total fatty acids and fecal bile acids, accompanied by a marked increase in fecal total fatty acids. Ergosterol linolenate effectively counteracted steatosis induced by a high-fat diet. Ergosterol linolenate also altered the mRNA expression of key intestinal and hepatic genes involved in lipid absorption and metabolism. Of them, ergosterol linolenate significantly reduced the mRNA expression of intestinal microsomal triglyceride transfer protein (MTP), a key component in the formation of chylomicrons. Therefore, the plasma TG-reducing action of ergosterol linolenate can be largely attributed to reduced lipid absorption and increased fecal lipid excretion.

Hypolipidemic Effect of Mulberry Leaf Extract in Rats Fed a High-cholesterol Diet (P06-014-19)

ObjectivesThe purpose of this study was to evaluate the hypolipidemic effect of high hydrostatic pressure extract of mulberry leaf on in rats fed a high-cholesterol diet. MethodsMale Sprague-Dawley rats were randomly allocated into four groups. Each group fed a normal diet (NOR), a high-cholesterol diet (HC), a HC containing 0.5% high hydrostatic pressure extract of mulberry leaves (ML), or a HC containing 1.0% high hydrostatic pressure extract of mulberry leaves (MH) for 4 weeks. ResultsBody weight and food intake were not different among the four groups. The levels of serum triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and atherosclerotic index (AI) significantly reduced in the ML and MH groups compared to HC group. While, in MH group, serum high-density lipoprotein cholesterol (HDL-C) was increased compared to HC group. Liver cholesterol was lower in the ML and MH groups than those in the HC group. Fecal excretion of the total lipid, TG, TC, and bile acid were higher in the ML and MH groups than those in the HC group. The mRNA related to cholesterol efflux and hepatic bile acid synthesis in liver, such as liver X receptor-a (LXRa), ATP-binding cassette sub-family G member 5(ABCG5), ATP-binding cassette sub-family G member 8 (ABCG8), and cholesterol 7- alpha hydroxylase gene (CYP7A1) were significantly upregulated in MH group compared to HC group. ConclusionsThese results suggest that hypolipidemic effect of mulberry leaf extracts partially associated with modulating gene expression related to hepatic cholesterol efflux, hepatic bile acid synthesis, and increasing fecal lipid excretion. Funding SourcesNone.

Dietary Eriodictyol Alleviates Adiposity, Hepatic Steatosis, Insulin Resistance, and Inflammation in Diet-Induced Obese Mice.

The present study aimed to investigate the molecular mechanisms underlying the anti-obesity effect of flavonoid eriodictyol (ED) supplementation in mice fed with a high-fat diet (HFD). C57BL/6N mice were fed with normal diet (ND), HFD (40 kcal% fat), or HFD + 0.005% (w/w) ED for 16 weeks. In HFD-induced obese mice, dietary ED supplementation significantly alleviated dyslipidemia and adiposity by downregulating the expression of lipogenesis-related genes in white adipose tissue (WAT), while enhancing fecal lipid excretion. ED additionally improved hepatic steatosis and decreased the production of pro-inflammatory cytokines by downregulating the expression of hepatic enzymes and the genes involved in lipogenesis and upregulating the expression of hepatic fatty acid oxidation-related enzymes and genes. In addition, ED improved insulin resistance (IR) by suppressing hepatic gluconeogenesis, enhancing glucose utilization, and modulating the production and release of two incretin hormones, namely gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). Taken together, the current findings indicated that ED can protect against diet-induced obesity and related metabolic disturbances, including dyslipidemia, inflammation, fatty liver disease, and IR in diet-induced obese mice.

Schizandrin A supplementation improves nonalcoholic fatty liver disease in mice fed a high-fat and high-cholesterol diet

We hypothesized that schizandrin (SCH) A, a lignan found in the fruits of the Schisandra genus, would exert protective effects against high-fat and high-cholesterol (HFHC) diet–induced nonalcoholic fatty liver disease (NAFLD) via regulation of lipid metabolism and oxidative stress. To test our hypothesis, male C57BL/6J mice were fed an HFHC diet with or without SCH A for 15 weeks. There were no significant differences in food intake, body weight, fat mass, and plasma total cholesterol level between the 2 groups. However, supplementation of SCH A significantly decreased levels of plasma free fatty acid and triglyceride, whereas plasma high-density lipoprotein cholesterol level was increased in the SCH A-supplemented mice. Moreover, hepatic free fatty acid, triglyceride, and cholesterol content, as well as hepatic lipid droplet accumulation, were markedly lower in the SCH A group in contrast to the control group. Activity of hepatic enzymes involved in fatty acid and triglyceride synthesis was significantly decreased by SCH A supplementation, whereas SCH A markedly increased hepatic β-oxidation and fatty acid oxidation-related gene expression as well as fecal excretion of free fatty acid and triglyceride. SCH A also significantly increased expression of genes involved in cholesterol homeostasis (biliary cholesterol excretion and cholesterol efflux to high-density lipoprotein) in the liver. Moreover, SCH A significantly decreased hepatic lipid peroxidation, which was accompanied by increased hepatic antioxidant enzymes activity. These results suggest that SCH A could alleviate HFHC diet–induced NAFLD by regulating hepatic lipid metabolism and oxidative stress as well as fecal lipid excretion.

Effect of Dietary Partial Hydrolysate of Phospholipids, Rich in Docosahexaenoic Acid-Bound Lysophospholipids, on Lipid and Fatty Acid Composition in Rat Serum and Liver.

Lysophospholipids have been recognized as potent biologically active lipid mediators. However, attention has not been paid to the health benefits of dietary partial hydrolysate of phospholipids (PH-PL), which is rich in docosahexaenoic acid (DHA)-bound lysophospholipids. In this study, the effects of PH-PL on serum and liver lipid profiles of rats upon administration of PH-PL are demonstrated in comparison to those of fish oil (FO), which comprises eicosapentaenoic acid (EPA) and DHA-bound triglyceride (TG). PH-PL containing EPA and DHA was prepared via enzymatic modification of squid (Todarodes pacificus) meal that is rich in phospholipids. Male Wistar rats were fed a basal diet containing soybean oil alone (7%), FO, and PH-PL. The FO and PH-PL diets had similar EPA and DHA contents. After the rats had been fed their respective diets for 28 d, their serum and liver lipid contents, fecal lipid excretion, and hepatic gene expression level were measured. The results demonstrated that compared with the soybean oil diet alone, the PH-PL diet decreased serum and liver TG contents partially because of the enhancement of liver acyl-CoA oxidase activity and suppression of liver fatty acid synthase activity. In addition, compared with the soybean oil diet, the PH-PL group exhibited lower serum cholesterol content at least in part because of the reduction of hepatic 3-hydroxy-3-methylglutaryl-CoA reductase mRNA expression level. We found that dietary administration of EPA and DHA containing PH-PL has a hypolipidemic effect that may help prevent the development lifestyle-related diseases.

Dietary sn-2 palmitic triacylglycerols reduced faecal lipids, calcium contents and altered lipid metabolism in Sprague–Dawley rats

In this study, the impact of dietary sn-2 palmitic triacylglycerol (sn-2 PTAG) on faecal lipids, calcium excretion and lipid metabolic alternation was investigated in Sprague–Dawley (SD) rats fed with high-fat diet containing either palm olein (PO, sn-2 palmitic acid (PA) of 14.8%), sn-2 PTAG50 (sn-2 PA of 56.4%) or sn-2 PTAG70 (sn-2 PA of 72.4%), respectively. After 4-week feeding period, SD rats fed with sn-2 PTAGs showed reduced faecal soap fatty acids, neutral lipid and calcium excretion compared to those of PO-fed rats, whereas a significant difference was only observed for the sn-2 PTAG70-fed rats (p < .05). Moreover, dietary sn-2 PTAG70 also showed a significant effect on decreasing serum triacylglycerol (TAG) level, reducing perirenal adipocyte size and regulating lipid metabolism in small intestine and perirenal adipose tissue of SD rats. Significantly increased mRNA levels of genes involved in intestinal lipid anabolism as well as lipid catabolism were both observed in the sn-2 PTAG70-fed rats (p < .05). Meanwhile, dietary sn-2 PTAG70 also significantly up-regulated lipolysis, mitochondrial fatty acid oxidation and thermogenesis-related gene and protein levels in perirenal adipose tissue, which might be correlated with the reduced perirenal adipocyte size. Taken together, our findings indicated that sn-2 PTAG70 may have some beneficial effects on intestinal lipid utilisation and lipid metabolic activity for energy supply in visceral adipose tissue.

비파 잎 및 열매 추출물이 고콜레스테롤 식이를 급여한 흰쥐의 콜레스테롤 저하효과 비교

This study compared the cholesterol lowering effects of loquat leaf and the fruit ethanol extracts on rats fed a high-cholesterol diet. Male Sprague-Dawley rats were divided into 4 groups: normal diet group (ND), high-cholesterol diet group (HCD), high-cholesterol diet and loquat leaf with 400 mg/kg treated group (HCD-LLE), and high-cholesterol diet and loquat fruit with 400 mg/kg treated group (HCD-LFE). No significant differences were found in body weight gain, food intake, adipose tissue weight, serum LDH activities, triglyceride (TG), and hepatic and fecal total lipid contents in both the normal (ND) and high-cholesterol diet fed groups (HCD, HCD-LLE, HCD-LFE). The serum ALT, AST and ALP activities, total cholesterol (TC), LDL-cholesterol, atherogenic index, cardiac risk factor, and hepatic TC contents were significantly lower in the HCD-LLE and HCD-LFE groups, whereas the HCD-LLE group showed a significantly higher serum HLD-cholesterol, and fecal TC and total bile acid content than the HCD and HCD-LLE groups. The cholesterol-lowering effects were greater in the HCD-LLE group than in the HCD-LFE group. These results suggest that loquat ethanol extracts may improve the serum and hepatic lipid profiles, and enhance the fecal excretion of lipids in mice fed a high-cholesterol diet.

Ginger Extract Ameliorates Obesity and Inflammation via Regulating MicroRNA-21/132 Expression and AMPK Activation in White Adipose Tissue.

Ginger is a plant whose rhizome is used as a spice or folk medicine. We aimed to investigate the effect of ginger root extract on obesity and inflammation in rats fed a high-fat diet. Sprague-Dawley rats were divided into three groups and fed either a 45% high-fat diet (HF), HF + hot-water extract of ginger (WEG; 8 g/kg diet), or HF + high-hydrostatic pressure extract of ginger (HPG; 8 g/kg diet) for 10 weeks. The HPG group had lower body weight and white adipose tissue (WAT) mass compared to the HF group. Serum and hepatic lipid levels of HPG group were lower, while fecal lipid excretion of the HPG group was higher than that of the HF group. In the WAT of the WEG and HPG groups, mRNA levels of adipogenic genes were lower than those of the HF group. Moreover, HPG group had lower mRNA levels of pro-inflammatory cytokines than did the HF group. MicroRNA (miR)-21 expression was down-regulated by both WEG and HPG. Additionally, miR-132 expression was down-regulated by HPG. The adenosine monophosphate-activated protein kinase (AMPK) activity of HPG group was greater than that of the HF group. HPG may have beneficial effects on obesity and inflammation, partially mediated by regulation of miR-21/132 expression and AMPK activation in WAT.

The effect of micronized corn fiber on body weight, glycemia, and lipid metabolism in rats fed cafeteria diet

Abstract During corn industrial dry milling, a residue rich in dietary fibers is generated. This study aimed to evaluate the effects of micronized corn fiber (MCF) as part of a cafeteria diet in the macronutrient metabolism and body weight. Wistar male rats, with initial body weight of 249 ± 14 g (n = 13), received AIN-93M diet (Group 1) or cafeteria diet (Groups 2, 3 and 4), composed of commercial ration, cookies, fried potato sticks, milk chocolate, bacon and chicken liver pâte. Groups 3 and 4 received MCF to replace 100 and 50% of the cellulose from the AIN-93M diet, respectively. After 35 days, blood, tissues and feces were collected. Data were analyzed by ANOVA followed by Tukey test (p < 0.10). The weight gain of the animals increased by 25.9%, 20.8% and 22.0%, when fed cafeteria diet or 100 and 50% of MCF respectively, compared to the control group, although food consumption did not differ between them. Body weight and food efficiency ratio did not differ between the groups fed cafeteria diet with or without MCF. The addition of MCF to the cafeteria diet did not alter the animal lipid profile and glycemia, however, the accumulation of lipids in their livers was similar to the control group. The intake of 100% MCF resulted in higher fecal weight and fecal excretion of lipids, and lower fecal nitrogen, lipid absorption and lipid deposition in the liver than the cafeteria diet. In conclusion, MCF has a potential to improve intestinal transit and lipid excretion, but showed no benefit on blood lipid and glucose levels.

Inulin Improves Postprandial Hypertriglyceridemia by Modulating Gene Expression in the Small Intestine.

Postprandial hyperlipidemia is an important risk factor for cardiovascular diseases in the context of obesity. Inulin is a non-digestible carbohydrate, known for its beneficial properties in metabolic disorders. We investigated the impact of inulin on postprandial hypertriglyceridemia and on lipid metabolism in a mouse model of diet-induced obesity. Mice received a control or a western diet for 4 weeks and were further supplemented or not with inulin for 2 weeks (0.2 g/day per mouse). We performed a lipid tolerance test, measured mRNA expression of genes involved in postprandial lipid metabolism, assessed post-heparin plasma and muscle lipoprotein lipase activity and measured lipid accumulation in the enterocytes and fecal lipid excretion. Inulin supplementation in western diet-fed mice decreases postprandial serum triglycerides concentration, decreases the mRNA expression levels of Cd36 (fatty acid receptor involved in lipid uptake and sensing) and apolipoprotein C3 (Apoc3, inhibitor of lipoprotein lipase) in the jejunum and increases fecal lipid excretion. In conclusion, inulin improves postprandial hypertriglyceridemia by targeting intestinal lipid metabolism. This work confirms the interest of using inulin supplementation in the management of dyslipidemia linked to obesity and cardiometabolic risk.