High-fat Diet-induced Metabolic Syndrome Research Articles

Organosulfur Compounds, S-Allyl-L-Cysteine and S-Ethyl-L-Cysteine, Target PCSK-9/LDL-R-Axis to Ameliorate Cardiovascular, Hepatic, and Metabolic Changes in High Carbohydrate and High Fat Diet-Induced Metabolic Syndrome in Rats.

Metabolic syndrome (MetS) is an ever-evolving set of diseases that poses a serious health risk in many countries worldwide. Existing evidence illustrates that individuals with MetS have a 30%-40% higher chance of acquiring type 2 diabetes mellitus (T2DM), cardiovascular disease (CVD), or both. This study was undertaken to uncover the regulatory role of natural organosulfur compounds (OSCs), S-allyl-L-cysteine (SAC), and S-ethyl-L-cysteine (SEC), in targeting high carbohydrate high fat (HCHF)-diet-induced MetS-associated risk management. Our findings suggested that SAC and SEC ameliorated HCHF-diet-induced diabetic profiles, plasma lipid and lipoprotein level, liver function, oxidative-stress, inflammatory cytokines, and chemokines including monocyte chemoattractant protein-1 (MCP-1), lipid peroxidation, plasma proprotein convertase subtilisin/kexin type-9 (PCSK-9), and high-sensitivity C-reactive protein (hs-CRP). Moreover, the assessment of the hepatic mRNA expression of the key genes involved in cholesterol homeostasis depicted that SAC and SEC downregulated the PCSK-9 mRNA expression via targeting the expression of HNF-1α, a transcriptional activator of PCSK-9. On the other hand, the LDL-receptor (LDL-R) expression was upregulated through the activation of its transcriptional regulator sterol regulatory element binding protein-2 (SREBP-2). In addition, the activity and the mRNA expression of 3-hydroxy-3-methylglutaryl coenzyme-A reductases (HMG-R) and peroxisome proliferator-activated receptors (PPARs) were also improved by the treatment of SAC and SEC. We concluded that SAC and SEC can protect against MetS via improving the lipid and lipoprotein content, glycemic indices, hepatic function, targeting the inflammatory cascades, and oxidative imbalance, regulation of the mRNA expression of PCSK-9, LDL-R, SREBP-2, HNF-1α, PPARs, and inflammatory biomarkers.

Metformin Regulates Cardiac Ferroptosis to Reduce Metabolic Syndrome-Induced Cardiac Dysfunction.

High-fat diet-induced metabolic syndrome (MetS) is closely associated with cardiac dysfunction. Recent research studies have indicated a potential association between MetS and ferroptosis. Furthermore, metformin can alleviate MetS-induced cardiac ferroptosis. Metformin is a classic biguanide anti-diabetic drug that has protective effects on cardiovascular diseases, which extend beyond its indirect glycemic control. This study aimed to assess whether MetS mediates cardiac ferroptosis, thereby causing oxidative stress and mitochondrial dysfunction. The results revealed that metformin can mitigate cardiac reactive oxygen species and mitochondrial damage, thereby preserving cardiac function. Mechanistic analysis revealed that metformin upregulates the expression of cardiac Nrf2. Moreover, Nrf2 downregulation compromises the cardio-protective effects of metformin. In summary, this study indicated that MetS promotes cardiac ferroptosis, and metformin plays a preventive and therapeutic role, partially through modulation of Nrf2 expression.

Protective effect of Fu Brick tea on high-fat diet-induced metabolic syndrome: Relevant to protecting the intestinal barrier and regulating the gut microbiota

Protective effect of Fu Brick tea on high-fat diet-induced metabolic syndrome: Relevant to protecting the intestinal barrier and regulating the gut microbiota

Effects of different fractions of polysaccharides from Dictyophora indusiata on high-fat diet-induced metabolic syndrome in mice

Dictyophora indusiata is a common edible mushroom with great potential in the field of medicine against metabolic disorders, inflammation, and immunodeficiency. Our previous studies have shown that different fractions of the polysaccharide from Dictyophora indusiata (DIP) have various structural characteristics and morphology. However, the impact of the structural features on the protective effects of DIP against metabolic syndrome remains unclear. In this study, three distinct polysaccharide fractions have been extracted from Dictyophora indusiata and a high-fat diet-induced metabolic syndrome (MetS) was constructed in mice. The effects of these fractions on a range of MetS-associated endpoints, including abnormal blood glucose, lipid profiles, body fat content, liver function, intestinal microbiota and their metabolites were investigated. Through correlation analysis, the potential link between the monosaccharide composition of the polysaccharides and their biological activities was determined. The study aimed to explore the potential mechanisms and ameliorative effects of these polysaccharide fractions on MetS, thereby providing statistical evidence for understanding the relationship between monosaccharides composition of Dictyophora indusiata polysaccharides and their potential utility in treating metabolic disorders.

Endothelin receptor B-deficient mice are protected from high-fat diet-induced metabolic syndrome

ObjectiveEndothelin receptor B (ETB) together with ETA mediates cellular effects of endothelin 1 (ET-1), an autocrine and endocrine peptide produced by the endothelium and other cells. It regulates vascular tone and controls kidney function. Metabolic syndrome is due to high caloric intake and is characterized by insulin resistance, dyslipidemia, and white adipose tissue (WAT) accumulation. ETA/ETB antagonism has been demonstrated to favorably influence insulin resistance. Our study explored the role of ETB in metabolic syndrome. MethodsWild type (etb+/+) and rescued ETB-deficient (etb−/−) mice were fed a high-fat diet, and energy, glucose, and insulin metabolism were analyzed, and hormones and lipids measured in serum and tissues. Cell culture experiments were performed in HepG2 cells. ResultsCompared to etb+/+ mice, etb−/− mice exhibited better glucose tolerance and insulin sensitivity, less WAT accumulation, lower serum triglycerides, and higher energy expenditure. Protection from metabolic syndrome was paralleled by higher hepatic production of fibroblast growth factor 21 (FGF21) and higher serum levels of free thyroxine (fT4), stimulators of energy expenditure. ConclusionsETB deficiency confers protection from metabolic syndrome by counteracting glucose intolerance, dyslipidemia, and WAT accumulation due to enhanced energy expenditure, effects at least in part dependent on enhanced production of thyroid hormone/FGF21. ETB antagonism may therefore be a novel therapeutic approach in metabolic syndrome.

Beneficial Effects of 6-Gingerol on Fatty Pancreas Disease in High-Fat High-Fructose Diet-Induced Metabolic Syndrome Rat Model.

To examine the effects of 6-gingerol (6-G) in overcoming fatty pancreas disease of high-fat high-fructose (HFHF) diet-induced metabolic syndrome in rats. Male Sprague-Dawley rats were randomly divided into 5 groups. The healthy-control group (normal diet, n = 5) received a standard diet. The HFHF group (HFHF; n = 20) received an HFHF diet and a single-dose intraperitoneal injection of streptozotocin (22 mg/kgBW) at week 8. Metabolic syndrome-confirmed rats received 6-G at doses of 50 (6-G 50, n = 5), 100 (6-G 100, n = 5), and 200 (6-G 200, n = 5) mg/kgBW, respectively, for 8 weeks. All rats were killed at week 16. Pancreatic tissue and blood samples were obtained for histological and amylase analysis. The serum amylase, MDA, mRNA of TNF-α, and IL-6 significantly increased, whereas GPx decreased in the HFHF group as compared with the normal diet group, respectively. Rats in the HFHF group showed pancreatic lipid accumulation and a decreased mean number of α- and β-cells in the pancreas. Meanwhile, all rats in 6-G at all dose groups showed improvement in all parameters and histopathological scores for lipid accumulation. 6-Gingerol could attenuate pancreatic lipid accumulation and improve the cell number of α- and β-cells in the pancreas, leading to improvements in fatty pancreas disease.

Reducing gut microbiome-driven adipose tissue inflammation alleviates metabolic syndrome

BackgroundThe gut microbiota contributes to macrophage-mediated inflammation in adipose tissue with consumption of an obesogenic diet, thus driving the development of metabolic syndrome. There is a need to identify and develop interventions that abrogate this condition. The hops-derived prenylated flavonoid xanthohumol (XN) and its semi-synthetic derivative tetrahydroxanthohumol (TXN) attenuate high-fat diet-induced obesity, hepatosteatosis, and metabolic syndrome in C57Bl/6J mice. This coincides with a decrease in pro-inflammatory gene expression in the gut and adipose tissue, together with alterations in the gut microbiota and bile acid composition.ResultsIn this study, we integrated and interrogated multi-omics data from different organs with fecal 16S rRNA sequences and systemic metabolic phenotypic data using a Transkingdom Network Analysis. By incorporating cell type information from single-cell RNA-seq data, we discovered TXN attenuates macrophage inflammatory processes in adipose tissue. TXN treatment also reduced levels of inflammation-inducing microbes, such as Oscillibacter valericigenes, that lead to adverse metabolic phenotypes. Furthermore, in vitro validation in macrophage cell lines and in vivo mouse supplementation showed addition of O. valericigenes supernatant induced the expression of metabolic macrophage signature genes that are downregulated by TXN in vivo.ConclusionsOur findings establish an important mechanism by which TXN mitigates adverse phenotypic outcomes of diet-induced obesity and metabolic syndrome. TXN primarily reduces the abundance of pro-inflammatory gut microbes that can otherwise promote macrophage-associated inflammation in white adipose tissue.7MrSGPEkxmDTc41cVX6rPoVideo

The Role of Green Tea on the Regulation of Gut Microbes and Prevention of High-Fat Diet-Induced Metabolic Syndrome in Mice.

Green tea is a popular non-alcoholic beverage consumed worldwide and has been shown to be beneficial for human health. However, further exploration is needed to fully understand its function in reducing obesity and regulating gut microbes. Here, we investigated the modulatory effects of green tea and its functional components on high-fat diet (HF)-induced metabolic alterations and gut microbiota in obese mice. Our results showed that 1%, 2%, and 4% of green tea promotes weight loss, with the 2% and 4% groups exhibiting distinct gut microflora clusters compared to the HF group. These results were comparable to those observed in the tea polyphenols (TPP)-treated group, suggesting the TPP in green tea plays a crucial role in body weight control and gut microbiota regulation. Additionally, 32 bacteria were identified as potential obesity markers via 16S rRNA gene sequencing. The 16SrDNA gene is a chromosomal gene present in all bacterial species, highly conserved in structure and function, that can reflect the differences between different taxa. The 16S rRNA-based analysis revealed that Akkermansia, a gut-beneficial bacteria, significantly increased in the TPP group.

Lactobacillus plantarum S9 alleviates lipid profile, insulin resistance, and inflammation in high-fat diet-induced metabolic syndrome rats

Probiotics are considered to play an crucial role in the treatment of high-fat diet (HFD)-induced lipid metabolic diseases, including metabolic syndrome (MS). This study aimed to investigate the effects of Lactobacillus plantarum S9 on MS in HFD-fed rats, and to explore the underlying role of probiotics in the treatment of MS. Sprague-Dawley rats were fed with HFD for 8 weeks, followed by the treatment of L. plantarum S9 for 6 weeks, and The body weight and blood glucose level of rats were detected on time. The results showed that L. plantarum S9 significantly decreased the body weight gain, Lee’s index, and liver index. Additionally, L. plantarum S9 reduced the levels of serum lipids and insulin resistance. L. plantarum S9 also decreased the levels of alanine aminotransferase (ALT) and aspartate transaminase (AST) in liver. Moreover, the serum levels of MS-related inflammatory signaling molecules, including lipopolysaccharide (LPS) and tumor necrosis factor-α (TNF-α), were significantly elevated. Western blot analysis showed that L. plantarum S9 inhibited the activation of nuclear factor-κB (NF-κB) pathway, decreased the expression level of Toll-like receptor 4 (TLR4), suppressed the activation of inflammatory signaling pathways, and reduced the expression levels of inflammatory factors in HFD-fed rats. Moreover, it further decreased the ratios of p-IκBα/IκBα, p-p65/NF-κB p65, and p-p38/p38. In summary, L. plantarum S9, as a potential functional strain, prevents or can prevent onset of MS.

Six types of tea extracts attenuated high-fat diet-induced metabolic syndrome via modulating gut microbiota in rats

An important puzzle for tea consumers is which type of tea is effective in treating metabolic syndrome (MS). In this study, the effects of six types of tea extracts (TEs) on high-fat diet (HFD)-induced MS, as well as chemical components of six TEs, were investigated and compared. Each TE consisted of representative tea originated from different places in China to avoid one-sidedness of sampling. All six TEs were found to attenuate MS and ameliorate intestinal barrier function in HFD-fed rats. Further, white tea performed better in body weight control, while dark tea had more advantages in protecting intestinal barrier. Moreover, all six TEs alleviated the gut microbiota dysbiosis, which was manifested by decreased Firmicutes/Bacteroidetes ratio and enriched beneficial bacteria, such as Akkermansia, Bacteroides, and Bifidobacterium. Together, all six TEs attenuate HFD-induced MS although their efficiency varies, and this therapeutic effect is related to the modulation of gut microbiota.

Rosuvastatin and co-enzyme Q10 improve high-fat and high-fructose diet-induced metabolic syndrome in rats via ameliorating inflammatory and oxidative burden

The prevalence of metabolic syndrome (MetS) has been rising alarmingly and it has now become a global concern causing an enormous economic burden on the health care system. MetS is generally linked to complications in lipid metabolism, oxidative stress and low grade inflammation. The aim of the current study was to evaluate the effect of rosuvastatin, co-enzyme Q10 (CoQ10), and their combination on blood pressure, blood sugar, dyslipidemia, and liver function in rats with MetS induced by high fructose and high fat diet (HF-HFD) and the possible underlying mechanism. Oral administration of rosuvastatin (10 mg/kg/day), CoQ10 (10 mg/kg/day) and their combination for 4 weeks in HF-HFD-fed rats elevated serum high density lipoprotein and reduced glutathione. On the other hand, treatment with rosuvastatin, CoQ10 or their combination decreased the serum levels of malondialdehyde, triglycerides, total cholesterol, and low density lipoprotein-cholesterol as well as systolic blood pressure, body weight and fasting blood glucose level. In addition, the drugs or their combination declined serum pro-inflammatory cytokines, namely tumor necrosis factor-α and interleukin-1β. In conclusion, our results showed that rosuvastatin or CoQ10 protected against HF-HFD-induced MetS through the regulation of dyslipidemia, elevated blood glucose, elevated blood pressure, antioxidant defenses and inflammatory response. Rosuvastatin or CoQ10 also alleviated the impairment of liver function that was induced by HF-HFD. Interestingly, CoQ10 augmented rosuvastatin's effect in ameliorating MetS, via exerting synergistic modulatory effects on oxidative stress and inflammation. Thus, rosuvastatin and CoQ10 combination therapy may have possible applications in ameliorating metabolic disorders.

Polyphenols and Polysaccharides from Morus alba L. Fruit Attenuate High-Fat Diet-Induced Metabolic Syndrome Modifying the Gut Microbiota and Metabolite Profile.

Morus alba L. fruit, a medicinal and edible fruit in East Asia, showed potential health-promoting effects against metabolic syndrome (MetS). However, both the protective effects and mechanisms of different fractions extracted from Morus alba L. fruit against MetS remain unclear. Additionally, the gut microbiota and its metabolites are regarded as key factors in the development of MetS. This study aimed to investigate the potential role of polyphenols and polysaccharides derived from Morus alba L. fruit against MetS in high-fat diet (HFD)-fed mice, individually and in combination, focusing on remodeling effects on gut microbiota and metabolite profiles. In the study, polyphenols and polysaccharides derived from Morus alba L. fruit improved the traditional pharmacodynamic parameters of MetS, including reductions in body weight (BW) and fat accumulation, improvement in insulin resistance, regulation of dyslipidemia, prevention of pathological changes in liver, kidney and proximal colon tissue, and suppressive actions against oxidative stress. In particular, the group treated with polyphenols and polysaccharides in combination showed better efficacy. The relative abundance of beneficial bacterial genera Muribaculum and Lachnospiraceae_NK4A136_group were increased to various degrees, while opportunistic pathogens such as Prevotella_2, Bacteroides, Faecalibacterium and Fusobacterium were markedly decreased after treatments. Moreover, fecal metabolite profiles revealed 23 differential metabolites related to treatments with polyphenols and polysaccharides derived from Morus alba L. fruit, individually and in combination. Altogether, these results demonstrated that polyphenols and polysaccharides derived from Morus alba L. fruit attenuated MetS in HFD-fed mice, and improved the gut microbiota composition and fecal metabolite profiles.

Impact of protocatechuic acid on high fat diet-induced metabolic syndrome sequelae in rats

The study aimed to assess the possible protective impact of protocatechuic acid (PCA) on high fat diet (HFD)-induced metabolic syndrome (Mets) sequelae in rats. Forty-two male Sprague–Dawley (SD) rats were randomly grouped as follows: CTR group; PCA group; HFD group; HFD-PCA group and HFD-MET group. Rats were fed on standard diet or HFD for 14 weeks. HFD-fed rats exhibited significant decreases in food intake and adiponectin (ADP) level; yet, body weight and anthropometrical parameters were significantly increased. Moreover, insulin sensitivity was impaired as indicated by significant elevation in glucose AUC during oral glucose tolerance test (OGTT), fasting serum glucose, fasting serum insulin and homeostasis model assessment of insulin resistance (HOMA-IR) index. Furthermore, chronic HFD feeding elicited significant increases in serum lipid profile and free fatty acids (FFAs) with concomitant hepatic steatosis. Additionally, serum C-reactive protein (CRP), interleukin 1b (Il-1b) and monocyte chemoattractant protein 1(MCP-1) levels were increased. Also, HFD-fed rats exhibited an increase in MDA level, while superoxide dismutase (SOD) and glutathione (GSH) activities were decreased. Moreover, the insulin-signaling pathway was markedly impaired in soleus muscles as indicated by a decrease in insulin-induced AKT phosphorylation. Histopathologically, adipose tissues showed significant increase in adipocyte size. Also, flow cytometry analysis of adipose tissue confirmed a significant increase in the percentage of number of CD68+ cells. PCA administration succeeded to attenuate HFD-induced obesity, insulin resistance, oxidative stress and inflammation. In conclusion, PCA administration could protect against HFD-induced Mets, possibly via its hypoglycemic, insulin-sensitizing, anti-oxidant and anti-inflammatory effects.

Polysaccharide from Flammulina velutipes attenuates markers of metabolic syndrome by modulating the gut microbiota and lipid metabolism in high fat diet-fed mice.

Natural biological macromolecules with putative functions of gut microbiota regulation possess the advantage of improving metabolic syndrome (MS). In this research, we aimed to determine the effects of Flammulina velutipes polysaccharide (FVP) (Expt. 1) and fecal microbiota transplantation (FMT) (Expt. 2) on MS-related disorders, gut microbiota structure changes and their underlying mechanisms in a murine model fed with high-fat diet (HFD). In Expt. 1, six-week-old male C57BL/6J mice were fed with a control diet (10% calories from fat) or a high fat diet (45% calories from fat), administered with saline or FVP (0.4 mg per g b.w.) by gavage over a 12-week period. In Expt. 2, mice were fed with a HFD, administered with fecal supernatants from healthy and FVP-fed donor mice for 12 weeks simultaneously. The body mass, blood lipid levels and blood glucose homeostasis of mice were analyzed, and total RNA from mouse liver and adipose tissue were extracted by TRIzol and the lipid metabolism-related gene expressions were calculated by qRT-PCR. Gut microbiota changes were evaluated by high-throughput sequencing. Results indicated that FVP and FMT supplementations showed an attenuation effect on mouse obesity, hyperlipidemia and insulin resistance. Up-regulated expressions of Ampkα1 and Ppara were found both in FVP and FMT treatment groups. Different changes were found in the gut microbiota caused by FVP and FMT, respectively. PICRUSt analysis indicated that compared with FVP supplementation, FMT showed a significant effect on regulating lipid metabolism in HFD-fed mice. The findings from this study indicated that oral administrations of FVP or FMT could significantly attenuate MS-related obesity, hyperlipidemia and insulin resistance in HFD-fed mice, and the beneficial effects may be mediated through lipid metabolism and gut microbiota regulation in different ways. These results improve the understanding of the functional activity of FVP as prebiotics.

Solasodine with Coenzyme Q10 Supplementation Ameliorates High Fat Diet-Induced Metabolic Syndrome in Rats by Modulating Adipokines and Lipid Peroxidation

Solasodine with Coenzyme Q10 Supplementation Ameliorates High Fat Diet-Induced Metabolic Syndrome in Rats by Modulating Adipokines and Lipid Peroxidation

Celastrol targets adenylyl cyclase-associated protein 1 to reduce macrophages-mediated inflammation and ameliorates high fat diet-induced metabolic syndrome in mice

Metabolic syndrome is a clustering of metabolic disorder with unclear molecular mechanism. Increasing studies have found that the pathogenesis and progression of metabolic syndrome are closely related to inflammation. Here, we report celastrol, a traditional Chinese medicine, can improve high fat diet-induced metabolic syndrome through suppressing resistin-induced inflammation. Mechanistically, celastrol binds to adenylyl cyclase associated protein 1 (CAP1) and inhibits the interaction between CAP1 and resistin, which restrains the cyclic adenylate monophosphate (cAMP)–protein kinase A (PKA)–nuclear factor kappa-B (NF-κB) signaling pathway and ameliorates high fat diet-induced murine metabolic syndrome. Knockdown of CAP1 in macrophages abrogated the resistin-mediated inflammatory activity. In contrast, overexpression of CAP1 in macrophages aggravated inflammation. Taken together, our study identifies celastrol, which directly targets CAP1 in macrophages, might be a promising drug candidate for the treatment of inflammatory metabolic diseases, such as metabolic syndrome.

Sulfated polysaccharides from Undaria pinnatifida improved high fat diet-induced metabolic syndrome, gut microbiota dysbiosis and inflammation in BALB/c mice

Undaria pinnatifida was shown to reduce serum lipids and fat accumulation and produce beneficial effect on type 2 diabetes, but its effect on intestinal micro-ecology remains unclear. This study showed that sulfated polysaccharides from U. pinnatifida (UPSP) reduced weight gain, fat accumulation and metabolic disorders in mice fed with high fat diet (HFD). UPSP not only alleviated HFD-induced microbiota dysbiosis indicated as increased abundances of some Bacteroidales members that had positive correlations with the improvement of physiological indexes, but also maintained gut barrier integrity and reduced metabolic endotoxemia. A dose-effect relationship was observed between the dose of UPSP and its effect on some physiological indexes, gut microbiota community and nutrient utilization. The in vitro result showed that the use of Bacteroides species within Bacteroidales on UPSP was species-dependent, and the dose of UPSP affected the growth properties of some Bacteroides species. It implied that UPSP can be considered as prebiotic agent to prevent gut dysbiosis and obesity-related diseases in obese individuals.

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.

Development of Fortified Citrus Olive Oils: From Their Production to Their Nutraceutical Properties on the Cardiovascular System.

Recently the use of food by-products as natural sources of biologically active substances has been extensively investigated especially for the development of functional foods fortified with natural antioxidants. Due to their content of bioactive compounds, such as carotenoids, flavonoids and limonoids, citrus peels could be suitable to formulate enriched olive oils able to boost healthy nutrition. The aim of this study was: (i) to determine the compositional and sensory profiles of citrus olive oil; and (ii) to evaluate its nutraceutical properties in rats with high fat diet-induced metabolic syndrome and oxidative stress. The results obtained show the potential of using citrus peels as a source of bioactive compounds to improve the sensory profile as well as the phytochemical composition of olive oil. We demonstrated that the production system of Citrus x aurantium olive oil and Citrus limon olive oil improves its organoleptic properties without altering its beneficial effects, which, like control extra virgin olive oil, showed protective effects relating to glucose and serum lipid levels, metabolic activity of adipocytes, myocardial tissue functionality, oxidative stress markers and endothelial function at blood vessel level.

Chemical activation of SAT1 corrects diet-induced metabolic syndrome.

The pharmacological targeting of polyamine metabolism is currently under the spotlight for its potential in the prevention and treatment of several age-associated disorders. Here, we report the finding that triethylenetetramine dihydrochloride (TETA), a copper-chelator agent that can be safely administered to patients for the long-term treatment of Wilson disease, exerts therapeutic benefits in animals challenged with hypercaloric dietary regimens. TETA reduced obesity induced by high-fat diet, excessive sucrose intake, or leptin deficiency, as it reduced glucose intolerance and hepatosteatosis,but induced autophagy. Mechanistically, these effects did not involve the depletion of copper from plasma or internal organs. Rather, the TETA effectsrelied on the activation of an energy-consuming polyamine catabolism, secondary to the stabilization of spermidine/spermine N1-acetyltransferase-1 (SAT1) by TETA, resulting in enhanced enzymatic activity ofSAT. All the positiveeffects of TETA on high-fat diet-induced metabolic syndromewere lost in SAT1-deficientmice.Altogether, these results suggest novel health-promoting effects of TETA that might be taken advantage of for the prevention or treatment of obesity.