Lipid Excretion Research Articles

Lactobacillus paragasseri SBT2055 attenuates obesity via the adipose tissue-muscle-gut axis in obese mice

The anti-obesity effects of Lactobacillus paragasseri (L. paragasseri) have been reported, but the exact mechanisms have not been elucidated. There are also no reports on the impact of L. paragasseri on the gut microbiota environment. Recently, the incidence of sarcopenia due to obesity has increased regardless of age, exacerbating metabolic disorders caused by obesity. Therefore, we investigate the beneficial effects of L. paragasseri SBT2055 (LG2055) on obesity along with obese sarcopenia and gut microbiome changes. C57BL/6 J mice were fed a high-fat diet (HFD) and LG2055 (1×108 or 1×1010 CFU/mice, low-dose LG2055 (LP) or high-dose LG2055 (HP), respectively was administered orally. LG2055 supplementation significantly reduced white adipose tissues compared to the HFD group and modified plasma lipid profiles to normal levels. The anti-obesity efficacy of LG2055 was due to increased lipid excretion into feces by reducing the mRNA levels of fatty acid binding protein 1 (Fabp1), fatty acid binding protein 2 (Fabp2), fatty acid transport protein 4 (Fatp4), cluster of differentiation 36 (Cd36), and apolipoprotein 48 (ApoB48) in the small intestine. The body fat reduction inhibits ectopic lipid accumulation in the muscles, leading to improvements in muscle mass, grip strength, hind leg thickness, muscle protein levels, and muscle fiber size in both LP and HP groups. LG2055 increased gut microbiota diversity and elevated the levels of Bacteroidota, resulting in a lower Firmicutes/Bacteroidota ratio compared to the HFD group. Changes in the Bacteroidota showed a negative correlation with body fat and plasma free fatty acid (FFA) while exhibiting a positive correlation with lean body mass, grip strength, and hind leg thickness. Our results demonstrated the anti-obesity effects of LG2055 through the white adipose tissue (WAT)-muscle-gut axis, suggesting its potential as an anti-obesity agent.

Dietary bamboo charcoal powder ameliorates high-fat diet-induced hyperlipidemia by enhancing fecal lipid excretions in Sprague-Dawley rats.

Bamboo charcoal powder (BCP) is increasingly used as a food colorant. This study aims to evaluate the effects of BCP consumption on improving high-fat diet-induced hyperlipidemia. Fifty male SD rats were randomly assigned into five groups, with 10 rats in each group: the control group was fed a low-fat diet (LFD); the model control group was fed a high-fat diet (HFD); the low-BCP dose group was fed a HFD and given 2.81 g of BCP/kg of body weight (BCP-L) by gavage; the medium-BCP dose group was fed a HFD and given 5.62 g of BCP/kg of body weight (BCP-M) by gavage; the high-BCP dose group was fed a HFD and given 11.24 g of BCP/kg of body weight (BCP-H) by gavage. After 90 days, the consumption of BCP caused a decrease in body weight, plasma lipids (triglyceride, cholesterol, and low-density lipoprotein (LDL)), liver triglyceride, and cholesterol levels, and liver histopathological scores. BCP caused a significant increase in superoxide dismutase (SOD) activity and total antioxidant capacity (T-AOC) in liver tissues. BCP also led to an increase in 72-h fecal dry weight and crude fat in a rat metabolic cage. The analysis of fecal samples with liquid chromatography time-of-flight mass spectrometry (LC-Q-TOF-MS) showed that the biomarkers associated with BCP consumption were mainly related to fatty and amino acid metabolism. Notably, BCP treatment significantly promoted linoleic acid metabolism. These results suggest that BCP may have a preventive effect against diet-induced hyperlipidemia through the promotion of fecal fat excretion. BCP may potentially be used as an alternative functional food component for people with diet-induced hyperlipidemia.

Effects of Immature Soybeans on Lipid Metabolism in Rats Fed Normal and High-Fat High-Fructose NAFLD Diets.

Edamame and chamame (brown edamame) are immature soybeans that contain abundant protein, vitamins, and dietary fiber. Edamame has a different nutrient composition compared with mature soybeans, as evidenced by its higher content of vitamins and folic acid. Recent studies have shown that proteins in mature soybeans, such as β-conglycinin, and dietary fiber influence the metabolism of lipids such as triglyceride and cholesterol. However, the effect of edamame on lipid metabolism has not been reported. In the present study, we investigated whether oral consumption of edamame or chamame affects lipid metabolism. We focused on the analysis of hepatic lipids, serum cholesterol, and fecal lipids in rats after feeding them a normal or non-alcoholic fatty liver disease (NAFLD) diet containing edamame or chamame for 6 wk. We found that the consumption of dietary edamame and chamame significantly lowered hepatic triglyceride and serum cholesterol levels compared with those in the control groups fed with normal and NAFLD diets. Intake of edamame and chamame improved the NAFLD-like fatty liver. Finally, intake of edamame and chamame resulted in a significantly higher amount of fecal lipids and bile acid than in the control, suggesting the stimulation of lipid excretion. Together, dietary edamame and chamame decrease hepatic and serum cholesterol by promoting lipid excretion, not by the regulation of hepatic gene expression, leading to the improvement of lipid metabolism in both normal and NAFLD model rats.

Anti-atherosclerotic effect of alfalfa flavonoid extract by regulating inflammation and oxidative stress in HUVEC cells and rats

Atherosclerosis is characterized by accumulation of lipid that triggers arterial inflammation. This study aims to investigate the protective effect of alfalfa flavonoid extract (AFE) on HUVEC cells treated with lipopolysaccharide (LPS) and rats fed with high-fat diet (HFD). AFE reduced the expression of proinflammatory factors (COX-2, iNOS, IL-1β, IL-6 and TNF-α), intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, and inhibited activation of NF-κB and MAPK pathways. AFE alleviated vascular endothelial lesions by reducing HFD-enhanced levels of triglyceride, total cholesterol and low-density lipoprotein but increased high-density lipoprotein. Mechanically, AFE ameliorated HFD-enhanced liver steatosis through downregulating gene expression for lipid biosynthesis (SREBP2, HMGCR and FASN) and lipid uptake (LDLR), and through upregulating CYP7A1 expression for lipid catabolism and excretion. These data suggest that AFE possesses the anti-atherosclerotic potential through controlling inflammation, hyperlipidemia and lipid metabolism, and can be used as a functional food additive to benefit patients with atherosclerosis.

Platycodon D reduces obesity and non-alcoholic fatty liver disease induced by a high-fat diet through inhibiting intestinal fat absorption.

Platycodin D (PD) has been reported to treat metabolic diseases, including non-alcoholic fatty liver disease. In addition, platycodin D has been reported to activate intestinal 5'AMP-activated protein kinase (AMPK) phosphorylation levels, thereby reducing lipid absorption. Therefore, the aim of this study is to explore whether PD activation of intestinal AMPK and reduced lipid absorption can improve non-alcoholic fatty liver disease. Clean-grade male C57/BL mice were fed a high-fat diet (HFD) (containing 60% calories) for 16 weeks, and oral PD (10mg/kg/day) was administered at the same time. The liver and intestines were the collected, and the intestines were tested. The expressions of lipid absorption genes (CD36, NPC1L1, and ApoB), the serum total triglyceride (TG) and total cholesterol (TC) levels in the intestines and livers, the fecal free fatty acid (FFA) levels, and the expression of AMPK phosphorylated proteins in the intestines were examined using Western blot analyses. The lipid distribution in the livers, intestines, and fat was detected using Oil Red O and hematoxylin and eosin (H&E) staining. A colon cancer cell line (Caco2) was used to confirm the effect of PD on the cellular lipid uptake in vitro. In addition, serum inflammatory factors and liver enzymes were measured to clarify the impact of PD on the circulation of metabolic syndrome. Leptin-deficient mice (OB) were then used to further explore the improvement of PD on body weight and blood lipids. PD had a very significant therapeutic or preventive effect on metabolic syndrome and fatty liver induced by a high-fat diet. PD improved body weight, insulin sensitivity, and glucose tolerance in mice fed a high-fat diet and also prevented non-alcoholic fatty liver disease, reduced blood lipid levels, and increased fecal lipid excretion. In addition, PD reduced lipid absorption by activating the intestinal AMPK protein, which may have involved the inhibition of the gene expression levels of intestinal lipid absorption genes (CD36, NPC1L1, and ApoB). The combined effect of these factors improved hepatic lipid accumulation and lipid accumulation in adipose tissue. It was further found that PD also improved the body weights and blood lipid levels of leptin-deficient mice (OB) mice. PD had a very strong therapeutic effect on mice under a high-fat diet. PD reduced high-fat diet-induced obesity and non-alcoholic fatty liver disease by inhibiting intestinal fat absorption.

Dietary Cholest-4-en-3-one, a Cholesterol Metabolite of Gut Microbiota, Alleviates Hyperlipidemia, Hepatic Cholesterol Accumulation, and Hyperinsulinemia in Obese, Diabetic db/db Mice.

Previous studies have shown that dietary cholest-4-en-3-one (4-cholestenone, 4-STN) exerts anti-obesity and lipid-lowering effects in mice. However, its underlying mechanisms are not fully understood. In the present study, we evaluated whether 4-STN supplementation would protect obese diabetic db/db mice from obesity-related metabolic disorders. After four weeks of feeding of a 0.25% 4-STN-containing diet, dietary 4-STN was found to have significantly alleviated hyperlipidemia, hepatic cholesterol accumulation, and hyperinsulinemia; however, the effect was not sufficient to improve hepatic triglyceride accumulation or obesity. Further analysis demonstrated that dietary 4-STN significantly increased the content of free fatty acids and neutral steroids in the feces of db/db mice, indicating that the alleviation of hyperlipidemia by 4-STN was due to an increase in lipid excretion. In addition, dietary 4-STN significantly reduced the levels of desmosterol, a cholesterol precursor, in the plasma but not in the liver, suggesting that normalization of cholesterol metabolism by 4-STN is partly attributable to the suppression of cholesterol synthesis in extrahepatic tissues. In addition, dietary 4-STN increased the plasma and hepatic levels of 4-STN metabolites cholestanol (5α-cholestan-3β-ol) and coprostanol (5β-cholestan-3β-ol). Our results show that dietary 4-STN alleviates obesity-related metabolic disorders, such as hyperlipidemia, hepatic cholesterol accumulation, and hyperinsulinemia, in db/db mice.

Heat-killed Lactiplantibacillus plantarum Shinshu N-07 exerts antiobesity effects in western diet-induced obese mice.

The aim of this study was to evaluate the antiobesity effects of heat-killed Lactiplantibacillus plantarum Shinshu N-07 (N-07) isolated from fermented Brassica rapa L. Male mice were divided into three groups (n=10/group); normal diet, western diet (WD), or WD+N-07 (N-07) group and administered each diet for 56 days. The N-07 group showed significant suppression of body weight gain and epididymal fat, perirenal fat, and liver weights compared with the WD group. Higher levels of fecal total cholesterol, triglyceride (TG), and free fatty acid (FFA) were observed in the N-07 group than in the WD group. The mRNA expression of the cholesterol transporter ATP-binding cassette transporter G5 (ABCG5) was significantly increased in the small intestine of N-07-fed mice compared with WD-fed mice. Moreover, N-07 supplementation significantly increased the mRNA expression of ABCG5 and ABCG8 in Caco-2 cells. Furthermore, the TG- and FFA-removal ability of N-07 was confirmed to evaluate its soybean oil- and oleic acid-binding capacities in in vitro experiments. The antiobesity effects of N-07 might be due to its ability to promote lipid excretion by regulating cholesterol transporter expression and lipid-binding ability.

A novel fatty acid mimetic with pan-PPAR partial agonist activity inhibits diet-induced obesity and metabolic dysfunction-associated steatotic liver disease

ObjectiveThe prevalence of metabolic diseases is increasing globally at an alarming rate; thus, it is essential that effective, accessible, low-cost therapeutics are developed. Peroxisome proliferator-activated receptors (PPARs) are transcription factors that tightly regulate glucose homeostasis and lipid metabolism and are important drug targets for the treatment of type 2 diabetes and dyslipidemia. We previously identified LDT409, a fatty acid-like compound derived from cashew nut shell liquid, as a novel pan-active PPARα/γ/δ compound. Herein, we aimed to assess the efficacy of LDT409 in vivo and investigate the molecular mechanisms governing the actions of the fatty acid mimetic LDT409 in diet-induced obese mice. MethodsC57Bl/6 mice (6–11-month-old) were fed a chow or high fat diet (HFD) for 4 weeks; mice thereafter received once daily intraperitoneal injections of vehicle, 10 mg/kg Rosiglitazone, 40 mg/kg WY14643, or 40 mg/kg LDT409 for 18 days while continuing the HFD. During treatments, body weight, food intake, glucose and insulin tolerance, energy expenditure, and intestinal lipid absorption were measured. On day 18 of treatment, tissues and plasma were collected for histological, molecular, and biochemical analysis. ResultsWe found that treatment with LDT409 was effective at reversing HFD-induced obesity and associated metabolic abnormalities in mice. LDT409 lowered food intake and hyperlipidemia, while improving insulin tolerance. Despite being a substrate of both PPARα and PPARγ, LDT409 was crucial for promoting hepatic fatty acid oxidation and reducing hepatic steatosis in HFD-fed mice. We also highlighted a role for LDT409 in white and brown adipocytes in vitro and in vivo where it decreased fat accumulation, increased lipolysis, induced browning of WAT, and upregulated thermogenic gene Ucp1. Remarkably, LDT409 reversed HFD-induced weight gain back to chow-fed control levels. We determined that the LDT409-induced weight-loss was associated with a combination of increased energy expenditure (detectable before weight loss was apparent), decreased food intake, increased systemic fat utilization, and increased fecal lipid excretion in HFD-fed mice. ConclusionsCollectively, LDT409 represents a fatty acid mimetic that generates a uniquely favorable metabolic response for the treatment of multiple abnormalities including obesity, dyslipidemia, metabolic dysfunction-associated steatotic liver disease, and diabetes. LDT409 is derived from a highly abundant natural product-based starting material and its development could be pursued as a therapeutic solution to the global metabolic health crisis.

Intestinal Acyl-CoA synthetase 5 (ACSL5) deficiency potentiates postprandial GLP-1 & PYY secretion, reduces food intake, and protects against diet-induced obesity

ObjectiveIn the small intestine, the products of digestion of dietary triacylglycerol (TAG), fatty acids (FA) and monoacylglycerol, are taken up by absorptive cells, enterocytes, for systemic energy delivery. These digestion products can also bind receptors on endocrine cells to stimulate the release of hormones capable of influencing systemic energy metabolism. The initial phase of intestinal FA absorption involves the acylation of FAs to acyl-CoA by the acyl-CoA long chain synthetase (ACSL) enzymes. ACSL5 is abundantly expressed in the small intestinal epithelium where it is the major ACSL isoform, contributing approximately 80% of total ACSL activity. In mice with whole body deficiency of ACSL5, the rate of dietary fat absorption is reduced and energy expenditure is increased. However, the mechanisms by which intestinal ACSL5 contributes to intestinal FA metabolism, enteroendocrine signaling, and regulation of energy expenditure remain undefined. Here, we test the hypothesis that intestinal ACSL5 regulates energy metabolism by influencing dietary fat absorption and enteroendocrine signaling. MethodsTo explore the role of intestinal ACSL5 in energy balance and intestinal dietary fat absorption, a novel mouse model of intestine specific ACSL5 deficiency (ACSL5IKO) was generated by breeding ACSL5 floxed (ACSL5loxP/loxP) to mice harboring the tamoxifen inducible, villin-Cre recombinase. ACSL5IKO and control, ACSL5loxP/loxP mice were fed chow (low in fat) or a 60% high fat diet (HFD), and metabolic phenotyping was performed including, body weight, body composition, insulin and glucose tolerance tests, energy expenditure, physical activity, and food intake studies. Pair-feeding studies were performed to determine the role of food intake in regulating development of obesity. Studies of dietary fat absorption, fecal lipid excretion, intestinal mucosal FA content, and circulating levels of glucagon like peptide 1 (GLP-1) and peptide YY (PYY) in response to a TAG challenge were performed. Treatment with a GLP-1 receptor antagonist was performed to determine the contribution of GLP-1 to acute regulation of food intake. ResultsWe found that ACSL5IKO mice experienced rapid and sustained protection from body weight and fat mass accumulation during HFD feeding. While intestine specific deficiency of ACSL5 delayed gastric emptying and reduced dietary fat secretion, it did not result in increased excretion of dietary lipid in feces. Energy expenditure and physical activity were not increased in ACSL5IKO mice. Mice deficient in intestinal ACSL5 display significantly reduced energy intake during HFD, but not chow feeding. When HFD intake of control mice was matched to ACSL5IKO during pair-feeding studies, no differences in body weight or fat mass gain were observed between groups. Postprandial GLP-1 and PYY were significantly elevated in ACSL5IKO mice secondary to increased FA content in the distal small intestine. Blockade of GLP-1 signaling by administration of a long-acting GLP-1 receptor antagonist partially restored HFD intake of ACSL5IKO. ConclusionsThese data indicate that intestinal ACSL5 serves as a critical regulator of energy balance, protecting mice from diet-induced obesity exclusively by increasing satiety and reducing food intake during HFD feeding. The reduction in food intake observed in ACSL5IKO mice is driven, in part, by increased postprandial GLP-1 and PYY secretion. These effects are only observed during HFD feeding, suggesting that altered processing of dietary fat following intestinal ACSL5 ablation contributes to GLP-1 and PYY mediated increases in satiety.

Consumption of green tea infusion causes loss of nutrients through faeces in Wistar rats

Relationship between consumption of green tea infusion and faecal nutrient content was studied. Twelve male Wistar rats (aged 10 to 12 weeks and weighed 87 to 120 g) were divided into two groups of six rats each. The control group was placed on tap water, while the test group was placed on green tea infusion (0.20 g/50 ml) daily as the only source of fluid; for 28 days. Both groups consumed rat feed ad libitum. Phytochemicals detected in the infusion were tannins, saponins, alkaloids, flavonoids and phytosterols. The infusion increased test animals’ appetite for food (% coefficient of variation, % CV = 5.44) but decreased their appetite for the infusion (% CV = 72.41). Animals placed on the infusion (test group) did not gain more weight (% CV = 3.86) nor had better feed conversion ratio (% CV = 1.41). Faecal ash and fibre contents were not affected by tea consumption (% CV = 3.38 and 2.03, respectively). Control rats lost more carbohydrate and moisture (% CV = 27.58 and 9.58, respectively) but test rats lost more protein and lipids. Energy lost by test rats through faecal matter was not appreciably higher (101.31 vs 96.24 kcal/ 100 g sample; % CV = 2.56). Loss of certain nutrients in the test rats may have been triggered by the inhibitory action of polyphenols such as tannins present in the infusion on their digestive enzymes. In conclusion, the tea infusion elicited increased feacal excretion of proteins and lipids in treated animals.

Ingestion of Bean Leaves Reduces Metabolic Complications and Restores Intestinal Integrity in C57BL/6 Mice with Obesity Induced by a High-Fat and High-Fructose Diet.

Consumption of foods with fiber and compounds can promote gastrointestinal health and reduce obesity complications. Therefore, treatment with common bean leaves (BL) against obesity was evaluated in mice with a high-fat and high-fructose diet (HFFD) for 14 weeks. The bromatological and phytochemical characterization of BL were determined. Afterwards, the animals were supplemented with BL (10%) or a standard diet (SD) as a strategy to encourage a healthy diet for 12 additional weeks. Changes in body composition, lipid profile, and intestinal integrity were analyzed. The characterization of BL stood out for its content of 27.2% dietary fiber, total phenolics (475.04 mg/100 g), and saponins (2.2 mg/100 g). The visceral adipose tissue (VAT) decreased in the BL group by 52% compared to the HFFD group. Additionally, triglyceride levels were 23% lower in the BL consumption group compared to the HFFD group. The improvement in lipid profile was attributed to the 1.77-fold higher fecal lipid excretion in the BL consumption group compared to the HFFD group and the inhibition of pancreatic lipase by 29%. Furthermore, BL supplementation reduced the serum levels of IL-6 (4.4-fold) and FITC-dextran by 50% compared with those in the HFFD group. Metabolic endotoxemia was inhibited after BL supplementation (-33%) compared to the HFFD group. BL consumption as a treatment in obese mice reduces adipose tissue accumulation and improves the lipid profile. Furthermore, we report for the first time that BL consumption improves intestinal integrity.

A polyphenol-rich plant extract prevents hypercholesterolemia and modulates gut microbiota in western diet-fed mice.

Totum-070 is a combination of five plant extracts enriched in polyphenols to target hypercholesterolemia, one of the main risk factors for cardiovascular diseases. The aim of this study was to investigate the effects of Totum-070 on cholesterol levels in an animal model of diet-induced hypercholesterolemia. C57BL/6JOlaHsd male mice were fed a Western diet and received Totum-070, or not, by daily gavage (1g/kg and 3g/kg body weight) for 6 weeks. The Western diet induced obesity, fat accumulation, hepatic steatosis and increased plasma cholesterol compared with the control group. All these metabolic perturbations were alleviated by Totum-070 supplementation in a dose-dependent manner. Lipid excretion in feces was higher in mice supplemented with Totum-070, suggesting inhibition of intestinal lipid absorption. Totum-070 also increased the fecal concentration of short chain fatty acids, demonstrating a direct effect on intestinal microbiota. The characterization of fecal microbiota by 16S amplicon sequencing showed that Totum-070 supplementation modulated the dysbiosis associated with metabolic disorders. Specifically, Totum-070 increased the relative abundance of Muribaculum (a beneficial bacterium) and reduced that of Lactococcus (a genus positively correlated with increased plasma cholesterol level). Together, these findings indicate that the cholesterol-lowering effect of Totum-070 bioactive molecules could be mediated through multiple actions on the intestine and gut microbiota.

Biomimetic ROS-responsive hyaluronic acid nanoparticles loaded with methotrexate for targeted anti-atherosclerosis.

Atherosclerosis (AS), an inflammatory disease characterized by lipid accumulation, has a high global incidence and mortality rate. Recently, nanotherapeutic approaches that target pathological sites and improve drug bioavailability and biocompatibility hold great promise for AS treatment. In this study, a biomimetic ROS-responsive hyaluronic acid-based nanomaterial was prepared for targeted anti-AS. Specifically, a safe ROS-responsive carrier based on hyaluronic acid (HSP) was prepared to load methotrexate (MTX), a drug known for its ability to enhance lipid excretion, resulting in the formation of MTX-loaded nanoparticles (MTXNPs). Furthermore, the macrophage membrane was coated on the surface of MTXNPs to obtain MM/MTXNPs. Both MTXNPs and MM/MTXNPs exhibited ROS responsiveness and demonstrated excellent biocompatibility. In vitro experiments revealed that MM/MTXNPs could evade macrophage phagocytosis and exhibited high uptake rates by inflamed endothelial cells. MM/MTXNPs also reduced lipid accumulation in foam cells. In vivo experiments showed that MM/MTXNPs exhibited superior accumulation at AS plaque sites, facilitated by the surface membrane layer containing integrin α4β1 and CD47, resulting in an enhanced therapeutic effect in inhibiting plaque development compared to free MTX and MTXNPs. Therefore, HSP represents a promising nanocarrier to load hydrophobic MTX, enabling effective and biocompatible enhancement of AS treatment.

A comparative study of the hypolipidemic effects and mechanisms of action of Laminaria japonica- and Ascophyllum nodosum-derived fucoidans in apolipoprotein E-deficient mice.

The structural characteristics of fucoidans exhibit species and regional diversity. Previous studies have demonstrated that Laminaria japonica- and Ascophyllum nodosum-derived fucoidans have type I and type II fucosyl chains, respectively. These chemical differences may contribute to distinct hypolipidemic effects and mechanisms of action. Chemical analysis demonstrated that the percentage contents of sulfate, glucuronic acid, and galactose were higher in L. japonica-derived fucoidans than those of A. nodosum-derived fucoidans. In hyperlipidemic apolipoprotein E-deficient mice, both A. nodosum- and L. japonica-derived fucoidans significantly decreased the plasma and hepatic levels of total cholesterol and triglyceride, leading to the reduction of atherosclerotic plaques. Western blotting experiments demonstrated that these fucoidans significantly enhanced the expression and levels of scavenger receptor B type 1, cholesterol 7 alpha-hydroxylase A1, and peroxisome proliferator-activated receptor (PPAR)-α, contributing to circulating lipoprotein clearance and fatty acid degradation, respectively. Differentially, L. japonica-derived fucoidan significantly increased the LXR/ATP-binding cassette G8 signaling pathway in the small intestine, as revealed by real-time quantitative PCR, which may lead to further cholesterol and other lipid excretion. Collectively, these data are useful for understanding the hypolipidemic mechanisms of action of seaweed-derived fucoidans, and their potential application for the prevention and/or treatment of atherosclerotic cardiovascular diseases.

Dietary supplementation with capsaicinoids alleviates obesity in mice fed a high-fat-high-fructose diet.

Capsaicinoids are the pungent compounds in chili peppers. The present study investigated the effect of capsaicinoids on obesity in mice induced by a high-fat-high-fructose diet. Thirty-two male C57BL/6J mice were randomly divided into four groups (n = 8) and fed one of the following diets, namely, a low-fat diet (LFD), a high-fat-high-fructose diet (HFF), an HFF + 0.015% capsaicinoids (LCP), and an HFF + 0.045% capsaicinoids (HCP), for 12 weeks. Results showed that capsaicinoids significantly reversed HFF-induced obesity. Supplementation with capsaicinoids improved glucose tolerance, reduced plasma lipids, and attenuated inflammation. Capsaicinoids also reduced hepatic lipid accumulation by upregulating the expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). In addition, capsaicinoids enhanced the production of fecal short-chain fatty acids (SCFAs) and increased the fecal excretion of lipids. Gut microbiota analysis revealed that capsaicinoids decreased the Firmicutes/Bacteroidetes ratio and beneficially reconstructed the microbial community. However, the effects of capsaicinoids on intestinal villus length and lipid tolerance were negligible. In conclusion, capsaicinoids effectively attenuated HFF-induced obesity and metabolic syndrome by favorably modulating lipid metabolism, improving SCFA production, and reshaping gut microbial structure.

Plasma cholesterol level reduction in albino rats by β-d glucan (pleuran) from Plurotus ostreatus

Abstract Background: The progression of atherosclerotic lesions and coronary artery disease is known to be accelerated by hypercholesterolemia. Objective: This study investigated at the effects of adding an extract of oyster mushroom fruiting bodies to rats with high and normal cholesterol levels on their biochemical and histological changes. This study was aimed to assess the effect of Pleurotus ostreatus extraction on hypercholesterolemia in albino rats and show the revelation of the relationship of these with some biochemical parameters. Materials and Methods: Three sets of ten albino rats each were formed from 6-week-old rats. To lower plasma total cholesterol, triglycerides, low-density lipoprotein (LDL), total lipid, phospholipids, and LDL/high-density lipoprotein, extracts of P. ostreatus fruiting bodies were fed to hypercholesterolemic rats. Results: In rats with high cholesterol, feeding oyster mushrooms drastically lowered body weight. The excretion of total lipids and cholesterol in feces was enhanced by feeding mushrooms. Conclusion: These findings imply that P. ostreatus food supplement improved health by altering hypercholesterolemic rats’ atherogenic lipid profiles.

Divergence in aerobic capacity influences hepatic and systemic metabolic adaptations to bile acid sequestrant and short-term high-fat/sucrose feeding in rats.

High versus low aerobic capacity significantly impacts the risk for metabolic diseases. Rats selectively bred for high or low intrinsic aerobic capacity differently modify hepatic bile acid metabolism in response to high-fat diets (HFDs). Here we tested if a bile acid sequestrant would alter hepatic and whole body metabolism differently in rats with high and low aerobic capacity fed a 1-wk HFD. Male rats (8 mo of age) that were artificially selected to be high (HCR) and low-capacity runners (LCR) with divergent intrinsic aerobic capacities were transitioned from a low-fat diet (LFD, 10% fat) to an HFD (45% fat) with or without a bile acid sequestrant (BA-Seq, 2% cholestyramine resin) for 7 days while maintained in an indirect calorimetry system. HFD + BA-Seq increased fecal excretion of lipids and bile acids and prevented weight and fat mass gain in both strains. Interestingly, HCR rats had increased adaptability to enhance fecal bile acid and lipid loss, resulting in more significant energy loss than their LCR counterpart. In addition, BA-Seq induced a greater expression of hepatic CYP7A1 gene expression, the rate-limiting enzyme of bile acid synthesis in HCR rats both on HFD and HFD + BA-Seq diets. HCR displayed a more significant reduction of RQ in response to HFD than LCR, but HFD + BA-Seq lowered RQ in both groups compared with HFD alone, demonstrating a pronounced impact on metabolic flexibility. In conclusion, BA-Seq provides uniform metabolic benefits for metabolic flexibility and adiposity, but rats with higher aerobic capacity display adaptability for hepatic bile acid metabolism.NEW & NOTEWORTHY The administration of bile acid sequestrant (BA-Seq) has uniform metabolic benefits in terms of metabolic flexibility and adiposity in rats with high and low aerobic capacity. However, rats with higher aerobic capacity demonstrate greater adaptability in hepatic bile acid metabolism, resulting in increased fecal bile acid and lipid loss, as well as enhanced fecal energy loss.

Combating Obesity: Harnessing the Synergy of Postbiotics and Prebiotics for Enhanced Lipid Excretion and Microbiota Regulation

Obesity is a chronic metabolic disease that can be induced by a high-fat diet (HFD) and predisposes to a variety of complications. In recent years, various bioactive substances, such as probiotics, prebiotics, and postbiotics, have been widely discussed because of their good anti-lipid and anti-inflammatory activities. In this paper, soybean protein isolate was used as a substrate to prepare the postbiotic. Compound prebiotics (galactose oligosaccharides, fructose oligosaccharides, and lactitol) preparation Aunulife Postbiotics and Prebiotics Composition (AYS) is the research object. Weight loss and bowel movements in mice induced by a high-fat diet were studied. Moreover, qualitative and quantitative analyses of small-molecule metabolites in AYS were performed to identify the functional molecules in AYS. After 12 weeks of feeding, the weight gain of mice that were fed with high-dose AYS (group H) and low-dose AYS (group L) from 4 to 12 weeks was 6.72 g and 5.25 g (p < 0.05), both of which were significantly lower than that of the high-fat diet (group DM, control group) group (7.73 g) (p < 0.05). Serum biochemical analysis showed that TC, TG, and LDL-C levels were significantly lower in mice from the H and L groups (p < 0.05). In addition, the fecal lipid content of mice in the L group reached 5.89%, which was significantly higher than that of the DM group at 4.02% (p < 0.05). The study showed that AYS changed the structure of the intestinal microbiota in mice on a high-fat diet, resulting in a decrease in the relative abundance of Firmicutes and Muribaculaceae and an increase in the relative abundance of Bacteroidetes, Verrucomicrobia, and Lactobacillus. The metabolomics study results of AYS showed that carboxylic acids and derivatives, and organonitrogen compounds accounted for 51.51% of the AYS metabolites, among which pantothenate, stachyose, betaine, and citrate had the effect of preventing obesity in mice. In conclusion, the administration of prebiotics and postbiotic-rich AYS reduces weight gain and increases fecal lipid defecation in obese mice, potentially by regulating the intestinal microbiota of mice on a high-fat diet.

221 Increasing Functional Amino Acid Ratios Does Not Improve Growth Performance in Pigs Raised Under Poor Sanitary Conditions When Fed with Individual Precision Feeding Or Conventional Feeding Systems

Abstract Immune system activation redirects dietary nutrients to defense mechanisms, thereby impairing growth performance of pigs. Supplementing pigs with functional amino acids (AA) such as Met, Thr and Trp was shown to support the immune system and reduce the negative effects on growth. However, pigs respond differently to immune stressors which increase herd variability. In this context, individual precision feeding (IPF) might be an alternative approach to reduce herd variability and increase nutrient efficiency in immune challenged pigs. This study aimed to evaluate growth performance, body composition, nitrogen (N) efficiency and haptoglobin and triglycerides serum concentration in growing pigs raised in poor sanitary conditions (PoorSC). The PoorSC was characterized by oral inoculation with 2 × 109 cfu of Salmonella typhimurium and manure spreading on the pen floor. Sixty gilts (23 ± 2.8 kg BW) were distributed in BW blocks according to a 2 dietary (D) × 2 feeding system (FS) factorial arrangement composed of to 2 diets [control (CN): INRA ideal AA ratio or supplemented (AA+) 120% of the ideal ratio for Met, Thr and Trp] and 2 feeding systems [conventional (GP) or IPF]. GP pigs were fed with a unique diet that matched the SID Lys requirement of the 80th-percentile pig at the beginning of the trial whereas the IPF pigs received a diet tailored daily to each pig requirement. All pigs were housed in the same pen and fed ad libitum during 28 experimental days with automatic feeding stations able to provide to each pig the assigned diet. Body composition was obtained by dual X-ray absorptiometry at days 0 and 28 and blood samples were collected at d 28. Data were analyzed with D and FS and their interaction as main fixed factors and body weight (BW) blocks as a random effect (Table 1). Haptoglobin serum concentration increased from d 0 to 28 regardless of FS and D (P < 0.10). IPF pigs fed with CN diet had the lightest BW at the end of the trial (P ≤ 0.10; FS × D), whereas BW was similar for the other treatments. However, across diets, IPF pigs had final BW, and protein, ADG, G:F, protein and lipid deposition, N intake and excretion and circulating triglycerides that were less than GP pigs. N utilization efficiency was similar across treatments. Additionally, increasing the provision of the studied functional AA did not improve pig performance. Thus, showing no benefits in increasing AA ratios for growth and immune response. The increased triglycerides concentration and low protein and lipid deposition suggests that IPF pigs prioritized the immune system to the expense of protein and lipid accretion. In conclusion, AA supplementation and IPF do not improve growth performance and N efficiency of pigs raised in poor sanitary conditions.

Dietary Bamboo Charcoal Decreased Visceral Adipose Tissue Weight by Enhancing Fecal Lipid Excretions in Mice with High-Fat Diet-Induced Obesity.

Bamboo charcoal (BC) powder is prepared from thick bamboo stems via dry distillation and is often used for food coloring. Due to the unique structure of the micropores in bamboo stems, BC powder also serves as an indigestible carrier to prevent the absorption of toxic substances and nutrients from the digestive tract. This study evaluated the health-promoting function of BC, particularly its effects in decreasing visceral adipose tissue in a mouse model with high-fat diet (HFD)-induced obesity. Four-week-old male C57BL/6J mice were divided into three groups and fed either a low-fat (LF) diet (7% fat), HF diet (25% fat), or HF diet with 0.5% BC (HF-BC). After 80 days, the HF-BC diet was found to have decreased epididymal and mesenteric white adipose tissue weights compared to HFD. The inhibition of visceral fat accumulation by BC intake was partly due to enhanced fecal fatty acid excretion induced by its bile acid-binding and pancreatic lipase inhibition. Contrarily, the gut microbiota, known to influence systemic energy metabolism, did not change significantly between the HF and HF-BC groups. These results indicate that dietary BC inhibits visceral fat accumulation, which could reduce obesity development.