Reduced Fat Accumulation Research Articles

Pueraria lobata Resistant Starch Regulating Lipid Metabolism and Gut Microbiota in High‐Fat Diet Mice

AbstractPueraria lobata resistant starch (PLRS) is prepared by modifying Pueraria lobata starch with pullulanase, and the PLRS modulate lipid metabolism disorders and gut microbiota structure are hypothesized in high‐fat diet (HFD) mice. The results reveal that the PLRS can alleviate lipid metabolism disorders by significantly upregulating the abundance of Akkermansia, Lactobacillus, Blautia, and Dubosiella, but markedly downregulating Staphylococcus in HFD mice. The PLRS may decrease the gain of weight, biochemical index, ameliorate hepatic impairment, and histopathological. Molecular mechanisms have elucidated that the PLRS may exert reducing fat accumulation and stabilize the gut microbiota effects through the modulation of the fatty acid metabolic signaling pathway and the PPAR signaling pathway. Therefore, these results suggest that this prebiotic carbohydrate may regulate lipid metabolism and gut microbiota in HFD mice and can be used to prepare healthy lipid‐lowering functional foods to attenuate obesity problems.

Effect of Bacillus subtilis BS-Z15 metabolite mycosubtilin on body weight gain in mice

Our previous study reported that the metabolite of Bacillus subtilis BS-Z15 n-butanol site could reduce body weight gain in mice, showing anti-obesity effects. This study further demonstrated the effects of purified mycosubtilin on the body weight gain and gut microbiota of Kunming mice. 30 male Kunming white mice were randomly selected into three groups at four weeks of age: Control (group A), gavage-administered with saline daily; n-butanol site treated (group B), gavage-administered with n-butanol site metabolites (90 mg/kg); and mycosubtilin treated (group C), gavage-administered with mycosubtilin (6 mg/kg). Different groups’ gut microbiota compositions were analyzed using high-throughput sequencing technology. The results showed that the effects of mycosubtilin and n-butanol sites were consistent; the treatment groups showed a significant reduction in body weight gain as well as triglyceride and low-density lipoprotein contents as compared to the control group (P <0.05). Moreover, the size and contents of epididymal adipocytes were also significantly reduced (P <0.05), and the gavage administration of mycosubtilin could significantly increase the expression levels of lipolysis gene adipose triglyceride lipase (ATGL) in the mice liver. Mycosubtilin and n-butanol site treatments could significantly alter the composition of the gut microbiota as compared to the physiologic saline treatment. B. subtilis BS-Z15 metabolites may regulate weight gain primarily by mycosubtilin, according to these findings. The mycosubtilin might reduce weight gain in mice by regulating lipid metabolism, thereby reducing fat accumulation and altering the composition of gut microbiota.

Molecular cloning and gene expression of acc2 from grass carp (Ctenopharyngodon idella) and the regulation of glucose metabolism by ACCs inhibitor.

Acetyl-CoA carboxylase (ACC) catalyzes the carboxylation of acetyl-CoA to malonyl-CoA. Malonyl-CoA, which plays a key role in regulating glucose and lipid metabolism, is not only a substrate for fatty acid synthesis but also an inhibitor of the oxidation pathway. ACC exists as two isoenzymes that are encoded by two different genes. ACC1 in grass carp (Ctenopharyngodon idellus) has been cloned and sequenced. However, studies on the cloning, tissue distribution, and function of ACC2 in grass carp were still rare. The full-length cDNA of acc2 was 8537bp with a 7146bp open reading frame encoding 2381 amino acids. ACC2 had a calculated molecular weight of 268.209kDa and an isoelectric point of 5.85. ACC2 of thegrass carp shared the closest relationship with that of the common carp (Sinocyclocheilus grahami). The expressions of acc1 and acc2 mRNA were detected in all examined tissues. Theexpression level of acc1 was high in the brain and fat but absent in the midgut and hindgut. Theexpression level of acc2 in the kidney was significantly higher than inother tissues, followed by the heart, brain, muscle, and spleen. ACCs inhibitor significantly reduced the levels of glucose, malonyl-CoA, and triglyceride in hepatocytes. This study showed that the function of ACC2 was evolutionarily conserved from fish to mammals. ACCs inhibitor inhibited the biological activity of ACCs, and reduced fat accumulation in grass carp.

Anti-obesity effect of Lactobacillus fermented Paeonia japonica, Cnidium officinale, and Angelica gigas nakai

Background and objective: This study evaluated the effects of Paeonia japonica, Cnidium officinale, and Angelica gigas nakai extracts fermented with Lactobacillus in obese mice induced by high-fat diets. Among the fermented liquids, Lactobacillus Paeonia japonica (LBPJ) exhibited high antioxidant activity and a significant total polyphenol content.Methods: Mice were divided into five groups: normal (NOR), high-fat diet (HFD), high-fat Lactobacillus Paeonia japonica (HLBPJ), high-fat Lactobacillus Cnidium officinale (HLBCO), and high-fat Lactobacillus Angelica gigas nakai (HLBAG). Obesity was induced with a high-fat diet for 8-weeks, and the fermented liquid was administered orally at a dose of 100 mg/kg per day.Results: The high-fat diet group showed significant weight gain and the group receiving the fermented liquid did not show weight loss. Blood tests showed increased levels of total cholesterol, triglyceride, and high-density lipoprotein (HDL) and decreased levels of low-density lipoprotein (LDL) in the HLBCO group. Creatinine levels remained unchanged, blood urea nitrogen (BUN) levels decreased, and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels increased. As a result of PCR analysis of liver tissue, LBPJ fermented liquid effectively reduced fat accumulation in the liver and inhibited the expression of fat-related genes such as PPARα, PPARγ, CPT-2, and HSL.Conclusion: These findings suggest that fermented liquids containing Angelica gigas nakai extracts prevent obesity by reducing body fat and blood sugar levels.

Docosahexaenoic and Eicosapentaenoic Acids Promote the Accumulation of Browning-Related Myokines via Calcium Signaling in Insulin-Resistant Mice

BackgroundMyokines have a prominent effect on improving insulin resistance (IR) by inducing browning of white adipose tissue (WAT). Although docosahexaenoic acids (DHA) and eicosapentaenoic acids (EPA) play roles in improving IR and stimulating browning, whether they mediate myokines directly remains unknown. ObjectiveThis study aims to investigate the effects of DHA and EPA on browning-related myokines under IR and clarify the mechanism via Ca2+ signaling. MethodsThe expression and secretion levels of myokines in IR mice and IR myotubes were detected after DHA/EPA treatment. The crosstalk between myotubes and adipocytes was evaluated through a method in which IR adipocytes were treated with the culture medium supernatant of myotubes treated with DHA/EPA. The expression of browning markers in the WAT of IR mice and adipocytes was determined. A calcium chelator was used to determine whether DHA and EPA regulate myokine production through a calcium ion-dependent pathway. ResultsIn vivo experiments: 3:1 and 1:3 DHA/EPA promoted the mRNA levels of Irisin, IL-6, IL-15, and FGF21 in skeletal muscle, stimulated WAT browning, reduced lipid accumulation; 3:1 DHA/EPA upregulated the serum concentration of Irisin; 1:3 DHA/EPA upregulated the serum concentrations of Irisin, IL-6, and FGF21. In vitro experiments: the levels of Irisin and IL-6 in C2C12 myotubes and their medium supernatant were significantly elevated in the 3:1 and 1:3 groups and the upregulation of browning markers and reduction in fat accumulation were observed in adipocytes treated with the medium supernatant of C2C12 myotubes in the 3:1 and 1:3 groups. However, the above phenomena disappeared when Ca2+ signaling was inhibited. ConclusionsTreatment with DHA and EPA at composition ratios of 3:1 and 1:3 induces browning of WAT in IR mice, which is likely related to the promotion of the accumulation of myokines, especially Irisin and IL-6, via Ca2+ signaling.

Facile adipocyte uptake and liver/adipose tissue delivery of conjugated linoleic acid-loaded tocol nanocarriers for a synergistic anti-adipogenesis effect

Obesity is a major risk to human health. Adipogenesis is blocked by α-tocopherol and conjugated linoleic acid (CLA). However, their effect at preventing obesity is uncertain. The effectiveness of the bioactive agents is associated with their delivery method. Herein, we designed CLA-loaded tocol nanostructured lipid carriers (NLCs) for enhancing the anti-adipogenic activity of α-tocopherol and CLA. Adipogenesis inhibition by the nanocarriers was examined using an in vitro adipocyte model and an in vivo rat model fed a high fat diet (HFD). The targeting of the tocol NLCs into adipocytes and adipose tissues were also investigated. A synergistic anti-adipogenesis effect was observed for the combination of free α-tocopherol and CLA. Nanoparticles with different amounts of solid lipid were developed with an average size of 121‒151 nm. The NLCs with the smallest size (121 nm) showed greater adipocyte internalization and differentiation prevention than the larger size. The small-sized NLCs promoted CLA delivery into adipocytes by 5.5-fold as compared to free control. The nanocarriers reduced fat accumulation in adipocytes by counteracting the expression of the adipogenic transcription factors peroxisome proliferator activated receptor (PPAR)γ and CCAAT/enhancer-binding protein (C/EBP)α, and lipogenic enzymes acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS). Localized administration of CLA-loaded tocol NLCs significantly reduced body weight, total cholesterol, and liver damage indicators in obese rats. The biodistribution study demonstrated that the nanoparticles mainly accumulated in liver and adipose tissues. The NLCs decreased adipocyte hypertrophy and cytokine overexpression in the groin and epididymis to a greater degree than the combination of free α-tocopherol and CLA. In conclusion, the lipid-based nanocarriers were verified to inhibit adipogenesis in an efficient and safe way.

An Ilex latifolia‐containing compound tea regulates glucose–lipid metabolism and modulates gut microbiota in high‐fat diet‐fed mice

AbstractKuding Tea (Ilex latifolia) is a bitter‐tasting herbal tea that was used for the treatment of symptoms related with diabetes mellitus, hypertension, and hyperlipidemia. However, Kuding Tea is also difficultly accepted by people in daily life because of its poor palatability. In this study, Kuding Tea, green tea (GT) (Camellia sinensis L.), and Luohan (Siraitia grosvenorii) fruits were formulated into a compound Kuding Tea (CKT) to improve the taste and health benefits of this beverage. High‐fat diet‐fed male C57BL/6J mice were used as animal models to explore the effects of CKT (6 or 12 mg/mL, water ad libitum) on body weight, food intake, liver function, blood glucose and lipids, and gene expression. L02 and 3T3‐L1 cells were used to further demonstrate the effects of CKT on fat accumulation and hepatic lipid deposition. Our results suggest that CKT can regulate glucose and lipid metabolism by decreasing body weight, reducing white adipose deposition, improving glucose tolerance, increasing the expression of brown adipose genes, and reducing fat accumulation in the liver, and CKT inhibited fat accumulation better than GT. In addition, a low dose (6 mg/mL) of CKT reduced the abundance of Desulfovibrio bacteria, positively associated with obesity, and increased that of norank_f__Muribaculaceae, Lachnospiraceae_NK4A136_group, and Alloprevotella, which are beneficial to glucose and lipid metabolism. This study suggests that CKT not only has a better palatability but also has potential preventive effects on high‐fat diet‐induced glucose–lipid metabolic diseases.

Sulforaphane-A Compound with Potential Health Benefits for Disease Prevention and Treatment: Insights from Pharmacological and Toxicological Experimental Studies.

Sulforaphane (SFN), which is a hydrolysis product from glucoraphanin, a compound found in cruciferous vegetables, has been studied for its potential health benefits, particularly in disease prevention and treatment. SFN has proven to be effective in combating different types of cancer by inhibiting the proliferation of tumors and triggering apoptosis. This dual action has been demonstrated to result in a reduction in tumor size and an enhancement of survival rates in animal models. SFN has also shown antidiabetic and anti-obesity effects, improving glucose tolerance and reducing fat accumulation. SFN's ability to activate Nrf2, a transcription factor regulating oxidative stress and inflammation in cells, is a primary mechanism behind its anticancerogenic and antidiabetic effects. Its antioxidant, anti-inflammatory, and anti-apoptotic properties are also suggested to provide beneficial effects against neurodegenerative diseases. The potential health benefits of SFN have led to increased interest in its use as a dietary supplement or adjunct to chemotherapy, but there are insufficient data on its efficacy and optimal doses, as well as its safety. This review aims to present and discuss SFN's potential in treating various diseases, such as cancer, diabetes, cardiovascular diseases, obesity, and neurodegenerative diseases, focusing on its mechanisms of action. It also summarizes studies on the pharmacological and toxicological potential of SFN in in vitro and animal models and explores its protective role against toxic compounds through in vitro and animal studies.

Effects of different HIIT protocols on exercise performance, metabolic adaptation, and fat loss in middle-aged and older adults with overweight.

Introduction: There is evidence that aging and obesity are associated with increased oxidative stress and chronic inflammation. High-intensity interval training (HIIT) may be superior to moderate-intensity continuous training (MICT) in anti-inflammatory and anti-obesity benefits. Therefore, the objective of this study is to determine which HIIT prescriptions will be more effective in reducing fat accumulation, inflammation, and improving metabolic adaptation and exercise performance in middle-aged and older overweight adults. Methods: Thirty-six middle-aged with overweight adults were divided into one of three groups: 1. L-HIIT group: the long-interval HIIT group (4 × 4 min Exercise/4 min Rest), 2. M-HIIT group: the medium-interval HIIT group (8 × 2 min Exercise/2 min Rest), 3. Control group: no exercise training intervention. All groups underwent the training stage for eight weeks (three sessions per week), followed by a detraining stage of four weeks in order to investigate the effects induced by different HIIT interventions on inflammation, metabolic adaptation, anti-fatigue and exercise performance, and fat loss Results: There was a significant physiological response in the change rate of heart rate (HR) after an acute L-HIIT session compared with an acute M-HIIT session (ΔHR: ↑49.66±16.09% vs ↑33.22±14.37%, p=0.02); furthermore, systolic blood pressure (SBP) and diastolic blood pressure (DBP) decreased significantly following a single L-HIIT session. After an eight-week training stage, the L-HIIT and M-HIIT groups exhibited a significant increase in aerobic capacity (ΔVO2peak), with values of +27.93±16.79% (p<0.001) and +18.39±8.12% (p<0.001), respectively, in comparison to the control group. Furthermore, in the L-HIIT group, the anaerobic power of relative mean power (RMP) exhibited a significant increase (p=0.019). However, following a four-week detraining stage, the adiponectin concentration remained 1.78 times higher in the L-HIIT group than in the control group (p=0.033). The results of blood sugar, blood lipids, body composition, and inflammatory markers did not indicate any improved it did not indicate any improvements from the two different HIIT protocols. Conclusions: The results indicate that an eight-week L-HIIT or M-HIIT intervention (three sessions per week, 32 minutes per session) may be an effective approach for improving aerobic capacity. It can be posited that L-HIIT may be a more advantageous mode than M-HIIT for enhancing anaerobic power, adipokine levels, and improving blood pressure in an aged and overweight population due to the induced physiological responses.

4,4-Dimethylsterols Reduces Fat Accumulation via Inhibiting Fatty Acid Amide Hydrolase InVitro and InVivo.

4,4-Dimethylsterols constitute a unique class of phytosterols responsible for regulating endogenous cannabinoid system (ECS) functions. However, precise mechanism through which 4,4-dimethylsterols affect fat metabolism and the linkage to the ECS remain unresolved. In this study, we identified that 4,4-dimethylsterols, distinct from 4-demethseterols, act as inhibitors of fatty acid amide hydrolases (FAAHs) both invivo and invitro. Genetic ablation of FAAHs (faah-1) abolishes the effects of 4,4-dimethylsterols on fat accumulation and locomotion behavior in a Caenorhabditis elegans model. We confirmed that dietary intervention with 4,4-dimethylsterols in a high-fat diet (HFD) mouse model leads to a significant reduction in body weight (>11.28%) with improved lipid profiles in the liver and adipose tissues and increased fecal triacylglycerol excretion. Untargeted and targeted metabolomics further verified that 4,4-dimethylsterols influence unsaturated fatty acid biosynthesis and elevate oleoyl ethanolamine levels in the intestine. We propose a potential molecular mechanism in which 4,4-dimethylsterols engage in binding interactions with the catalytic pocket (Ser241) of FAAH-1 protein due to the shielded polarity, arising from the presence of 2 additional methyl groups (CH3). Consequently, 4,4-dimethylsterols represent an unexplored class of beneficial phytosterols that coordinate with FAAH-1 activity to reduce fat accumulation, which offers new insight into intervention strategies for treating diet-induced obesity.

Effect and mechanism of GPR75 in metabolic dysfunction-related steatosis liver disease.

Research on G protein-coupled receptor 75 (GPR75) in metabolic dysfunction-related steatosis liver disease (MASLD) reveals its potential role in regulating body weight and energy balance. Loss-of-function mutations in the GPR75 gene are significantly associated with lower body mass index and reduced body weight. Studies demonstrate that GPR75 knockout mice exhibit lower fasting blood glucose levels, improved glucose homeostasis, and significant prevention of high-fat diet-induced MASLD. The absence of GPR75 reduces fat accumulation by beneficially altering energy balance rather than restricting adipose tissue expansion. Moreover, female GPR75 knockout mice show greater protection against lipid accumulation on a high-fat diet compared to males, potentially attributed to higher physical activity and energy expenditure. However, current research primarily relies on mouse models, and its applicability to humans requires further validation. Future studies should explore the role of GPR75 across diverse populations, its clinical potential, and delve into its specific mechanisms and interactions with other metabolic pathways. Ultimately, targeted therapies based on GPR75 could offer novel strategies for the prevention and treatment of MASLD and other metabolic disorders.

In silico determination of fenthion, permethrin, and carbaryl as FFAR2 inhibitors: Type 2 diabetes mellitus pathomechanism study

Background: In the last few decades, many studies have shown that pesticides have a close relationship with increasing blood glucose levels and the incidence of diabetes. Some examples of pesticides include fenthion, permethrin, and carbaryl. Recently, free fatty acid receptor 2 (FFAR2) was identified as having a critical function in preventing insulin resistance. Activation of FFAR2 will reduce fat accumulation and induce glucagon-like peptide 1 (GLP-1) secretion, which plays an important role in regulating type 2 diabetes mellitus (T2DM) prevention.Objective: This study aims to determine a comparison of the binding ability between fenthion, permethrin, and carbaryl to FFAR2 protein for predicting the mechanism of pesticide toxicity to T2DM through an in silico study.Methods: This is an exploratory bioinformatic study. The protein structure was FFAR2 receptor (UniProt: O15552), while the ligand was fenthion (PubChem CID: 3346), permethrin (PubChem CID: 40326), and carbaryl (PubChem CID: 6129). This molecular docking was conducted in October 2022 using Asus X202XE with Intel® Core™ i3-3217U CPU equipped with BIOVIA Discovery Studio, AutoDockTools, and AutoDock Vina. Results: The binding affinity values generated after docking between fenthion, permethrin, and carbaryl with FFAR2 indicate that the binding affinity comparison is permethrin &lt; carbaryl &lt; fenthion. This explains that permethrin could form a stronger bond with FFAR2 protein than other pesticides. However, the visualisation results of the form of bond interactions show that permethrin does not bind to the active site of FFAR2, so it could not be called an inhibitor. This is different from fenthion and carbaryl, which could bind to several amino acid residues on the active site of FFAR2 and have the potential to become inhibitors.Conclusion: Carbaryl is a pesticide with the strongest FFAR2 inhibitor. Carbaryl could cause type 2 DM through its inhibitory pathway to FFAR2.

Tryptophan Prevents the Development of Non-Alcoholic Fatty Liver Disease.

The main aim of this research is to study the protective effects of tryptophan on the histomorphological and biochemical abnormalities in the liver caused by a high-calorie diet (HCD), as well as its ability to normalize mitochondrial functions in order to prevent the development of non-alcoholic fatty liver disease (NAFLD). The study was conducted in male Wistar rats aged 3 months at the start of the experiment. Control animals (group I) were fed a standard diet. Group II experimental animals were fed a diet with an excess of fat (45%) and carbohydrates (31%) for 12 weeks. Group III experimental animals also received L-tryptophan at a dose of 80 mg/kg body weight in addition to the HCD. The presence of NAFLD, functional activity, physiological regeneration, and the state of the liver parenchyma and connective tissue were assessed using physiological, morphological, histo-morphometric, biochemical, and biophysical research methods. HCD induced the development of NAFLD, which is characterized by an increase in liver weight, hypertrophy of hepatocytes and an increase in the concentration of lipids, cholesterol and triglycerides in liver tissue. Increased alanine aminotransferase activity in the liver of obese rats also confirm hepatocytes damage. Tryptophan added to the diet lowered the severity of NAFLD by reducing fat accumulation and violations of bioelectric properties, and prevented a decrease in mitochondrial ATP synthesis. The addition of tryptophan can have a potential positive effect on the liver, reducing the severity of structural, biochemical, mitochondrial and bioelectric damage caused by HCD.

Rheological properties, biochemical changes, and potential health benefits of dehulled and defatted industrial hempseeds after fermentation

Dehulled hempseed (DHS), fermented dehulled hempseed (FDHS), hempseed cake (HSC), and fermented HSC (FHSC) were examined for their phytochemical composition, health benefits, and rheological characteristics. At 500 µg/mL concentration, DHS, FDHS, HSC, and FHSC extracts exhibited the ability to inhibit DPPH radicals, with 32.46 %, 47.35 %, 33.85 %, and 47.41 %, respectively. Similarly, they demonstrated potential to scavenge ABTS radicals by 13.7 %, 27.87 %, 14.40 % and 25.70 %, respectively. For lipase inhibition activity, FDHS (72.92 %) and FDHS (85.89 %) outperformed DHS (52.94 %) and HSC (43.08 %). Furthermore, FHSC enhanced the survival and reduced fat accumulation in glucose-supplemented Caenorhabditis elegans. We used HPLC and UHPLC-ESI-QTOF-MS for metabolite analysis, quantifying eight polyphenols using HPLC and identifying thirty-four metabolites with UHPLC-ESI-QTOF-MS. Generally, metabolomics indicated an improved metabolite profile after fermentation. Fermentation also showed impact on rheological characteristics, modifying viscosity, loss modulus, and storage modulus. These findings collectively demonstrate the ability of fermentation in enhancing overall value of hempseed.

Pleurotus abieticola Polysaccharide Alleviates Hyperlipidemia Symptoms via Inhibition of Nuclear Factor-κB/Signal Transducer and Activator of Transcription 3-Mediated Inflammatory Responses

Hyperlipidemia (HLP) is a metabolic syndrome induced by obesity, which has been widely recognized as a significant threat to human health. Pleurotus abieticola, an edible lignin-degrading fungus, remains relatively understudied in terms of its bioactivity and medicinal properties. In this study, the lipid-lowering effect of Pleurotus abieticola polysaccharide (PAPS1) was systematically explored in high-fat diet (HFD)-induced HLP mice. The findings demonstrated that the administration of PAPS1 significantly inhibited bodyweight gain, ameliorated blood glucose and lipid levels, reduced fat accumulation, and mitigated hepatic injury in HLP mice. In addition, PAPS1 demonstrated the capability to increase the levels of three distinct fecal metabolites while simultaneously reducing the levels of eight other fecal metabolites in HLP mice. According to biological detection, PAPS1 reduced the hepatic level of reactive oxygen species (ROS) and pro-inflammatory factors, such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β, -6, -17A, -22, and -23, and increased the expression of anti-inflammatory factor IL-10. Combined with proteomics, Western blot and immunohistochemistry analysis showed that PAPS1 exerted suppressive effects on inflammation and oxidative damage by inhibiting the nuclear factor-κB (NF-κB)/signal transducer and activator of transcription 3 (STAT3) signaling pathway in HLP mice. These findings offer evidence supporting the effectiveness of PAPS1 as a therapeutic agent in reducing lipid levels through its targeting of chronic inflammation.

An Investigation of Attitude toward Exercise and Services Expected from Fitness Center of People at Jiaying University

Background and Aim: This research investigates the attitudes of individuals towards exercise and the services they expect from the fitness center at Jiaying University. The study aims to achieve the following objectives: (1) To examine the attitudes of Jiaying University's community, including teachers, staff, and students, towards exercise and various forms of physical activity. And (2) To identify the specific services that people anticipate receiving from Jiaying University's fitness center. Materials and Methods: The research population comprises a total of 30,462 individuals, including teachers, staff, and students at Jiaying University, China, during the academic year 2022. The sample group for this study consisted of 379 participants who were selected using questionnaires as the primary data collection tool. Statistical analysis of the data involved calculating percentages, means, and standard deviations. Results: The research findings are summarized as follows: Analysis of the population's attitudes toward exercise revealed that the top three factors with the highest agreement among respondents were: enhancing cardiovascular health, reducing fat accumulation in blood vessels, and slowing down the aging process. Examination of the services expected from Jiaying University's fitness center identified the following top three priorities: ensuring the safety of members, providing attentive employees, and maintaining high-quality equipment standards. Conclusion: This study sheds light on the attitudes of Jiaying University's community towards exercise and their expectations regarding the services offered by the university's fitness center. The key areas of focus in this research encompass (1) the factors influencing exercise, (2) attitudes towards physical activity, (3) the management of the fitness center, and (4) the services anticipated from such a facility.

The senolytic agent Dasatinib reduces fat accumulation in the heart and bone marrow of type 2 diabetic, obese mice and adipogenesis of human bone marrow pericytes

Abstract Background Inflammaging, a chronic inflammatory state associated with aging and obesity, participates in the pathogenesis of cardiovascular disease and type 2 diabetes (T2D). Adipocyte accumulation in bone marrow (BM) may contribute to this phenomenon. Senolytic drugs, like Dasatinib, reportedly eliminate senescent preadipocytes. However, the effects of Dasatinib on fat deposits in the heart and BM remain unknown. Purposes This study aimed to identify the cellular source of adipocytes in human BM and determine whether treatment with Dasatinib reverses adiposity and improves cardiovascular function in T2D obese mice. Methods and results Human CD34neg CD45neg CD146pos pericytes (hBM-PCs) were sorted from BM mesenchymal stem cells (hBM-MSCs) by immunomagnetic beads. HBM-PCs showed a higher propensity to differentiate into Oil red O positive (pos) adipocytes after 21 days of stimulation in a pro-adipogenic medium (P=0.0299 vs. hBMSCs (hBM-MSCs except for hBM-PCs)). Dasatinib treatment reduced the number of viable cells (P=0.0034 vs. Vehicle (DMSO)) and the rate of adipocyte differentiation (P= 0.0179 vs. Vehicle). In a randomized blind study, Dasatinib (5 mg/kg) or vehicle (10% DMSO+90% PEG-300) was given by oral gavage to T2D, obese 21-week-old male BKS.Cg-+Leprdb/+Leprdb/OlaHsd (Db/Db) mice. Groups of animals were sacrificed at 1 or 4 weeks. Dasatinib reduced the Oil red O pos cells in the heart (P= 0.001 and 0.045) and BM (P= 0.018 and 0.0253) at both time points. Senescence marker p16INK4a expression and plasma adipokines levels were similar between the two groups at one week. With long-term treatment, the expression of senescence marker p16INK4a was significantly reduced in the murine hearts (P=0.035) and BM (P=0.068), whereas adipokines levels were similar. In vitro treatment of murine BM-MSCs with Dasatinib reduced the expression of p21Waf1/Cip1 (P= 0.030). VisualSonics 3D echocardiography showed similar diastolic and systolic function in Dasatinib- or Vehicle-treated mice: stroke volume (P= 0.494); ejection fraction (P= 0.701); fractional shorten (P= 0.807); and cardiac output (P= 0.437). Conclusion Pericytes are the primary source of adipocytes in human BM. The senolytic agent Dasatinib reduces pericyte commitment to adipogenesis. The senolytic agent prevented fat accumulation and cell senescence in the BM and heart of T2D mice. However, more prolonged treatment may be necessary for the reduced adiposity to translate into improvements in heart function.

Myo-inositol improves osmoregulation by promoting lipid utilization in Nile tilapia (Oreochromis niloticus)

This research explores the influence of myo-inositol (MI) on the hypertonic stress adaptation of Nile tilapia (Oreochromis niloticus) by increasing lipid utilization under long-term salinity stress. A two-factor interactive experiment was used, and diets containing either normal lipids (NL, 7%) or high lipids (HL, 15%) contained three MI concentrations of 0, 400, and 1200 mg/kg in each lipid diet. Fish were fed six diets under 20 psu (practical salinity units [psu]) for eight weeks. Under long-term hypertonic stress, dietary MI supplementation significantly improved the growth performance of O. niloticus (P < 0.05). Dietary 1200 mg/kg MI supplementation significantly promoted protein deposition and reduced fat accumulation in the whole fish (P < 0.05). The HL diet significantly caused lipid accumulation in the liver, while dietary 1200 mg/kg MI addition alleviated lipid accumulation by promoting the expression of genes related to lipolysis (PPAR-α; ATGL and CPT) and inhibiting the expression of genes related to lipid synthesis (SREBP; DGAT and FAS) (P < 0.05). In addition, 400 mg/kg MI significantly reduced serum lipids (TG and LDL-C) (P < 0.05). qPCR showed that the purity of dietary 1200 mg/kg MI significantly upregulated the expression of an ion transporter-related gene (NKA) in gills (P < 0.05). Meanwhile, 400 mg/kg and 1200 mg/kg MI significantly affected the content of fatty acids in the liver and gill (P < 0.05). In addition, dietary 1200 mg/kg MI supplementation significantly increased the antioxidant capacity in the liver of O. niloticus. In conclusion, dietary supplementation with 1200 mg/kg MI could regulate lipid metabolism, promote lipid utilization and improve the osmotic regulation ability of O. niloticus.

Nutritional quality and health benefits of roselle calyces

Abstract Roselle calyces (Hibiscus sabdariffa L.) were evaluated through a critical study of existing research works on health benefits, mineral compositions, bioactive compositions, mechanisms, and possible research gaps. The use of roselle calyces as an alternative to synthetic food dyes, addressing growing global challenges of overweight, obesity, and cardiovascular diseases, was evaluated and encouraged. Studies indicate the attenuation of obesity by chlorogenic acid (the predominant phenolic compound in roselle calyx) via mechanisms associated with the UCP-1 and PGC-1α pathways, resulting in reduced blood lipid levels, reduced fat accumulation in the liver, and increased thermogenesis through fat metabolism. Minimum inhibitory concentration (MIC) of known bacteria and fungi, such as Listeria monocytogenes, Escherichia coli, Bacillus cereus, Salmonella typhimurium, Candida tropicalis, and Candida krusei, were studied. More research, however, needs to be conducted on organic acids present in roselle calyces to look into their possible applications and maximize their possible benefits.

Mechanisms of weight-loss effect in obese mice by the endogenous cannabinoid receptor 2 agonist beta-caryophyllene

Background and aimsThe endogenous cannabinoid system (ECS) is involved in the regulation of a variety of physiological activities in the body, such as metabolism and energy uptake, and cannabinoid receptor 2 (CNR2) is one of these receptors that is predominantly distributed in the periphery. β-caryophyllene (BCP) is an agonist of CNR2 which is known to possess pharmacological activities such as anti-inflammatory and antioxidant properties. In this study, we wanted to investigate whether BCP possesses pharmacological effects on obese mice and its mechanism. MethodsReversed feeding rhythm, propylthiouracil was delivered intraperitoneally, and BCP was gavaged once daily for four weeks to establish a hyperlipidemic obese mouse model. A glucose tolerance test, lipid level measurements, liver, peritoneal, and subcutaneous fat removal, HE and Oil Red O staining of the liver, and immunohistochemistry (IHC) staining with an anti-CNR2 antibody were all carried out. The liver was examined using tools like GO and KEGG databases for differentially expressed genes and signaling pathways linked to medication effectiveness. ResultsBCP had significant effects on weight reduction and improvement of dyslipidemia. What’s more, it significantly reduced body fat percentage, improved steatosis and ballooning of liver cells, and reduced fat accumulation, while inhibiting the proliferation of peri-abdominal adipocytes. BCP exerted its effects to improve dyslipidemia and reduce body weight probably through circadian regulation and cholesterol metabolic pathways. Finally, and its efficacy in improving dyslipidemia and reducing body weight may be mainly through activating CNR2, activating SIRT1/PGC-1α/PPARγ and SIRT1/AMPK pathways. ConclusionBCP activates the CNR2, SIRT1/PGC-1α/PPARγ signaling pathway, and SIRT1/AMPK signaling pathway to exert dyslipidemia-improving and weight-loss effects.