High-fat And High-fructose Diet Research Articles

Effects of Sacha Inchi (Plukenetia volubilis) Oil on Serum Interleukin 6 Levels and Foam Cell Count in Male Wistar Rats (Rattus norvegicus) Fed a High Fat and Fructose Diet

A high-fat, high-fructose diet induces pro-inflammatory agents such as Interleukin-6 (IL-6) and hyperlipidemia, leading to atherosclerosis. Sacha inchi oil, rich in alpha-linolenic acid (ALA), has anti-inflammatory and lipid-modulating properties. This study aimed to examine the effect of sacha inchi oil on serum IL-6 levels and foam cell count in the aorta of wistar rats on a high-fat, high-fructose diet. This experiment is a true experimental study with a post-test-only control group design, 30 male wistar rats were divided into five groups: normal control (K0), high fat and fructose diet (HFFD) (K1), and three treatment groups receiving HFFD with sacha inchi oil at doses of 0.27 ml/200gBW/day (P1), 0.54 ml/200gBW/day (P2), and 1.08 ml/200gBW/day (P3) for 28 days. On day 29, serum IL-6 levels were measured using ELISA. Mean serum IL-6 levels were K1 (8.465 ng/L), P1 (4.294 ng/L), P2 (3.197 ng/L), P3 (1.379 ng/L), and K0 (1.340 ng/L), with significant differences among groups (p<0.05) except between K0 and P3 (p>0.05). Mean foam cell counts were K1 (55.3 cells/fov), P1 (47.1 cells/fov), P2 (53.2 cells/fov), P3 (52.6 cells/fov), and K0 (44.4 cells/fov), with significant differences between K0 and K1, K1 and P1, K0 and P2, and K0 and P3 (p<0.05). Sacha inchi oil significantly reduced IL-6 levels at all doses compared to the negative control (p<0.05), with the 1.08 ml/200 g/day dose being most effective. The 0.27 ml/200 g/day dose inhibited foam cell formation in HFFD rat. In conclusion, sacha inchi oil reduces serum IL-6 levels and inhibits foam cell formation in male wistar rats on a high-fat, high-fructose diet.

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.

Metagenomics and metaproteomics alterations are associated with kidney disease in opisthorchiasis hamsters fed a high-fat and high-fructose diet.

Opisthorchis viverrini (O. viverrini, Ov) infection and consumption of high-fat and high-fructose (HFF) diet exacerbate liver and kidney disease. Here, we investigated the effects of a combination of O. viverrini infection and HFF diet on kidney pathology via changes in the gut microbiome and host proteome in hamsters. Twenty animals were divided into four groups; 1) fed a normal diet not infected with O. viverrini (normal group), 2) fed an HFF diet and not infected with O. viverrini (HFF), 3) fed a normal diet and infected with O. viverrini (Ov), and 4) fed an HFF diet and infected with O. viverrini (HFFOv). DNA was extracted from fecal samples and the V3-V4 region of the bacterial 16S rRNA gene sequenced on an Illumina MiSeq sequencing platform. In addition, LC/MS-MS analysis was done. Histopathological studies and biochemical assays were also conducted. The results indicated that the HFFOv group exhibited the most severe kidney injury, manifested as elevated KIM-1 expression and accumulation of fibrosis in kidney tissue. The microbiome of the HFFOv group was more diverse than in the HFF group: there were increased numbers of Ruminococcaceae, Lachnospiraceae, Desulfovibrionaceae and Akkermansiaceae, but fewer Eggerthellaceae. In total, 243 host proteins were identified across all groups. Analysis using STITCH predicted that host proteome changes may lead to leaking of the gut, allowing molecules such as soluble CD14 and p-cresol to pass through to promote kidney disease. In addition, differential expression of TGF-beta-activated kinase 1 and MAP3K7-binding protein 2 (Tab2, involving renal inflammation and injury) are predicted to be associated with kidney disease. The combination of HFF diet and O. viverrini infection may promote kidney injury through alterations in the gut microbiome and host proteome. This knowledge may suggest an effective strategy to prevent kidney disease beyond the early stages.

The polysaccharides from the fruits of Lycium barbarum ameliorate high-fat and high-fructose diet-induced cognitive impairment via regulating blood glucose and mediating gut microbiota

High-fat and high-fructose diet (HFFD) consumption can induce cognitive dysfunction and gut microbiota disorder. In the present study, the effects of the polysaccharides from the fruits of Lycium barbarum L. (LBPs) on HFFD-induced cognitive deficits and gut microbiota dysbiosis were investigated. The results showed that intervention of LBPs (200 mg/kg/day) for 14 weeks could significantly prevent learning and memory deficits in HFFD-fed mice, evidenced by a reduction of latency and increment of crossing parameters of platform quadrant in Morris water maze test. Moreover, oral administration of LBPs enhanced the expression of postsynaptic density protein 95 and brain-derived neurotrophic factor and reduced the activation of glial cells in hippocampus. Besides, LBPs treatment enriched the relative abundances of Allobaculum and Lactococcus and reduced the relative abundance of Proteobacteria in gut bacterial community of HFFD-fed mice, accompanied by increased levels of short-chain fatty acids (SCFAs) as well as expression of associated G protein-coupled receptors. Furthermore, LBPs intervention prevented insulin resistance, obesity and colonic inflammation. Finally, a significant correlation was observed among neuroinflammation associated parameters, gut microbiota and SCFAs through Pearson correlation analysis. Collectively, these findings suggested that the regulation of gut microbiota might be the potential mechanism of LBPs on preventing cognitive dysfunction induced by HFFD.

Chronic jet lag alters gut microbiome and mycobiome and promotes the progression of MAFLD in HFHFD-fed mice.

Metabolic dysfunction-associated fatty liver disease (MAFLD) is the most common chronic liver disease worldwide. Circadian disruptors, such as chronic jet lag (CJ), may be new risk factors for MAFLD development. However, the roles of CJ on MAFLD are insufficiently understood, with mechanisms remaining elusive. Studies suggest a link between gut microbiome dysbiosis and MAFLD, but most of the studies are mainly focused on gut bacteria, ignoring other components of gut microbes, such as gut fungi (mycobiome), and few studies have addressed the rhythm of the gut fungi. This study explored the effects of CJ on MAFLD and its related microbiotic and mycobiotic mechanisms in mice fed a high fat and high fructose diet (HFHFD). Forty-eight C57BL6J male mice were divided into four groups: mice on a normal diet exposed to a normal circadian cycle (ND-NC), mice on a normal diet subjected to CJ (ND-CJ), mice on a HFHFD exposed to a normal circadian cycle (HFHFD-NC), and mice on a HFHFD subjected to CJ (HFHFD-CJ). After 16 weeks, the composition and rhythm of microbiota and mycobiome in colon contents were compared among groups. The results showed that CJ exacerbated hepatic steatohepatitis in the HFHFD-fed mice. Compared with HFHFD-NC mice, HFHFD-CJ mice had increases in Aspergillus, Blumeria and lower abundances of Akkermansia, Lactococcus, Prevotella, Clostridium, Bifidobacterium, Wickerhamomyces, and Saccharomycopsis genera. The fungi-bacterial interaction network became more complex after HFHFD and/or CJ interventions. The study revealed that CJ altered the composition and structure of the gut bacteria and fungi, disrupted the rhythmic oscillation of the gut microbiota and mycobiome, affected interactions among the gut microbiome, and promoted the progression of MAFLD in HFHFD mice.

Transcriptomics reveal a molecular signature in the progression of nonalcoholic steatohepatitis and identifies PAI‑1 and MMP‑9 as biomarkers in invivo and invitro studies.

Nonalcoholic steatohepatitis (NASH) is emerging as the primary driver of liver disease‑induced fibrosis. The imperative need for noninvasive biomarkers to ascertain disease progression stage is evident. The present study elucidated the biological roles of hub genes that could potentially serve as diagnostic markers for NASH. Using an invivo approach, C57BL/6J mice were subjected to a high‑fat and fructose diet (HFFD) for 6, 10, 14, 18 or 22weeks. Serological biochemical indices were assessed and liver specimens were obtained to identify potential markers linked to the NASH process, employing a comprehensive strategy that combined transcriptomic and histopathological analyses. The HFFD regimen induced hyperlipidemia, obesity and insulin resistance, progressively culminating in NASH with fibrosis over time. The transcriptomic analyses indicated temporal patterns of pivotal gene sets intricately connected to NASH progression, which encompassed processes such as glucose homeostasis, inflammatory responses, reactive oxygen species‑mediated damage, lipid metabolism disruptions and the formation of fibrotic tissue. Among these genes, Serpine1 and Mmp9 demonstrated promising diagnostic potential for NASH, with their intrahepatic mRNA expression levels serving as robust indicators. Moreover, the levels of PAI‑1 (encoded by the Serpine1 gene) and MMP‑9 in the serum of mice demonstrated a parallel increase with the duration of HFFD intervention. Invitro experiments utilizing HepG2 cells further validated these findings, demonstrating a significant elevation in the protein expression levels of both PAI‑1 and MMP‑9 upon exposure to free fatty acids, in agreement with the results of the animal study. Consequently, PAI‑1 and MMP‑9 are promising noninvasive biomarkers for assessing the progression of NASH.

Artemether Attenuates Gut Barrier Dysfunction and Intestinal Flora Imbalance in High-Fat and High-Fructose Diet-Fed Mice

Intestinal inflammation is a key determinant of intestinal and systemic health, and when our intestines are damaged, there is disruption of the intestinal barrier, which in turn induces a systemic inflammatory response. However, the etiology and pathogenesis of inflammatory diseases of the intestine are still not fully understood. Artemether (ART), one of the artemisinin derivatives, has been widely used to treat malaria. Nevertheless, the effect of ART on intestinal inflammation remains unclear. The present study intended to elucidate the potential mechanism of ART in diet-induced intestinal injury. A high-fat and high-fructose (HFHF) diet-induced mouse model of intestinal injury was constructed, and the mice were treated with ART to examine their role in intestinal injury. RT-qPCR, Western blotting, immunohistochemical staining, and 16S rRNA gene sequencing were used to investigate the anti-intestinal inflammation effect and mechanism of ART. The results indicated that ART intervention may significantly ameliorate the intestinal flora imbalance caused by the HFHF diet and alleviate intestinal barrier function disorders and inflammatory responses by raising the expression of tight junction proteins ZO-1 and occludin and decreasing the expression of pro-inflammatory factors TNF-α and IL-1β. Moreover, ART intervention restrained HFHF-induced activation of the TLR4/NF-κB p65 pathway in colon tissue, which may be concerned with the potential protective effect of ART on intestinal inflammation. ART might provide new insights into further explaining the mechanism of action of other metabolic diseases caused by intestinal disorders.

Colonic L-cell impairment in aged subjects with type 2 diabetes leads to diminished GLP-1 production

AimsGlucagon-like peptide 1 (GLP-1) is produced by the L subtype of enteroendocrine cells (EECs). Patients with type 2 diabetes (T2D) exhibit reduced incretin effect, but the pathophysiology and functional change of the L-cells remain unclear. Deciphering the mechanisms of the biological changes in L-cells under T2D conditions may assist in the research of gut-based strategies for T2D therapy. MethodsWe investigated the fasting serum GLP-1 levels and the distribution of colonic L-cells in young and aged participants with and without T2D. Additionally, we established an aged male T2D Wistar rat model subjected to a long-term high-fat and high-fructose (HFHF) diet. Histological investigations and single-cell RNA sequencing (scRNA-seq) analyses were performed to explore the mechanisms underlying functional changes in the colonic EECs. ResultsWe observed a decline in circulating GLP-1 levels and a reduced number of colonic L-cells in elderly patients with T2D. The mechanisms underlying impaired L-cell formation and disturbed GLP-1 production were revealed using aged T2D rats induced by a long-term HFHF diet. The scRNA-seq results showed that the transcription factors that regulate L-cell commitment, such as Foxa1, were downregulated, and the expression of genes that participate in encoding GLP-1, GLP-1 posttranslational processing, hormone secretion, and nutrient sensing was disturbed. ConclusionsTaken together, the reduced L-cell lineage commitment and disturbed L-cell functions might be the major cause of the reduced GLP-1 production in aged populations with T2D. Our study provides new insights for identifying novel targets in colonic L-cells for improving endogenous GLP-1 production.

Effect of Dangke consumption on body weight, blood glucose, and total cholesterol in rats subjected to high-fat and fructose diet

Obesity occurs due to an imbalance in caloric intake, leading to excess fat accumulation in adipose tissue. This condition is associated with hyperglycemia and abnormal lipid levels. Dangke, a traditional Indonesian cheese, contains lactic acid bacteria and bioactive peptides known for their health benefits. This study aims to assess the effects of dangke consumption on body weight, glucose, and total cholesterol levels in rats subjected to a high-fat and fructose diet (HFFD). This research employed an experimental laboratory design. Twenty-four Sprague-Dawley rats, with weights ranging from 100 to 200 g, were divided into six groups, each consisting of four rats. Group 1 (ND) (received a normal diet. Group 2 (HFFD) was provided with a high-fat and fructose diet).

Protective effect of moringa seed extract on kidney damage in rats fed a high-fat and high-fructose diet

ObjectiveMoringa is a common plant that contains high levels of antioxidants. In this study, we aimed to analyze the protective effect of moringa seed extract on the kidneys of a rat model maintained on a high-fat and high-fructose (HFHF) diet. MethodsAn experiment with a pretest-posttest control group design was used to measure metabolic parameters and determine kidney function, while a posttest-only method was used for the control group to determine glomerular volume and superoxide dismutase (SOD) expression. Purposive sampling was used on 28 rats divided into four groups: a control (K1) group, and three groups fed a HFHF diet for 53 days (K2, K3, and K4). Subsequently, K3 and K4 were given 150 and 200 mg/kg BW per day moringa seed extract for 28 days. Data were analyzed using IBM® SPSS® Statistics version 22 software. ResultsAnalysis showed that the diet increased the risk of metabolic syndrome, as evidenced by weight gain, glucose, and triglycerides. The optimal dose of moringa seed extract significantly improved glomerular volume (p = 0.001). The expression of SOD in kidney tubules and glomeruli was significantly different with each group (p = 0.002 and p = 0.001) respectively. ConclusionThe administration of moringa seed extract provided a protective effect on the kidney by reducing serum creatinine levels, improving overall structure, and increasing the expression of SOD, a key antioxidant.

10-OR: The Triple Roles of Tubular Mitochondria AKT in the Regulation of Renal Function, Insulin Resistance, and Body Composition during Development of Diabetic Nephropathy

Diabetic nephropathy is a major cause of end-stage renal disease. We have recently shown translocation of AKT to mitochondria in proximal tubules played a renoprotective role in murine ischemia/reperfusion injury. In this study, we tested the hypothesis that activation of mitochondrial AKT (mito-AKT) signaling in renal proximal tubules improves kidney function in diabetic nephropathy and modulates overall glucose homeostasis. We used renal tubule-specific bigenic mice that harbor tamoxifen-inducible mitochondria-targeting constitutively active AKT1 (KMCAKT), which were fed with either normal chow diet or high fat and fructose diet (HFFD). Wild type mice fed with HFFD developed nephropathy after 24 wks. Activation of renal tubular mito-AKT significantly attenuated urinary albumin, creatinine, and glucose excretion in the KMCAKT mice on HFFD. Interestingly, activation of tubular mito-AKT also decreased fasting hyperglycemia, and improved glucose tolerance of HFFD-fed mice. Insulin resistance (HOMA-IR) was significantly reduced when tubular mito-AKT was activated. In addition, mito-AKT activation reduced plasma cholesterol. Furthermore, mito-AKT activation increased total body weight and fat mass of HFFD-fed mice, but had no effect on their water and food intake. To dissect the underlying mechanism, we used 18F-fluoro-4-thia-oleate PET scan to define organ specific fatty acid uptake, and revealed a significant increase of uptake in white and brown adipose tissues in KMCAKT mice on HFFD. In conclusion, this is the first report to demonstrate critical roles of mitochondrial AKT in renal tubules in the regulation of whole-body metabolism, insulin sensitivity, and body composition beyond its local effect on kidney function in diabetic nephropathy, which suggests kidney function and nephropathy associated metabolic dysfunction could be mediated through a common pathway in tubular mitochondria. Disclosure E.Salem: None. A.Ta: None. H.Y.H.Lin: None. J.Li: None. P.H.Wang: Research Support; ViaCyte, Inc. Funding Shannon & Amy Ko Foundation

Monascin and ankaflavin prevents metabolic disorder by blood glucose regulatory, hypolipidemic, and anti-inflammatory effects in high fructose and high fat diet-induced hyperglycemic rat

Monascin (MS) and ankaflavin (AK) produced by Monascus purpureus fermented red mold dioscorea (RMD) elicit an anti-diabetes effect in streptozocin-induced type 1 diabetes. However, their effects on preventing metabolic disorder with type 2 diabetes induced by long-term high fat and high fructose diet (HFFD) remain unclear. In this study, RMD, MS, and AK were orally administered to HFFD-fed rats for 10 weeks. The result showed that orally administered MS, AK, and RMD were able to prevent the develop-ment. MS had a more potent effect on lowering blood glucose, fructosamine, and insulin resistance, and increasing hepatic glucose transporters-2, adipocyte glucose transporters-4, and hypoxia-inducible factor 1-α. AK had a greater effect on lowering blood lipid, adipose pad, and adipose inflammatory factors (interlukin-1β, tumor necrosis factor-α, and interlukin-6) levels. Therefore, the prevention of type 2 diabetes and metabolic disorders of RMD could be mainly attributed to the synergistic effect of MS and AK.

Lycopene prevents non-alcoholic fatty liver disease through regulating hepatic NF-κB/NLRP3 inflammasome pathway and intestinal microbiota in mice fed with high-fat and high-fructose diet.

Lycopene (LY) belongs to carotenoids and is abundant in red fruits and vegetables. Several previous studies suggested that LY is beneficial for ameliorating non-alcoholic fatty liver disease (NAFLD), while the potential mechanisms are unclear. The present study aimed to clarify the potential mechanisms of LY in preventing NAFLD via exploring the hepatic NF-κB/NLRP3 inflammasome pathway and intestinal microbiota composition in high-fat and high-fructose diet (HFFD)-fed mice. Fifty eight-week-old male C57BL/6J mice were randomly assigned into 5 groups: Normal control group (NC); HFFD group; HFFD with low dose of lycopene group (LLY, 20 mg/kg/d); HFFD with high dose of lycopene group (HLY, 60 mg/kg/d) and HFFD with resveratrol group (RSV, 50 mg/kg/d, positive control). After 8 weeks, feces were collected and the 12 h fasted mice were sacrificed to acquire tissues and blood for parameters measurement. The results showed that the mice in LLY, HLY and RSV groups had significantly lower body weight gain, weight of white adipose tissue, serum levels of high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), lipopolysaccharide (LPS), alanine aminotransferase (ALT), and hepatic concentrations of triglyceride (TG) and interleukin-6 (IL-6) than that in the HFFD group (p < 0.05). HLY and RSV groups also displayed lower serum levels of TG, total cholesterol (TC) and hepatic levels of tumor necrosis factor-α (TNF-α) than the HFFD group (p < 0.05). Liver protein expressions of NLRP3, Pro-Caspase-1, Caspase-1 and NF-κB were lower in the LLY, HLY and RSV groups than those in the HFFD group (p < 0.05). The feces of LY -treated mice had higher relative levels of SCFAs producing bacteria Allobaculum and lower destructive bacteria, including Firmicutes, Lachnospiraceae_NK4A136_group, Desulfovibrio, and Alistipes over the HFFD group (p < 0.05). RSV group also displayed lower fecal levels of Lachnospiraceae_NK4A136_group, Desulfovibrio, and Alistipes than the HFFD group (p < 0.05). In conclusion, LY might prevent NAFLD by suppressing hepatic NF-κB/NLRP3 inflammasome pathway and attenuating gut microbiota dysbiosis.

Improvement of obesity-induced fatty liver disease by intermittent hypoxia exposure in a murine model.

Background: The high prevalence of non-alcoholic fatty liver disease (NAFLD) in the world raises an important concern for human health. The western diet containing high fat and fructose is the risk factor for NAFLD development. Intermittent hypoxia (IH), known as the basis of obstructive sleep apnea (OSA), normally is correlated with impaired liver function. However, the role of IH in liver injury prevention has been revealed by many other studies based on the different IH paradigms. The current study, therefore, tests the impact of IH on the liver of high-fat and high-fructose diet (HFHFD) fed mice. Material and Method: Mice were exposed to IH (2min cycle, FiO2 8% for 20s, FiO2 20.9% for 100s; 12h/day) or intermittent air (FiO2 20.9%) for 15weeks, with normal diet (ND) or high-fat and high-fructose diet (HFHFD). Indices of liver injury and metabolism were measured. Results: IH causes no overt liver injury in mice fed an ND. However, HFHFD-induced lipid accumulation, lipid peroxidation, neutrophil infiltration, and apoptotic process were significantly attenuated by IH exposure. Importantly, IH exposure altered bile acids composition and shifted the hepatic bile acids towards FXR agonism, which was involved in the protection of IH against HFHFD. Conclusion: These results support that the IH pattern in our model prevents liver injury from HFHFD in experimental NAFLD.

β-(1,3)-D-glucan from &lt;em&gt;Pleurotus ostreatus&lt;/em&gt; correlates with lower plasma IL-6, IL-1β, HOMA-IR, and higher pancreatic beta cell count in High-Fat and High-Fructose Diet (HFFD) rats

Introduction: The increasing consumption of high-fat and high-fructose foods contributes to the increasing prevalence of global obesity. Low-grade chronic inflammation in obesity is a significant risk factor for insulin resistance and type 2 diabetes. Therefore, this study aimed to determine the effect of β-(1,3)-D-glucan from oyster mushroom (Pleurotus ostreatus) extract on rats fed with a high-fat and high-fructose diet. Design and Methods: This experimental study was conducted on 35 male Sprague-Dawley rats aged eight weeks. The rats were divided into groups given a normal (N) diet, a high-fat and high-fructose diet (HFFD), D1 (HFFD+125 mg/kg BW β-glucan), D2 (HFFD+250 mg/kg BW β glucan), and D3 (HFFD+375 mg/kg BW β-glucan) with an intervention of 14 weeks. IL-6 and IL-1β levels were measured by the ELISA method, while HOMA-IR (Homeostatic Model Assessment for Insulin Resistance) was calculated by the fasting insulin (ng/mL) x fasting blood glucose (mg/dL)/405 formula. Pancreatic beta-cell counts were measured by hematoxylin and eosin (H&amp;E) staining. Results: The results showed no differences in IL-6 and IL-1β between the treatment groups. However, there were significant differences in HOMA-IR and pancreatic beta-cell counts between groups. There were negative correlations between the dose of β-glucan and IL-6, IL-1β, and HOMA-IR levels. Also, there was a positive correlation between the dose of β-glucan and the number of pancreatic beta cells. Conclusions: Administration of β-(1,3)-D-glucan from oyster mushroom (Pleurotus ostreatus) extract prevented hyperglycemia and insulin resistance, also reduced inflammation in rats fed with HFFD regardless of weight gain.

The intervention effects of konjac glucomannan with different molecular weights on high-fat and high-fructose diet-fed obese mice based on the regulation of gut microbiota

Konjac is a high-quality dietary fiber rich in β-glucomannan, which has been reported to possess anti-obesity effects. To explore the effective components and the structure–activity relationships of konjac glucomannan (KGM), three different molecular weight components (KGM-1 (90 kDa), KGM-2 (5 kDa), KGM-3 (1 kDa)) were obtained, and systematical comparisons of their effects on high-fat and high-fructose diet (HFFD)-induced obese mice were investigated in the present study. Our results indicated that KGM-1, with its larger molecular weight, reduced mouse body weight and improved their insulin resistance status. KGM-1 markedly inhibited lipid accumulation in mouse livers induced by HFFD by downregulating Pparg expression and upregulating Hsl and Cpt1 expressions. Further investigation revealed that dietary supplementation with konjac glucomannan at different molecular weights caused β-diversity changes in gut microbes. The potential weight loss effect of KGM-1 maybe attributed to the abundance of changes in Coprobacter, Streptococcus, Clostridium IV, and Parasutterella. The results provide a scientific basis for the in-depth development and utilization of konjac resources.

Effects of Different Vegetable Oils on the Nonalcoholic Fatty Liver Disease in C57/BL Mice.

Nonalcoholic fatty liver disease (NAFLD) is the most common hepatic disorder, affecting 22-28% of the adult population and more than 50% of obese people all over the world. Modulation of the fatty acids in diet as a means of prevention against nonalcoholic fatty liver disease in animal models (NAFLD) remains unclear. The treatment of NAFLD has not been described in specific guidelines so far. Thus, the justification for the study is to check modifications in macronutrients composition, fatty acids, in particular, play a significant role in the treatment of NAFLD regardless of weight loss. To investigate different vegetable oils in prevention and progression of NAFLD in animal models. For the experiment were used fifty C57BL/6J mice male fed with high fat and fructose diet (HFD) to induce the NAFLD status and they received different commercial vegetable oils for 16 weeks to prevent steatosis. Liver steatosis and oxidative stress parameters were analyzed using biochemical and histological methods. Fatty acids profile in the oils and in the liver samples was obtained. The high fat and fructose diet led to obesity and the vegetable oils offered were effective in maintaining body weight similar to the control group. At the end of the experiment (16 weeks), the HFHFr group had a greater body weight compared to control and treated groups (HFHFr: 44.20 ± 2.34 g/animal vs. control: 34.80 ± 3.45 g/animal; p < 0.001; HFHFr/OL: 35.40 ± 4.19 g/animal; HFHFr/C: 36.10 ± 3.92 g/animal; HFHFr/S: 36.25 ± 5.70 g/animal; p < 0.01). Furthermore, the HFD diet has caused an increase in total liver fat compared to control (p < 0.01). Among the treated groups, the animals receiving canola oil showed a reduction of hepatic and retroperitoneal fat (p < 0.05). These biochemical levels were positively correlated with the hepatic histology findings. Hepatic levels of omega-3 decreased in the olive oil and high fat diet groups compared to the control group, whereas these levels increased in the groups receiving canola and soybean oil compared to control and the high fat groups. In conclusion, the commercial vegetable oils either contributed to the prevention or reduction of induced nonalcoholic fatty liver with high fat and fructose diet, especially canola oil.

Hypolipidaemic effects of papaya (Carica papaya L.) juice on rats fed on a high fat and fructose diet.

Papaya (Carica papaya L.) is a highly nutritious and less-caloric fruit, commonly consumed for its minerals and vitamins and hence may help in controlling obesity and abdominal discomforts. The present study investigated the hypolipidaemic effects of papaya juice extract on male Albino Wistar rats (7 weeks old; 185 ± 17 g) fed on a high fat and fructose diet (HFFD) for 6 weeks. The rats were divided into groups I-IV of five rats each and fed on either a HFFD (i.e. the Control), HFFD + 200 mg papaya, HFFD + 350 mg papaya or a HFFD + 500 mg papaya. On day 34, after an overnight fast, blood samples were obtained by cardiac puncture under 99⋅8% Chloroform anaesthesia for the determination of serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c) and high-density cholesterol (HDL-c). The atherogenic (AI) and coronary risk (CRI) indices were also calculated. Statistical analysis was performed using ANOVA where means were separated using Tukey's HSD test. Resulted showed that all rats given papaya juice had an increasing, non-significant HDL-c and reduced LDL-c levels while rats fed on HFFD had the highest TC (53⋅2 mg/dl) and TG (37⋅6 mg/dl) levels. Papaya juice statistically reduced the AI and CRI of the rats. In conclusion, consumption of HFFD + 500 mg was the most effective in the reduction of rats' blood lipids and fats, due to its anti-obesity and hypolipidaemic properties, thus can be used in the management of dyspilidaemic disorders.

Water extract of goji berries improves neuroinflammation induced by a high-fat and high-fructose diet based on the bile acid-mediated gut-brain axis pathway.

The high-fat and high-fructose diet (HFFD) is a common diet in westernized societies, which worsens disturbances in gut microbiota and bile acid (BA) metabolism. Herein, the present study aimed to investigate the effects of the water extract of Lycium barbarum fruits (LBE) on gut microbiota and BA metabolism in mice with HFFD-induced neuroinflammation. The results showed that supplementation of LBE for 14 weeks remarkably ameliorated weight gain and insulin resistance and suppressed microglial activation and neural neuroinflammation induced by HFFD. The results of Morris water maze and Y-maze tests demonstrated that LBE attenuated HFFD-induced cognitive impairment. Moreover, LBE elevated hepatic BA biosynthesis and excretion of BAs and increased elimination of BAs via the feces. Notably, LBE supplementation resulted in the enrichment of tauroursodeoxycholic acid in the cortex and hippocampus. Furthermore, the 16S rDNA sequencing results showed that LBE could modulate the structure of gut microbiota, and in the meantime decrease the relative abundance of Clostridium_XlVa, which is associated with BA homeostasis. Additionally, LBE exerted neuroprotective effects involving the increment of Lactococcus, known as a potentially beneficial bacterium. These results demonstrated that LBE could ameliorate neuroinflammation and cognitive impairment in HFFD-induced mice through the gut-liver-brain axis, which might be due to the regulation of BA homeostasis and gut microbiota in mice.

Serum Phospholipids Are Potential Therapeutic Targets of Aqueous Extracts of Roselle (Hibiscus sabdariffa) against Obesity and Insulin Resistance

Roselle (Hibiscus sabdariffa) is rich in phenolic compounds with antiobesogenic and antidiabetic effects. In this study, the effects of aqueous extracts of two varieties of Hibiscus sabdariffa, Alma blanca (white-yellow color) and Cuarenteña (purple color), were evaluated for the prevention of obesity and insulin resistance in rats fed a high-fat and high-fructose diet (HFFD), identifying targeted molecules through global metabolomics. After sixteen weeks, both roselle aqueous extracts prevented body weight gain, and white roselle extract ameliorated insulin resistance and decreased serum free fatty acid levels. Moreover, white roselle extract decreased 18:0 and 20:4 lysophosphatidylethanolamines and purple roselle extract increased 16:0 and 20:4 lysophosphatidylinositol compared to HFFD-fed rats. These results demonstrate that roselle's beneficial health effects are variety-dependent. Interestingly, the white roselle extract showed a greater beneficial effect, probably due to its high contents of organic and phenolic acids, though its consumption is not as popular as that of the red/purple varieties.