Reduced Weight Gain Research Articles

Enhanced Oxidation Resistance of Pt‐Containing Inconel 718 Alloy through Facilitated Formation of Protective Chromia

This study investigates the influence of Pt addition on the oxidation behavior of a Cr2O3‐forming superalloy. Inconel 718 (IN718) alloys with varying Pt content were prepared and subjected to isothermal oxidation tests. The results demonstrate that Pt significantly enhances the oxidation resistance of IN718, as evidenced by reduced weight gain, thinner oxide layers, and smaller oxide particles. Pt addition also increases the activation energy for both initial interface oxidation and ion diffusion during long‐term oxidation. Furthermore, Pt promotes the formation of a Cr2O3 layer while suppressing the formation of other undesirable oxides, resulting in a more cohesive and stable oxide layer. The improved oxidation resistance is attributed to two key factors: during the initial oxidation stage, Pt, as a noble element, reduces the activity of the primary oxide‐forming element Cr to oxidative environments, thereby lowering its susceptibility to initial oxidation at the metal–oxidant interface. During long‐term oxidation, Pt preferentially substitutes for Ni in major phases such as γ‐Ni(Cr,Fe) and γ′‐Ni3(Al,Ti), locally increasing the Cr composition. This promotes Cr oxidation, effectively suppressing the oxidation of Ni or Fe. These findings suggest that Pt addition is a promising approach for enhancing oxidation resistance in alloy design.

Silencing ACE1 Gene with dsRNA of Different Lengths Impairs Larval Development in Leptinotarsa decemlineata

In the search for effective strategies to control the Colorado Potato Beetle, RNA interference technology has emerged as a promising method due to its capacity to suppress genes selectively. Factors such as the target gene and double-stranded RNA (dsRNA) length are critical for optimizing gene silencing efficiency. In this study, we designed and synthesized in vitro dsRNAs of varying lengths targeting the ACE1 gene, which encodes the AChE1 isoform of acetylcholinesterase in the beetle. All tested dsRNA lengths (222 bp, 543 bp, 670 bp, and 870 bp) promoted transcript reduction. The 670 bp dsRNA was the most effective, reducing transcript levels by approximately 40% by day seven, followed by the 543 bp dsRNA. No significant differences were observed between the 222 bp and 870 bp dsRNAs. Furthermore, all of the dsRNA lengths resulted in reduced weight gain and increased mortality in larvae, with the 670 bp dsRNA showing the highest mortality rate, leaving only 63% larval survival, a trend that persisted through day nine. These findings emphasize that dsRNA length is a key factor in the silencing response, underscoring the importance of selecting the optimal length while considering the gene’s target, stability, and delivery methods. This study contributes to establishing design criteria for dsRNA, aiding in the development of more effective and sustainable pest management strategies.

Dodecanedioic acid prevents and reverses metabolic-associated liver disease and obesity and ameliorates liver fibrosis in a rodent model of diet-induced obesity.

Dodecanedioic acid (DC12) is a dicarboxylic acid present in protective polymers of fruit and leaves. We explored the effects of DC12 on metabolic dysfunction-associated steatohepatitis (MASH) and obesity. DC12 supplementation (100 mg/kg/day) was added to a high-fat diet (HFD) for 8 weeks in rodents to assess its impact on obesity and MASH prevention. Rats given DC12 experienced significant reductions of weight gain, liver and visceral fat weight, and improved glucose tolerance and insulin sensitivity. Liver histology showed protection against diet-induced MASH, with reduced steatosis, hepatocyte ballooning, and fibrosis. For weight-loss and MASH reversion, rats were fed HFD for 14 weeks, followed by 6 weeks with or without DC12. DC12 supplementation (100 mg/kg/day) led to a significant reduction of weight gain and liver weight. DC12 induced white adipose tissue beiging and reduced adiposity with a decrease of visceral fat. It also improved glucose tolerance, insulin sensitivity, and reduced hepatic gluconeogenic gene expression. Liver histology revealed a significant reduction in steatosis, hepatocyte ballooning, and inflammation as well as fibrosis, indicating MASH reversal. DC12 reduced hepatic lipogenesis enzymes as well as de novo lipogenesis measured by deuterated water and increased fatty acid β-oxidation. Plasma lipid profile showed lower triglycerides and phosphatidylcholines in the DC12 group. Notably, DC12 decreased mINDY expression, the cell membrane Na+-coupled citrate transporter, reducing citrate uptake and de-novo lipogenesis, linking its effects to improved lipid metabolism and reduced steatosis. We found that during the hepatic first pass, half of the DC12 ingested with water was taken up by the liver. The concentration of DC12 in the portal vein falls within the range identified invitro as sufficient to inhibit citrate transport in hepatocytes.

Isoliquiritigenin Prevents the Development of Nephropathy by an HFD in Rats Through the Induction of Antioxidant Production and Inhibition of the MD-2/TLR4/NF-κB Pathway

This study tested the ISL against renal damage induced by a high-fat diet (HFD) and explored its underlying mechanisms. Adult male rats were assigned to four groups: (1) control on a standard diet (STD), (2) ISL on STD (30 mg/kg), (3) HFD, and (4) HFD + ISL (30 mg/kg). After 12 weeks of dietary intervention, ISL treatment led to significant reductions in body weight gain, visceral fat, and glucose and insulin levels in HFD-fed rats. Notably, ISL decreased serum urea and creatinine, increased serum albumin, and improved urinary profiles by lowering the urinary albumin and the albumin/creatinine ratio. Histological analyses revealed that ISL enhanced the glomerular structure and mitigated tubular damage, as evidenced by reduced urinary excretion of the kidney injury markers NGAL and KIM-1. Additionally, ISL significantly lowered cholesterol, triglycerides, and free fatty acids in both the control and HFD groups while also decreasing oxidized low-density lipoproteins (ox-LDLs) and malondialdehyde (MDA). Importantly, ISL enhanced renal antioxidant levels, increasing glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT). Moreover, ISL downregulated mRNA levels of MD-2, Toll-like receptor-4 (TLR-4), and NF-κB, leading to reduced NF-κB p65 levels in renal tissues. In conclusion, ISL offers substantial protection against HFD-induced renal toxicity through mechanisms that attenuate metabolic stress, enhance antioxidant defenses, and inhibit the MD-2/TLR4/NF-κB inflammatory pathway.

Toxicity assessment of copper oxide nanoparticles: In vivo study

Abstact Copper oxide nanoparticles (CuO NPs) have wide range of application in many fields of industry, agriculture, cosmetics, and health care with probable risk to human health. The present study was conducted to find the chronic toxicity of these nanoparticles in the vital organs. Male healthy Wister Albino rats were subjected on daily bases to 35 intraperitoneal administration of 25 nm CuO NPs (2 mg/kg). All animals were subjected to morphological, histological, histochemical, and ultrastructural examinations. Exposure to CuO NPs induced reduction in body weight gain, urine retention, back arching, and renal calculi formation. The renal tissues demonstrated tubular hydropic degeneration, glomerular hypercellularity, blood vessels congestion and dilatation, renal interstitial oedema, mitochondrial injury, and lysosomal hypertrophy. Conversely, the liver displayed hepatocyte insultation, sinusoidal dilatation, Kupffer cells hyperplasia, inflammatory cell infiltration, hepatocytes mitochondrial cristolysis, mitochondrial swelling, lysosomal hyperplasia, and nuclear alterations. Furthermore, the cardiac tissues demonstrated congestion, cardiocytes disarray, and disorganization. In addition, the neural tissue exhibited Purkinje cells degeneration and cerebral cortex spongiosis. The results suggest that CuO nanomaterials engage with the vital organs’ components, potentially leading to alterations that could affect the organs function. Further research is encouraged for better understanding the mechanisms involved in pathogenesis of CuO NPs.

Safety assessment of (S)-Equol: Subchronic toxicity study in Sprague Dawley Rats

(S)-Equol is a chemically synthesized nutraceutical compound and its consumption provides several health benefits for humans. The new nutraceutical, enantiopure (S)-Equol was studied for acute and sub-chronic toxicity in Sprague Dawley Rats. The oral acute toxicity study showed that (S)-Equol is safe > 2000–5000 mg/kg body weight and it classified into GHS category 5/Unclassified. The repeated dose administration of (S)-Equol at dose levels of 20, 60, and 160 mg/kg body weight for 14 days and 250, 500, and 1000 mg/kg body weight for 90-consecitve days. The 14 days repeated-dose toxicity study showed no adverse effects in Sprague Dawley rats. The 90-day repeated dose toxicity study showed a reduction in body weight gain than that of control group. No treatment-related contrary effects were perceived on haematology, clinical chemistry, coagulation, urine parameters analysed, organ weights (absolute and relative), neurological and ophthalmological examination. No treatment-related abnormal gross pathological findings were obtained from gross necropsy. However, as a treatment-related effect, a significant decrease in cholesterol levels for 14 and 90 days of repeated dose administration was observed, which is considered as a pharmacological class effect of the (S)-Equol. In comparison to the corresponding vehicle control group, the high dose treatment group for both sexes showed no treatment-related histopathological abnormalities. For female rats, the no-observed-adverse-effect-level (NOAEL) was 250 mg/kg/day and for male rats, the lowest-observed-adverse-effect level (LOAEL) was 250 mg/kg/day.

Effects of metformin supplementation in high-carbohydrate diets on growth performance, glucose metabolism, intestinal flora, and PI3K/AKT signaling pathway of hybrid grouper (Epinephelus fuscoguttatus♀×Epinephelus lanceolatu♂)

Metformin, or 1,1-dimethylbiguanide, is a hypoglycemic drug that lowers blood glucose by reducing glycogen synthesis and increasing glucose uptake in peripheral tissues. Six diets with iso-nitrogenous and iso-lipid compositions were prepared, including a positive control (20 % carbohydrate, PC) and a negative control (30 % carbohydrate, T0). The experimental diets contained 0.2 % (T2), 0.4 % (T4), 0.6 % (T6), and 0.8 % (T8) metformin based on the negative control diet. A total of 540 hybrid groupers, with consistent size and health conditions, were randomly assigned to six groups. Each group contained 30 fish, with three replicates per group, and they were fed for eight weeks. The high-carbohydrate diet reduced weight gain, digestive enzyme activities and specific growth rates (P>0.05), while significantly increasing hepatosomatic indices (P<0.05). Metformin supplementation reduced both hepatosomatic and viscerosomatic indices (P<0.05). The high-carbohydrate diet led to increased levels of glucose, triglycerides, low-density lipoprotein, hepatic fructose 1,6-bisphosphatase, and glucose-6-phosphatase in the serum (P<0.05). In contrast, metformin supplementation significantly lowered glucose, insulin, triglycerides, and low-density lipoprotein levels (P<0.05), while enhancing the activities of hepatic glucokinase, phosphofructokinase-1, and pyruvate kinase (P<0.05). It significantly reduced the activities of PEPCK and G6Pase and downregulated the expression of ir, pi3k, pdk, ampkα1, and gs in fish on high-carbohydrate diets, while metformin supplementation upregulated the expression of ir, pi3k, pdk, ampkα1, and gs genes compared to the T0 group (P<0.05). In terms of microbiota, a high-carbohydrate diet increased pathogenic bacteria like Proteobacteria and Photobacterium, while metformin boosted beneficial bacteria such as Firmicutes and Brevibacillus. Overall, the high-carbohydrate diet impaired growth and insulin sensitivity, while metformin improved glucose metabolism, promoted beneficial bacteria, and supported intestinal health.

Enhancing the Hypolipidemic and Functional Properties of Flammulina velutipes Root Dietary Fiber via Steam Explosion.

Flammulina velutipes is an edible mushroom widely cultivated in China. As a by-product of Flammulina velutipes, the roots are rich in high-quality dietary fiber (DF). In order to obtain high-quality soluble dietary fiber (SDF), steam explosion (SE) is used as an effective modification method to improve the extraction rate and avoid the loss of active substances. Mounting evidence shows that SDF alleviates lipid metabolism disorders. However, it is not well understood how the influence of SDF with SE pretreatment could benefit lipid metabolism. In this study, we extracted a soluble dietary fiber from Flammulina velutipes root with an SE treatment, named SE-SDF, using enzymatic assisted extraction. The physicochemical and structural properties of the SE-SDF were investigated, and its hypolipidemic effects were also analyzed using oleic-acid-induced HepG2 cells. In addition, the anti-obesity and hypolipidemic effects of SE-SDF were investigated using a high-fat diet (HFD) mouse model. The results indicate that SE treatment (1.0 MPa, 105 s) increased the SDF content to 8.73 ± 0.23%. The SE-SDF was primarily composed of glucose, galactose, and mannose. In HFD-fed mice, SE-SDF significantly reduced weight gain and improved lipid profiles, while restoring liver function and reducing injury. This work provides an effective method for the processing of fungi waste and adds to its economic value. In future studies, the structural characteristics and the anti-obesity and gut microbiota regulation mechanisms of SE-SDF will be explored in depth, supporting its high-value utilization in healthcare products.

Repetitive daily oxytocin treatment reduces weight gain but not acute neonatal procedural pain.

While the incidence of neonatal intensive care unit (NICU) admission steadily increases, neonatology lacks evidence of a safe, effective, and preventive analgesic for treating procedural pain. Given its role in nociception and promoting healthy neurodevelopment, the endogenous neuropeptide oxytocin (OT) emerges as a promising candidate. This study investigates the use of daily repeated subcutaneous OT (1 mg/kg) treatment in an established model of neonatal repetitive procedural pain and assesses the effectivity of OT treatment on mechanical sensitivity and body weight. Contrary to our hypothesis repeated daily OT treatment did not prevent the development of mechanical hypersensitivity following needle pricks. Furthermore, treatment with OT diminished body weight gain in neonatal pups, a major side effect observed throughout the neonatal week. These results highlight the unique nature of the maturing nociceptive system that makes the identification and selection of analgesic options for the treatment of acute neonatal procedural pain a major challenge. In conclusion, our preclinical results do not support the use of repeated OT for acute pain relief in the NICU, and the side effects on body weight gain raise concerns about the use of OT in the NICU. Repeated daily OT treatment inhibits weight gain in neonatal rat pus. Repetitive daily OT administration does not prevent the development of mechanical hypersensitivity in a model of neonatal procedural pain. Future research must focus on the unique physiology of the developing nociceptive system to establish safe, effective and protective treatment of neonatal procedural pain.

Blood circulation effect of fermented citrus bioconversion product (FCBP) in EA.hy926 endothelial cells and high-fat diet-fed mouse model.

The escalating global burden of cardiovascular diseases, largely driven by unhealthy lifestyle choices and dietary patterns, has intensified the search for effective and safe interventions. With current treatments often marred by significant side effects, the exploration of natural compounds such as flavonoids presents a compelling alternative. This study investigated the effects of fermented citrus bioconversion product (FCBP), a fermented citrus bioflavonoid, on various markers of cardiovascular health in the context of a high-fat diet. In vivo, a high-fat diet-induced mouse model was used to assess the effects of FCBP on body weight, serum nitric oxide (NO) levels, activated partial thromboplastin time (aPTT), phosphatidylserine (PS) exposure on red blood cells, and the expression of inflammatory markers Intercellular Adhesion Molecule (ICAM)-1 and Vascular Cell Adhesion Molecule (VCAM)-1 in the thoracic aorta. In vitro, EA.hy926 endothelial cells were used to evaluate the compound's effects on cell viability, NO production, endothelial nitric oxide synthase (eNOS) expression, and cell adhesion molecule (CAM) levels to further understand the mechanisms behind the in vivo findings. In vivo, FCBP supplementation led to a dose-dependent reduction in weight gain, a significant decrease in serum NO levels at 10 mg/kg, and reduced ICAM-1 and VCAM-1 expressions in the thoracic aorta, indicating anti-inflammatory properties. PS exposure on red blood cells was also reduced, suggesting decreased procoagulant activity, while aPTT remained unchanged. In vitro, FCBP was non-cytotoxic to endothelial cells, showed a trend toward increased NO production and eNOS expression, and reduced the expression of ICAM-1 and VCAM-1, supporting its potential anti-inflammatory effects. FCBP demonstrates potential as a bioactive compound for managing cardiovascular health by reducing inflammation, mitigating weight gain, and influencing blood circulation-related parameters under high-fat diet conditions. Further studies, including diverse models and human trials, are warranted to elucidate its mechanisms and compare its efficacy with established cardiovascular therapeutics.

Establishment of a mouse model of ovarian oxidative stress induced by hydrogen peroxide.

Oxidative stress, resulting from environmental changes, significantly affects female fertility. Developing a mouse model to study oxidative stress lays the groundwork for research into human reproductive health and livestock fertility. In this study, we established and evaluated an oxidative stress model by administering hydrogen peroxide (H2O2) to mice. ICR mice of similar age (7-8 weeks old) and average body weight (31.58 ± 1.12 g) were randomly assigned to four groups (A, B, C, and D). Group A served as the control and was injected with a saline solution, while groups B, C, and D received saline solutions containing 0.75%, 1.50%, and 3.0% H2O2, respectively, over one week. We measured the body weights of all mice before and after the experimental period. Our findings showed that the average body weight of mice in groups A and B increased, while groups C and D experienced weight loss. Group C showed a significantly lower average weight gain compared to groups A and B, and group D exhibited an even more pronounced reduction in weight gain. Although group D had a high mortality rate, there was no significant difference in mortality rates among groups B, C, and D. Serum malondialdehyde (MDA) content increased with higher concentrations of H2O2, with a significant difference noted between groups C and A. Catalase (CAT) activity in group B was significantly higher than in group A, while superoxide dismutase (SOD) activity in group C was notably elevated compared to groups A and B. Conversely, glutathione peroxidase (GSH-Px) activity in group C was significantly lower than in both group A and group B. Hematoxylin and eosin (HE) staining revealed changes in ovarian morphology and follicle dynamics. The percentage of atretic follicles in group C was significantly higher than in the control group, and group D had a significantly lower total number of healthy follicles compared to the untreated group. Increased H2O2 content resulted in a reduction of ovary size and an irregular appearance in group D. Based on our findings, treatment with 1.50% H2O2 effectively established an oxidative stress model in mice within 1 week. This model serves as a valuable reference for future clinical studies on oxidative stress and reproductive disorders in female animals and humans.

Subcutaneously transplanted xenogeneic protein recruits treg cells and M2 macrophages to induce browning of inguinal white adipose tissue.

To study whether subcutaneously embedding xenogeneic protein threads or synthetic polymer absorbable threads can improve obesity phenotypes and metabolic conditions, and to further explore its underlying mechanism. Thirty-six 8-week-old ob/ob mice were randomly allocated to three groups, respectively, receiving catgut embedding, PGA thread embedding or sham treatment bilaterally to the groin. Individual parameters including weight, food intake, and core temperature are recorded and metabolism assessment, energy expenditure analysis, and PET/CT scanning are also performed at fixed timepoints. After surgical incision, the inguinal white adipose tissue was histologically examined and its expression profile was tested and compared among groups 4 weeks and 12 weeks after operation. Catgut embedding reduced weight gain and improved metabolic status in ob/ob mice. Browning of bilateral inguinal WAT (white adipose tissue) was induced after catgut embedding, with massive infiltration of Treg cells and M2 macrophages in the tissue slices of fat pads. IL-10 and TGF-β released by Treg cells targeted macrophages and the induced M2 macrophages increased the expression of thermogenic and anti-inflammatory genes in fat. The secretion of catecholamines by polarized M2 macrophages led to the activation of β3-AR-related pathways in adipocytes and the browning of adipose tissue. Abdominal subcutaneous catgut embedding has the potential to combat obesity through the induction of WAT browning mediated by infiltrated Treg cells and macrophages.

Investigating the Resilience of Kidneys in Rats Exposed to Chronic Partial Sleep Deprivation and Circadian Rhythm Disruption as Disruptive Interventions

Sleep is a vital biological function that significantly influences overall health. While sleep deprivation (SD) and circadian rhythm disruption are known to negatively impact various organs, their specific effects on kidney function remain understudied. This study aimed to investigate the impact of chronic partial sleep deprivation and circadian rhythm disruption on renal function in rats, providing insights into the relationship between sleep disturbances and kidney health. A total of 40 male Wistar rats were divided into five groups: a control group, a group with circadian rhythm disruption (CIR), a group with sleep deprivation during the light phase (SD-AM), a group with sleep deprivation during the dark phase (SD-PM), and a group with combined sleep deprivation and circadian rhythm disruption (SD-CIR). Sleep deprivation was induced using a specialized machine, depriving rats of sleep for four hours daily, while circadian rhythm disruption was achieved through a 3.5-hour light/dark cycle. After four weeks, kidney tissues and blood samples were collected for histological and biochemical analyses. The results showed that all experimental groups exhibited reduced water intake, with the CIR and SD-CIR groups also showing significantly lower food intake and reduced weight gain compared to controls. Oxidative stress markers revealed increased serum malondialdehyde (MDA) levels in the SD-PM and SD-CIR groups. Despite these metabolic and oxidative changes, histological examination of the kidneys revealed no significant alterations in renal structure or function across the groups. This study highlights the negative effects of chronic partial sleep deprivation and circadian rhythm disruption on feeding behavior, weight gain, and oxidative stress in rats. However, these interventions did not significantly alter renal structure or function. Further research is needed to explore the physiological mechanisms underlying these findings and the potential long-term effects of sleep disturbances on kidney health.

Sibling presence during fostering ameliorates endocrine stress profile changes in a social rodent species (Octodon degus) in a sex-specific manner

During early life, disruption of the parent-offspring bond can substantially impact development of offspring physiology and behavior. In rodents, it has been well-documented that parental separation, reduction in parental care, and cross-fostering can affect development of the endocrine stress response. For social species, however, several social factors may mitigate the stress of cross-fostering, such as remaining with other known adult caregivers or siblings. In this study, we cross-fostered a social rodent species (Octodon degus) with or without their siblings at postnatal day (PND) 8 and measured their endocrine stress response immediately after fostering (PND9) and at weaning (PND28). We found that female singly-fostered offspring displayed elevated baseline cortisol levels and reduced weight gain immediately after fostering. At weaning, female singly-fostered offspring continued to display elevated baseline cortisol levels compared to non-fostered female offspring, while singly-fostered males demonstrated weaker cortisol negative feedback strength compared to male offspring that were not fostered or were fostered with their siblings. These results suggest that sibling presence may help mitigate the stress of fostering, and that future studies should further examine other social conditions that may help reduce developmental consequences of long-term parental bond disruption.

Natural Honey Proteins Prevent Diet-Induced Obesity and Metabolic Disorders in Rats.

Previous studies have shown that oral whole honey reduces weight gain in rats on a normal diet (ND) or high-fat diet (HFD) and suppresses inflammation by modulating immunological cytokines in human neutrophils and macrophages. We hypothesize that the honey proteins (HP) are responsible for the reduced weight gain in rats on ND and HFD and that HP would alleviate obesity parameters. To test this, proteins were isolated from acacia honey through the salting-out method. Wistar rats (N = 24) were randomized to get ND or HFD for 4 weeks, then further randomized to four groups and treated with HP or saline for another 4 weeks. Energy intake (EI), body weight gain, EI per gram body weight gain, serum glucose, and lipids were measured. Expression of adipose tissue genes fatty acid binding protein (FABP), lipase C (LIPC), and apolipoprotein A-1 (APOA1) was evaluated through the quantitative polymerase chain reaction. HFD increased the body weight versus ND in weeks 1-4. HP for the next 4 weeks reduced weight gain in ND-HP and HFD-HP groups versus saline controls (P < .01). EI was not significantly different among groups. However, EI per gram body weight gain among groups was markedly different (P < .01), demonstrating reduced weight gain efficiency by HP (P < .01). HP reduced glucose in ND but not in HFD groups. Triglycerides were lower in both HP groups. The expressions of FABP, LIPC, and APOA1 genes were significantly increased (P < .05) in HP-treated HFD rats. Collectively, weight gain efficiency was remarkably reduced without altering EI in rats following the HP treatment, suggesting HP increased metabolic rate or substrate partitioning. Studies of HP are suggested in humans.

Effect of ethanol extract from Enterolobium cyclocarpum fruit on Leghorn chickens exposed to Eimeria.

There are concerns about residues of drugs in meat that are used to prevent coccidiosis in chickens. Natural compounds are an alternative to drugs. Two studies investigated the effect of an extract of Enterolobium cyclocarpum fruits (EEC) in the feed of male Leghorn chickens exposed to Eimeria spp. In the first experiment, the administration of EEC after infection with Eimeria spp. was investigated over 16 days. One thousand chickens were randomly housed in 20 pens of 1 m2 each. The pens were randomly assigned to each treatment. Five treatments were administered, containing 150, 300 and 450mg/kg of EEC in the feed, the fourth treatment (C) contained 0.5g/kg of a commercial anticoccidial, and the fifth treatment provided no treatment (WA). The second experiment lasted 18 days. Administration of the EEC began five days before the chickens were infected with Eimeria spp. Four hundred and eighty chickens were randomly allocated to 24 pens of 1 m2. The pens were randomly assigned to each treatment. In the second experiment, the same five treatments were tested and one additional treatment containing 300mg EEC plus 1g of polyethylene glycol (PEG)/kg of feed (E300PEG). In the experiment one chickens in the EEC treatments had lower faecal oocyst excretion (OE) on day 14 post infection with Eimeria spp., than chickens in the WA treatment (P < 0.05). A reduction in live weight gain (LWG) was observed in the EEC treatments (P < 0.05). In the second experiment, the excretion of oocysts in chickens from the EEC and E300PEG treatments on day 13 post-infection with Eimeria spp. was the same as in the C treatment and lower than in the WA treatment (P < 0.05). LWG was lower in the EEC treatments than in the C treatment (P < 0.05). However, the Chickens in the E300PEG and C treatments had similar LWG (P > 0.05) suggesting that PEG inhibits the negative effect of EEC tannins on LWG. In conclusion, the addition of EEC to chicken feed reduced both OE and LWG. Treatment with EEC and PEG (E300PEG) reduced the excretion of oocysts without negative effects on LWG.

Water Extract of Pulsatilla koreana Nakai Inhibits Osteoclast Differentiation and Alleviates Ovariectomy-Induced Bone Loss.

Pulsatilla koreana Nakai (P. koreana) is a perennial herb traditionally used to treat malaria and fever. Although the pharmacological properties of P. koreana have been explored in various contexts, its effects on bone diseases, such as osteoporosis, remain poorly studied. In this study, we investigated the effects of water extracts of P. koreana (WEPK) on osteoclasts, which play a crucial role in bone remodeling, and an ovariectomized (OVX) mouse model, which mimics osteoporosis. Phytochemical profiling of WEPK revealed several compounds that regulate bone or fat metabolism. WEPK suppressed osteoclast differentiation by downregulating the expression of receptor activator of nuclear factor-κB ligand (RANKL), a cytokine that induces osteoclastogenesis. Additionally, WEPK directly inhibited RANKL-induced differentiation of osteoclast precursors by downregulating nuclear factor of activated T cells 1 (NFATc1), the master transcription factor for osteoclastogenesis, by modulating its upstream regulators. In vivo, oral administration of WEPK suppressed bone loss, reduced weight gain, and mitigated fat accumulation in the liver and gonadal tissues of OVX mice. Given its positive impact on bone and fat accumulation under estrogen deficiency, WEPK may serve as a promising alternative therapy for postmenopausal osteoporosis, especially when accompanied by other metabolic disorders, such as obesity and fatty liver.

Engineering Supramolecular Nanofiber Depots from a Glucagon-Like Peptide-1 Therapeutic.

Diabetes and obesity have emerged as major global health concerns. Glucagon-like peptide-1 (GLP-1), a natural incretin hormone, stimulates insulin production and suppresses glucagon secretion to stabilize and reduce blood glucose levels and control appetite. The therapeutic use of GLP-1 receptor agonists (e.g., semaglutide) has transformed the standard of care in recent years for treating type 2 diabetes and reversing obesity. The native GLP-1 sequence has a very short half-life, and therapeutic advances have come from molecular engineering to alter the pharmacokinetic profile of synthetic GLP-1 receptor agonists to enable once-weekly administration, reduce the frequency of injection, and improve adherence. Efforts to further extend this profile would offer additional convenience or enable entirely different treatment modalities. Here, an injectable GLP-1 receptor agonist depot is engineered through integration of a prosthetic self-assembling peptide motif to enable supramolecular nanofiber formation and hydrogelation. This supramolecular GLP-1 receptor agonistic (PA-GLP1) offers sustained release in vitro for multiple weeks, supporting long-lasting therapy. Moreover, in a rat model of type 2 diabetes, a single injection of the supramolecular PA-GLP1 formulation achieved sustained serum concentrations for at least 40 days, with an overall reduction in blood glucose levels and reduced weight gain, comparing favorably to daily injections of semaglutide. The general and modular approach is also extensible to other next-generation peptide therapies. Accordingly, the formation of supramolecular nanofiber depots offers a more convenient and long-lasting therapeutic option to manage diabetes and treat metabolic disorders.

Anticancer properties and prevention of metabolic syndrome by probiotic-enriched powdered human milk

This work aimed to develop a novel formulation based on human milk (HM) enriched with a probiotic formulation comprised of Lactobacillus acidophilus CL1285, Lactobacillus casei LBC80R and Lactobacillus rhamnosus CLR2 and to evaluate in vitro and in vivo anticancer properties and its impact on the prevention of risk factors of metabolic syndrome (MetS). In vitro studies were conducted on Hepa-1c1c7, HT-29, and CHO-K1 cell lines to assess the antiproliferative and anticancer properties of HM and probiotics. The in vivo study was conducted with 28 male Wistar rats fed a high-fat diet (HFD). Rats were daily force-fed with HM and HM + probiotics or water for 8 weeks. Inflammation and oxidative stress were monitored through blood cytokines and kidney investigation. Body weight and blood glucose were recorded throughout the study. The results showed that HM had antiproliferative properties and caused apoptosis of intestinal tumoral cells. Quinone reductase (QR) was induced up to 1.8x in Hepa-1c1c7 cell line demonstrating chemotherapeutic potential. HM enriched with probiotics reduced weight gain by 10% while renal oxidative damages were reduced by up to 97%. Blood insulin and Plasminogen Activator Inhibitor-1 (PAI-1) levels were also significantly reduced. The study showed that HM had antiproliferative and chemopreventive properties on cancer cell lines. The in vivo experiment suggests that the development of a formulation based on HM powder enriched with probiotics could be used to modulate the rate of inflammation and oxidative damage to tissues, thus reducing the risk of obesity-related diseases.

Dynamic Hydration and Viscosity Control of Konjac Glucomannan Enhance Long-Term Antiobesity Effects by Reducing Food Intake in High-Fat-Diet-Fed Mice.

The purpose of this study was to investigate the necessity and importance of dynamic hydration rate and ultimate viscosity control of konjac glucomannan (KGM) for long-term antiobesity effects in C57BL/6J mice on high-fat (HF) diets. KGM supplementation effectively attenuated HF-diet-induced increases in body and tissue weights. The hydration rate and viscosity changes of KGM in the digestive tract were found to have marked impacts on antiobesity effects. KGM with medium hydration and viscosity slowed gastric emptying and intestinal transit, leading to prolonged presence in the lower ileum, increased satiety-related hormones (GLP-1 and PYY), and an 18.27% reduction in daily food intake over 10 weeks (p < 0.05). This resulted in the greatest reduction in weight gain among HF-fed mice. In contrast, KGM with faster hydration and higher viscosity provided only short-term satiety due to rapid dilution. Furthermore, KGM improved metabolic health and altered glycolipid metabolism gene transcription while enriching beneficial gut bacteria; however, no significant differences were observed among the KGM groups in these effects. These findings highlight that synchronizing KGM's hydration rate and viscosity with digestive processes is crucial for regulating satiety and achieving long-term weight loss.