Serum Glucose Levels Research Articles

Potassium diformate affects the growth and development of broilers by improving intestinal function and digestive enzyme activity

Gut health of broiler chickens is essential for production performance. The present study aimed to evaluate the impact of dietary supplementation with potassium diformate (KDF) on growth performance and intestinal health in broiler chickens. A total of 180 Arbor Acres (AA) broiler chickens were randomly allocated into 3 treatments, with 6 replicates, containing 10 chicks in each replicate. The treatment groups were: control group (CON) was fed a basal diet; KDF-4 groups fed the basal diet with 4 g/kg KDF; KDF-8 groups fed the basal diet with 8 g/kg KDF. The experiment period lasted for 42 d. During the starter phase, the ADFI and F/G of broilers in KDF groups were lower (P < 0.05) compared to the CON group. Furthermore, the BW and ADG in KDF-4 group was improved (P<0.05). The treatment groups exhibited a significant increase (P < 0.05) in both ADG and ADFI during the grower and overall phase. Moreover, the F/G in KDF-4 group was lower (P < 0.05) compared to the CON and KDF-8 groups. The semi-eviscerated weight rate (SEWR), eviscerated carcass weight rate (ECWR), pectoral muscle rate (PMR), and leg muscle rate (LMR) of broilers were improved (P < 0.05) in KDF groups. The serum levels of glucose (GLU) and UREA (UA) were significantly higher (P < 0.05) in KDF-8 group. Additionally, the nutrient apparent utilization rate of dry matter (DM), energy (EE), and crude protein (CP) were improved (P < 0.05) in KDF-4 group. The villus height (VH) and villus height to crypt depth ratio (V/C) of duodenum, jejunum, and ileum were higher (P < 0.05) in KDF groups compared to the CON group, while crypt depth (CD) was significantly reduced (P < 0.05). The digestive enzyme activities of lipase (LIP), amylase (AMS), or trypsin (TPS) were significantly enhanced (P < 0.05) in the intestinal chyme, while the total bacterial count, Escherichia coli, Lactobacilli, Bifidobacteria, and Bacillus were reduced (P < 0.05) in the ileum. This study demonstrates that the inclusion of KDF in the diet of broilers leads to improvements in growth, slaughter performance, nutrient utilization rate, and maintenance of intestinal health.

Controlled synthesized of ternary Cu-Co-Ni-S sulfides nanoporous network structure on carbon fiber paper: a superior catalytic electrode for highly-sensitive glucose sensing

BackgroundEfficient monitoring of glucose concentration in the human body necessitates the utilization of electrochemically active sensing materials in nonenzymatic glucose sensors. However, prevailing limitations such as intricate fabrication processes, lower sensitivity, and instability impede their practical application. Herein, ternary Cu-Co-Ni-S sulfides nanoporous network structure was synthesized on carbon fiber paper (CP) by an ultrafast, facile, and controllable technique through on-step cyclic voltammetry, serving as a superior self-supporting catalytic electrode for the high-performance glucose sensor.ResultsThe direct growth of free-standing Cu-Co-Ni-S on the interconnected three-dimensional (3D) network of CP boosted the active site of the composites, improved ion diffusion kinetics, and significantly promoted the electron transfer rate. The multiple oxidation states and synergistic effects among Co, Ni, Cu, and S further promoted glucose electrooxidation. The well-architected Cu-Co-Ni-S/CP presented exceptional electrocatalytic properties for glucose with satisfied linearity of a broad range from 0.3 to 16,000 μM and high sensitivity of 6829 μA mM− 1 cm− 2. Furthermore, the novel sensor demonstrated excellent selectivity and storage stability, which could successfully evaluate the glucose levels in human serum. Notably, the novel Cu-Co-Ni-S/CP showed favorable biocompatibility, proving its potential for in vivo glucose monitoring.ConclusionThe proposed 3D hierarchical morphology self-supported electrode sensor, which demonstrates appealing analysis behavior for glucose electrooxidation, holds great promise for the next generation of high-performance glucose sensors.

Diosgenin reverses posttraumatic stress disorder in mice by augmenting neurochemical release and inhibiting HPA axis dysfunction, oxidative stress, and neuroinflammation

Post-traumatic stress disorder (PTSD) is a mental disorder linked to neurochemical, hypothalamic-pituitary-adrenal (HPA)-axis dysregulations, inflammatory and pro-oxidant challenges in response to traumatic events. It is one of the leading causes of neurocognitive declines, hence prompting the need for a pharmacological intervention. However, the impact of diosgenin, a naturally occurring steroidal saponin with adaptogenic-like action, on PTSD-induced neuropsychiatric disturbances and its underlying mechanisms are unknown. In this study, we investigated the outcome of diosgenin treatment in a multimodal traumatic, single prolonged stress (SPS)-induced PTSD in mice. Following the SPS-induced 7 days of PTSD, mice (n = 9) were thereafter treated with diosgenin (25 and 50 mg/kg) or fluoxetine (10 mg/kg) orally from days 8–20 (14 days). Locomotory, cognitive-, depressive- and anxiety-like behaviors were investigated. We assayed for changes in adrenal weight, serum glucose and corticosterone concentrations. Neurochemical, inflammatory, oxido-nitrergic dysfunctions and monoamine oxidase-B and acetylcholinesterase activities, were measured in the striatum, prefrontal-cortex and hippocampus. The results revealed that the SPS challenge inhibited locomotor, spatial/non-spatial memory functions, increased anxiety and depressive-like features, which were reversed by diosgenin. Diosgenin reduced SPS-induced increased monoamine oxidase-B, acetylcholinesterase activities, TNF-α, IL-6, malondialdehyde and nitrite levels in the striatum, prefrontal-cortex and hippocampus. Antioxidants such as glutathione, superoxide-dismutase, and catalase levels in SPS-mice brains were increased by diosgenin. Moreover, diosgenin attenuated SPS-induced hyper-HPA-axis mediation of PTSD by decreasing serum corticosterone, glucose levels and adrenal gland hypertrophy. Herewith, we suggest that diosgenin convenes adaptogenic-like protection against mice exposed to PTSD by enhancing antioxidant machinery, neurochemical modulations, and inhibition of oxido-nitrergic, inflammatory, and HPA-axis dysfunctions.

Excess Iodine Consumption Induces Oxidative Stress and Pancreatic Damage Independently of Chemical Form in Male Wistar Rats: Participation of PPAR-γ and C/EBP-β.

Human beings consume different chemical forms of iodine in their diet. These are transported by different mechanisms in the cell. The forms of iodine can be part of thyroid hormones, bind to lipids, be an antioxidant, or be an oxidant, depending on their chemical form. The excessive consumption of iodine has been associated with pancreatic damage and diabetes mellitus type 2, but the association between disease and the chemical form consumed in the diet is unknown. This research analyzes the effect of excessive iodine consumption as Lugol (molecular iodine/potassium iodide solution) and iodate on parameters of pancreatic function, thyroid and lipid profiles, antioxidant and oxidant status, the expression of IR/Akt/P-Akt/GLUT4, and transcription factors PPAR-γ and CEBP-β. Three groups of Wistar rats were treated with 300 μg/L of iodine in drinking water: (1) control, (2) KIO3, and (3) Lugol. Lugol and KIO3 consumption increased total iodine levels. Only KIO3 increased TSH levels. Both induced high serum glucose levels and increased oxidative stress and pancreatic alpha-amylase activity. Insulin levels and antioxidant status decreased significantly. PPAR-γ and C/EBP-β mRNA expression increased. The pancreatic damage, hypertriglyceridemia, and oxidative stress were independent of the chemical form of iodine consumed. These effects depended on PPAR-γ, C/EBP-β, GLUT-4, and IR.

The Lipid-Metabolism-Associated Anti-Obesity Properties of Rapeseed Diacylglycerol Oil.

To investigate the effects of rapeseed diacylglycerol oil (RDG) intake on lipid accumulation and metabolism in C57BL/6J mice, obese mice were fed a high-fat diet in which 45% of the total energy content came from RDG (RDGM group) or rapeseed triacylglycerol oil (RTGM group). This diet intervention was conducted for 12 weeks following the establishment of the obese mouse model. By the end of the experiment, the serum glucose levels of the mice in the RTGM and RDGM groups were 13.0 ± 1.3 mmol/L and 9.7 ± 1.5 mmol/L, respectively. Meanwhile, the serum triglyceride level in the RDGM group was 26.3% lower than that in the RTGM group. The weight-loss effect in the RDGM group was accompanied by a significant decrease in the white adipose tissue (WAT) index. The RDG intervention did not significantly change the antioxidant and anti-inflammatory properties of the rapeseed oil in vivo. The RDG diet improved the liver lipid metabolism abnormalities induced by a high-fat diet, leading to decreased liver damage index values (AST and ALT). Additionally, compared to that in the RTGM group, the expression of the adipogenic genes PPAR-γ and DGAT decreased in both the liver and intestine by 21.7% and 16.7% and by 38.7% and 47.2%, respectively, in the RDGM group. Further, most lipolytic genes in BAT showed no significant change after the RDG intervention. This implies that RDG regulates lipid metabolism by altering the expression of adipogenic genes in the liver, intestine, and adipose tissue, thereby reducing the accumulation of WAT. Furthermore, the RDG diet enhanced gut flora diversity, increasing the relative levels of unclassified Muribaculaceae and decreasing the levels of Dubosiella and Faecalibaculum in the mouse gut, potentially accelerating lipid metabolism. Thus, a three-month RDG diet intervention in obese mice exhibited benefits in regulating the somatotype, serum obesity-related indices, gut flora structure, and lipid metabolism in the adipose tissue, liver, and intestine.

Metabolic and microbial mechanisms related to the effects of dietary wheat levels on intramuscular fat content in finishing pigs

The current study aimed to investigate the metabolic and microbial mechanisms behind the effects of dietary wheat levels on intramuscular fat (IMF) content in the psoas major muscle (PM) of finishing pigs. Thirty-six barrows were arbitrarily assigned to two groups and fed with diets containing 25% or 55% wheat. Enhancing dietary wheat levels led to low energy states, resulting in reduced IMF content. This coincided with reduced serum glucose and low-density lipoprotein cholesterol levels. The AMP-activated protein kinase α2/sirtuin 1/peroxisome proliferator-activated receptor-γ coactivator 1α pathway may be activated by high-wheat diets, causing downregulation of adipogenesis and lipogenesis genes, and upregulation of lipolysis and gluconeogenesis genes. High-wheat diets decreased relative abundance of Lactobacillus and Coprococcus, whereas increased SMB53 proportion, subsequently decreasing colonic propionate content. Microbial glycolysis/gluconeogenesis, d-glutamine and D-glutamate metabolism, flagellar assembly, and caprolactam degradation were linked to IMF content. Metabolomic analysis indicated that enhancing dietary wheat levels promoted the protein digestion and absorption and affected amino acids and lipid metabolism. Enhancing dietary wheat levels reduced serum glucose and colonic propionate content, coupled with strengthened amino acid metabolism, contributing to the low energy states. Furthermore, alterations in microbial composition and propionate resulted from high-wheat diets were associated with primary bile acid biosynthesis, arachidonic acid metabolism, steroid hormone biosynthesis, and biosynthesis of unsaturated fatty acids, as well as IMF content. Colonic microbiota played a role in reducing IMF content through modulating the propionate-mediated peroxisome proliferators-activated receptor signaling pathway. In conclusion, body energy and gut microbiota balance collectively influenced lipid metabolism.

Neuroprotective Effect of Chlorogenic Acid in an Animal Model of Sporadic Alzheimer's Disease Induced by Streptozotocin.

Alzheimer's Disease is a degenerative neurological condition which leads to a decline in memory and cognitive function. Chlorogenic Acid (CGA) presents properties including neuroprotective, antioxidant and anti-inflammatory. The aim of this study was to examine the impact of CGA on cognitive impairments, neuroinflammation and neuronal damage in mice submitted to an experimental model of Sporadic Alzheimer Disease (SAD) induced by intracerebroventricular administration of streptozotocin (ICV-STZ). Male Swiss mice received bilateral ICV-STZ injections (3mg/Kg) on days 1 and 3. The treatment with CGA (5mg/Kg, orally) or vehicle (water, orally), was initiated and continued for 26days, starting 2h after the second induction procedure. At first, there was no change in serum glucose levels after SAD induction. ICV-STZ induces impairments in aversive, recognition, and spatial memory, while CGA treatment significantly alleviated these memory deficits. Furthermore, locomotor activity, working memory, and anxiety-related activities remained unaffected by the treatments. CGA treatment protects against ICV-STZ-induced increase in the nitrite/nitrate and TBARS levels. ICV-STZ induced a reduction in viable cells, depletion of BDNF, and triggered astrogliosis and microgliosis in the cortex and hippocampus. Treatment with CGA preserves viable cell count in the prefrontal cortex, CA1, and CA3 regions of the hippocampus. Additionally, it prevented BDNF depletion in the prefrontal cortex and hippocampus (CA1, CA3, and DG regions), and mitigated astrogliosis and microgliosis in the prefrontal cortex and hippocampus (CA1, CA3, and DG regions). These findings indicate the neuroprotective effects of CGA, underscoring their potential as therapeutic agents or adjuncts in the treatment of SAD.

Gckr depletion leads to growth retardation and diet-dependent visceral obesity in red crucian carp (Carassius auratus red var.)

There exists a notable contrast in the carbohydrate utilization capacity between fish and mammals. In mammals, the glucokinase regulatory protein (GCKR) is known to exert inhibitory effects on glycolysis by binding to glucokinase (GCK), but its role in fish remains unexplored. In this study, the function of gckr in red crucian carp (Carassius auratus red var.), hereafter referred to as RCC, was investigated through its knockout. Under normal dietary conditions, the growth rate of gckr knockout RCC was significantly lower compared to wild-type (WT) RCC reared in the same environment. Subsequent analysis found that gckr knockout RCC exhibited significantly higher serum glucose levels at 1 h post-feeding or glucose injection (hpi), while the difference was abolished at 3 h. Therefore, the metabolic characteristics at 1 and 3 hpi were evaluated between WT and gckr knockout RCC. The results revealed that gckr knockout led to impaired insulin signaling and glycolysis, as evidenced by a reduction in serum insulin level, hepatic insulin receptor a and pyruvate kinase expression, GCK contents, and pyruvate levels at 1 hpi. Additionally, gckr knockout resulted in compromised gluconeogenesis, as indicated by a significant decrease in hepatic expression of fructose-1,6-bisphosphatase 1 and glucose-6-phosphatase at 1 hpi, while it did not affect glycogen accumulation after glucose injection. Regarding lipid metabolism, gckr knockout caused a transient decrease in triglyceride level and reduced expression of fatty acid synthase after glucose injection. Moreover, decreased hepatic peroxisome proliferator activated receptor alpha (ppara) transcripts and proteins were observed in gckr knockout RCC at 1 dpi, indicating a reduced capacity for β-oxidation due to Gckr deficiency. Interestingly, when fed a high-lipid diet, gckr knockout resulted in a significant increase in visceral mass with higher triglyceride level, accompanied by attenuated PPARα signaling. Taken together, this study provides evidence that Gckr-mediated maintenance of Gck contributes to the facilitation of postprandial glycolysis, gluconeogenesis, lipogenesis, and fatty acid β-oxidation in RCC. This study further suggests that enhancing glycolysis may promote growth and liver health in fish under high lipid dietary conditions.

Correlations between Gut Microbiota and Hematological, Inflammatory, Biochemical and Oxidative Stress Parameters in Treatment-Naïve Psoriasis Patients.

Psoriasis is an inflammatory dermatosis with a complex pathogenesis, significantly impacting the quality of life of patients. The role of oxidative stress and gut microbiota in the pathogenesis of this disease is increasingly studied, appearing to underlie the comorbidities associated with this condition. We present the first prospective observational study conducted in Romania evaluating the interrelationship between gut microbiota and hematological, inflammatory, biochemical, and oxidative stress parameters in treatment-naïve psoriasis patients. Significant differences were observed in terms of microbiota composition, with lower levels of Firmicutes and Enterobacteriaceae in the psoriasis group compared to the control group. Moreover, a negative correlation was found between the serum triglyceride levels in patients with psoriasis and the Enterobacteriaceae family (p = 0.018, r = -0.722), and a positive correlation was found between the serum glucose levels and the Firmicutes/Bacteroides ratio (p = 0.03, r = 0.682). Regarding the oxidant-antioxidant status, a significant correlation was found between the FORT level and Lactobacillus (p = 0.034, r = 0.669). Lastly, the Firmicutes level negatively correlated with the DLQI level, independent of the clinical severity of the disease (p = 0.02, r = -0.685). In conclusion, even though the number of included patients is small, these results may serve as a starting point for future research into the involvement of the microbiota-inflammation-oxidative stress axis in psoriasis development.

Benefits of Badminton for Preventing Cognitive Decline and Dementia

Badminton is one of the most popular racket sports played by all age groups worldwide. Anyone can practice and play badminton as a leisure or competitive sport, regardless of age, experience, or skill level. It does not require physical contact among players or expensive equipment. Compared with closed-skill exercises (e.g., running and swimming), open-skill exercises (e.g., badminton and table tennis) have been reported to significantly improve cognitive function and prevent cognitive decline. This mini review aimed to investigate the findings related to badminton intervention for cognitive function, with attention to the modifiable risk factors of dementia in adults. Additionally, we outlined the characteristics of badminton’s physical demands. This narrative review encompassed studies reported from 2013 to 2023 from multiple databases, including PubMed and Google Scholar. Keywords such as “badminton”, “dementia”, “cognitive function”, “physical activity”, and “depression” were used to identify relevant articles. Various studies, including randomized controlled trials, cohort studies, and case–control studies, were selected to provide a comprehensive overview of badminton intervention. Quantitative data analysis suggests that at a cognitive level, high-intensity badminton can enhance cognitive function with at least 10 min of play once weekly or 20 min of play once weekly on average, whereas moderate-intensity badminton can be effective when played for at least 30 min once weekly or 35 min twice weekly on average. For modifiable risk factors, recreational badminton for about 3 h weekly could effectively manage blood pressure. For body fat percentage and fasting serum glucose levels, recreational badminton for about 10 h weekly exerted positive effects. For depressive states, a moderate-intensity badminton program for 100 min weekly was effective. For lipid profiles associated with dementia occurrence, prolonged badminton intervention for more than 3 months may be beneficial. The characteristics presented here indicate that intervention with regular badminton exercise could effectively improve cognitive function and prevent cognitive decline in older adults.

Prevalence, demographic characteristics, and clinical features of suicide risk in first episode drug-naïve schizophrenia patients with comorbid severe anxiety

BackgroundBoth anxiety symptoms and suicide risk are common in schizophrenia. However, previous findings about the association between anxiety and suicide risk in schizophrenia were controversial. This study is the first to examine the prevalence of suicide risk and related demographic, clinical features in a large sample of first episode drug-naïve (FEDN) schizophrenia patients with comorbid severe anxiety. MethodsIn total, 316 patients with FEDN schizophrenia were enrolled in this study. Patients' symptoms were assessed using the Hamilton Depression Scale (HAMD), Hamilton Anxiety Rating Scale (HAMA), and Positive and Negative Syndrome Scale (PANSS). Serum levels of glucose, insulin, uric acid, and lipids including total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C), were evaluated. ResultsIn the current study, 56.3% patients presented comorbid severe anxiety. The rate of suicide risk was higher in the severe anxiety group (55.6%) than in the mild-moderate anxiety group (33.3%). The interactions among severe anxiety, uric acid and HDL-C were associated with suicide risk. Compared with patients with normal uric acid, those with abnormal uric acid exhibited a stronger association between HAMA scores and HAMD-suicide item scores. This enhanced association was also observed for patients with abnormal HDL-C levels. ConclusionsIn FEDN schizophrenia patients with comorbid severe anxiety, our findings suggested a high incidence of suicide risk. Abnormal levels of uric acid and low levels of HDL-C, as well as high depression may be associated with an increased risk of suicide in FEDN schizophrenia patients with comorbid severe anxiety.

The effect of 12weeks of aerobic exercise training with or without saffron supplementation on diabetes-specific markers and inflammation in women with type 2 diabetes: A randomized double-blind placebo-controlled trial.

This study was conducted to investigate the effects of 12weeks of aerobic exercise (AT) and saffron supplementation on hemostasis, inflammatory markers, and insulin resistance in obese women diagnosed with type 2 diabetes (T2D). A total of 44 women with T2D (mean age: 54.12±5.63years, mean BMI: 31.15±1.50kg/m2, HbA1c: 85±4.2mmol/mol) were included in a randomized, double-blind, placebo-controlled study. We were randomly assigned to one of four groups (n=11 per group): saffron+training (ST), placebo+training (PT), saffron supplement (SS), and placebo (P). The ST and PT groups completed 12weeks of AT (three sessions per week of mild to moderate intensity). The ST and SS groups were administered a daily dose of 200mg of saffron powder for 12weeks. Fasting blood samples were collected 48h before the first AT session and/or nutritional supplementation and 48h after the last AT session and/or nutritional supplementation. Post-evaluation, homeostatic model assessment of insulin resistance value (HOMA-IR, p<0.001) and serum levels of glucose (p<0.001), fibrinogen (FIB, p<0.001), homocysteine (HCY, p<0.001), interleukin-6 (IL-6, p<0.001), and tumor necrosis factor α (TNFα, p<0.001) showed significant reduction in the ST, PT, and SS groups compared to the P group (p<0.05). In particular, the ST group showed a more significant reduction in all variables compared to the PT and SS groups (p<0.05). Our results suggest that a 12-week intervention with AT and saffron supplementation can independently improve markers related to hemostasis, inflammation, and insulin resistance. However, their combination showed the greatest effectiveness on the above markers.

Synergistic Effect of Maternal Micronutrient Supplementation on ORFV DNA Vaccine Immune Response in a Pregnant Model.

Contagious ecthyma is a contagious zoonotic disease caused by the Orf virus that can infect farm animals and humans, but no vaccine is available for pregnant mothers. Excessive oxidative stress during pregnancy can suppress the vaccine immune response in pregnant mothers; hence, maternal micronutrient supplementation could effectively improve the immune response, health, and oxidative status during pregnancy. In this study, we employed an 8-week-old pregnant rat model to receive a single intramuscular dose of 200µg of ORF DNA vaccine with or without vitamin E and selenium supplementation to evaluate their effect on immune responses (specific IgG and IgG isotypes), oxidative stress, liver enzymes, and blood glucose levels in maternal-neonatal serum and milk secretions. Additionally, antioxidant-related gene expressions were analyzed in the maternal placenta and pups' liver. The results showed that supplementation of vitamin E and selenium with ORF DNA vaccination increased the production of specific antibody and IgG isotypes (IgG1 and IgG2a) and reduced the oxidative stress in neonatal-maternal serum and milk compared to both the control group and those vaccinated without supplementation (p < 0.05). Notably, the ORF DNA vaccine did not cause oxidative stress and hepatic damage. However, combined supplementation of vitamin E and selenium with DNA vaccination significantly decreased serum malondialdehyde (MDA) levels and improved the antioxidant-related enzyme activities of glutathione peroxidase (GPX), superoxide dismutase 1 (SOD1), and selenoprotein P (SELP) in the maternal placenta and liver of pups (p < 0.05). In conclusion, maternal supplementation of vitamin E and selenium enhanced the immune responses of the ORF DNA vaccine by mitigating oxidative stress in pregnant rats and could thus be a promising strategy for better health outcomes for both mothers and neonates.

Optimal level of dietary arginine enhances growth performance, haemato-biochemical status, metabolic responses and growth-related gene expression of GIFT juveniles reared in inland saline water

The effects of arginine levels in diets on growth performance, survival, and haemato-biochemical responses and gene expression of genetically improved farmed tilapia (GIFT) juveniles raised in inland saline water (ISW) of 10 ppt were evaluated through a 60-day growth trial. Seven isoproteinaceous (⁓320 g protein/kg), isolipidic (80 g/kg) and isoenergetic (16.8 MJ DE/kg) diets with graded levels of arginine viz. A10 (10 g/kg), A12.5 (12.5 g/kg), A15 (15.0 g/kg), A17.5 (17.5 g/kg), A20 (20.0 g/kg), A22.5 (22.5 g/kg) and A25 (25.0 g/kg) were prepared. Acclimated GIFT juveniles (3.75 ± 0.017 g) were randomly assigned into seven treatments in triplicate with 15 fish/replicate and fed with respective diets thrice a day on a satiation basis. The percent weight gain, specific growth rate, protein efficiency ratio, whole carcass protein, tissue alanine and aspartic acid aminotransferase activities, serum total protein, albumin and globulin concentration and expression of IGF-1 & IGF-1R genes of fish significantly increased, while feed conversion ratio significantly decreased with increasing arginine in the diet up to 17.5 g/kg and decreased thereafter. Additionally, white blood cell count increased with rising arginine levels in the diet. However, body indices, survival, whole carcass lipid, total ash and essential amino acids contents, activities of digestive and antioxidant enzymes, serum glucose level and blood haemoglobin level and red blood cell count of fish remained unchanged for different treatments. Based on broken-line regression and second order polynomial regression models in relation to hepatic IGF-1 gene expression and percent weight gain, the dietary optimal arginine level was found to be 15.97 and 16.76 g/kg and 17.06 and 17.41 g/kg, respectively with the optimum range of 15.97 to 17.41 g/kg for successful culture of GIFT in ISW of 10 ppt salinity.

Novel insights into immune stress markers associated with myxosporeans gill infection in Nile tilapia (molecular and immunohistochemical studies).

Nile tilapia (Oreochromis niloticus) is valued in aquaculture because of its quick development and ability to thrive in various environments. Myxosporeans are among the fish parasites that affect fish productivity, as they impact fish growth and reproduction, resulting in large fish deaths in farms and hatcheries. This study has been focused on morpho-molecular identification for the myxosporean parasites infecting Nile tilapia from three governorates in Egypt and assessment of gene expression of different cytokines (Interleukin-1βeta (IL-1β), major histocompatibility complex class II (MHC-II), and clusters of differentiation 4 (CD-4) and 8 (CD-8)) in tissues. Additionally, this work aimed to correlate the developed histopathological alterations and inflammatory reactions in gills with immunohistochemical expression of inducible nitric oxide synthase (iNOS) and tumor necrosis factor-alpha (TNF-α). Finally, the infected fish's cortisol levels and blood glucose were assessed. Results of BLAST sequence analysis of the 18S rRNA for the collected protozoans confirmed Myxobolus agolus, M. brachysporus, M. tilapiae, and Henneguya species. The molecular characterization of the immunological status of gills revealed marked upregulation of different inflammatory cytokines in the gills of infected fish. There was a significantly increased serum cortisol and glucose level in infected fish compared with control, non-infected ones. Severe histopathological alterations were observed in the infected fish gills, associated with increased expression of iNOS and TNF-α and related to myxosporean infection. The present study provides new insights into oxidative stress biomarkers in Nile tilapia infected with Myxosporeans and elucidates the gill's immune status changes as a portal of entry for protozoa that contribute to tissue damage.

A randomized double blind placebo controlled trial to assess the safety and efficacy of a patented fenugreek (Trigonella foenum-graecum) seed extract in Type 2 diabetics.

Fenugreek plant (Trigonella foenum-graecum) constitutes a traditionally acclaimed herbal remedy for many human ailments including diabetes, obesity, neurodegenerative diseases, and reproductive disorders. It is also used as an effective anti-oxidative, anti-inflammatory, antibacterial, and anti-fungal agent. The seed of the plant is especially enriched in several bioactive molecules including polyphenols, saponins, alkaloids, and flavonoids and has demonstrated potential to act as an antidiabetic phytotherapeutic. A novel patented formulation (Fenfuro®) was developed in our laboratory from the fenugreek seeds which contained >45% furostanolic saponins (HPLC). A placebo-controlled clinical compliance study was designed to assess the effects of complementing Fenfuro® on a randomized group of human volunteers on antidiabetic therapy (Metformin and sulphonylurea) in controlling the glycemic index along with simultaneous safety assessment. In a randomized double-blind, placebo-controlled trial, 42 individuals (21 male and 21 female volunteers) in the treatment group (out of 57 enrolled) and 39 individuals (17 male and 22 female volunteers) in the placebo group (out of 47 enrolled), all on antidiabetic therapy with Metformin/Metformin with sulphonyl urea within the age group of 18-65 years were administered either 1,000 mg (500 mg × 2) (Fenfuro®) capsules or placebo over a period of 12 consecutive weeks. Fasting and postprandial glucose along with glycated hemoglobin were determined as primary outcomes to assess the antidiabetic potential of the formulation. Moreover, in order to evaluate the safety of the formulation, C-peptide and Thyroid Stimulating Hormone (TSH) levels as well as immunohematological parameters were assessed between the treatment and placebo groups at the completion of the study. After 12 weeks of administration, both fasting as well as postprandial serum glucose levels decreased by 38 and 44% respectively in the treatment group. Simultaneously, a significant reduction in glycated hemoglobin by about 34.7% was also noted. The formulation did not have any adverse effect on the study subjects as there was no significant change in C- peptide level and TSH level; liver, kidney, and cardiovascular function was also found to be normal as assessed by serum levels of key immunohematological parameters. No adverse events were reported. This clinical compliance study re-instated and established the safety and efficacy of Fenfuro® as an effective phytotherapeutic to treat hyperglycemia.

Frequency of Hypoglycemia in Cirrhotic Patients Undergoing Endoscopy.

Liver cirrhosis isthe replacement of normal liver parenchyma by fibrous tissue and nodularity. Cirrhosis liver has a negative effect on the body's ability to regulate blood glucose levels because the liver cannot release the amount of glucose it wouldultimately cirrhotic patients are atrisk of hypoglycemia. To determine the frequency of hypoglycemia in cirrhotic patients just before endoscopy after being nil per mouth (NPO) for 6 hours. This cross-sectional study was done at the Department of Gastroenterology Lady Reading Hospital, Peshawar from 1st April 2023 to 30th September 2023.Patients aged > 20 years of both genders, having Child-Pugh class C cirrhosis, and undergoing upper gastrointestinal (GI) endoscopy were enrolled in the study while patients with a history of diabetes using oral or parenteral hypoglycemic medications, patients taking steroids, patients with hepatocellular carcinoma and patients with hepatic encephalopathy were excluded. Diagnosis of liver cirrhosis was based on clinical examination, serum albumin level, and prothrombin time followed by characteristic findings on ultrasound. Serum glucose level was determined in the blood sample of the patient from the hospital laboratory. Results:One hundred and ninety-six patients were enrolled including 130 (67.4%) males and 66 (32.6%) females. Age of the patients ranged from 20 to 60 years. The mean age of the participants was 46.68±10.239 years. Hypoglycemia was found in 48% of patients with liver cirrhosis. A significant association of hypoglycemia was found with disease duration and Child-Pugh class. Hypoglycemia is a frequent finding in patients with liver cirrhosis and needs urgent management to prevent complications. Prolonged illness and patients with Child-Pugh class C cirrhosis are more likely to have hypoglycemia.

Effect of polymethoxylated flavonoids on glucose and lipid metabolism in rat model of obesity induced by a high-fat diet

This study established a rat model of obesity by using a high-fat diet(HFD) to explore the effect of polymethoxylated flavonoids on glucose and lipid metabolism in the model rats and decipher the role and mechanism of polymethoxylated flavonoids in mitigating obesity. Thirty normal SD rats were selected and randomized into normal, model, ezetimibe(0.1 mg·kg~(-1)), and polymethoxylated flavonoids(62.5 mg·kg~(-1) and 125 mg·kg~(-1)) groups based on the body weight. Except the normal group receiving a conventional diet, the other groups received a HFD. Rats were administrated with corresponding doses of drugs by gavage. During the administration period, the body weight of each group of rats was regularly weighed, and the serum lipid and glucose levels were measured by a fully automated biochemical analyzer. Islet homeostasis and serum levels of obesity factors were measured by ELISA. The 16S rRNA high-throughput sequencing was employed to study the gut microbiota. Hematoxylin-eosin staining was employed to observe the histomorphology of white fat, brown fat, and pancreas. After the wet weights of white fat and brown fat were measured, the organ index was calculated. Immunohistochemistry and Western blot were employed to determine the protein levels. The results showed that polymethoxylated flavonoids reduced the body weight and Lee's index and improved blood lipid levels of the model rats. Polymethoxylated flavonoids reduced blood glucose and insulin secretion, increased insulin responsiveness, and alleviated insulin resistance. In addition, polymethoxylated flavonoids regulated the serum levels of obesity factors and reduced the weights and indexes of white fat and brown fat, the diameter of white adipocytes, and the number of fat vacuoles in brown fat and pancreatic islet cells. The intervention with polymethoxylated flavonoids increased the diversity of gut microbiota in the model rats, increasing the beneficial bacteria associated with glucose and lipid metabolism and reduced the harmful bacteria at the genus level. In addition, polymethoxylated flavonoids up-regulated the protein levels of glucose transporter 4(GLUT4), phosphorylated AMP-activated protein kinase(p-AMPK), peroxisome proliferator-activated receptor gamma coactivator-1α(PGC-1α), and uncoupling protein 1(UCP1). In summary, polymethoxylated flavonoids may increase the body utilization of glucose and lipids by regulating the homeostasis of insulin, the serum levels of obesity factors, the diversity of gut microbiota, and the expression of mitochondrial metabolism-related proteins in brown adipocytes, thereby mitigating obesity in rats.

The Effect of Isotretinoin on Insulin Resistance and Serum Adiponectin Levels in Acne Vulgaris Patients: A Systematic Review and Meta-Analysis.

Isotretinoin is the drug of choice for severe acne. We sought to examine the potential link between isotretinoin and insulin resistance. We conducted a systematic review and meta-analysis in accordance with the PRISMA statement. A comprehensive search of the PubMed/MEDLINE, SCOPUS, and Cochrane databases was performed until 12 January 2022 utilizing the PICO (Patient, Intervention, Comparison, Outcome) tool. Fifteen English-language studies focusing on isotretinoin-treated acne patients were included. Serum levels of insulin, glucose, and adiponectin were evaluated before and after treatment, and insulin sensitivity was assessed using the HOMA-IR. A meta-analysis was conducted using RevMan 5.4.1 software, and a quality assessment was undertaken using the ROBINS-I tool. The meta-analysis unveiled a statistically significant rise in the post-treatment levels of adiponectin, an anti-inflammatory agent, which inhibits liver glucose production while enhancing insulin sensitivity (SMD = 0.86; 95% confidence interval (95% CI) = 0.48-1.25, p-value < 0.0001; I2 = 58%). Our subgroup analysis based on study type yielded consistent findings. However, no statistically significant outcomes were observed for insulin, glucose levels, and the HOMA-IR. There is not a clear association between isotretinoin and insulin resistance, but it appears to enhance the serum levels of adiponectin, which participates in glucose metabolism.

Glutaryl-CoA dehydrogenase suppresses tumor progression and shapes an anti-tumor microenvironment in hepatocellular carcinoma

Crotonylation, a crotonyl-CoA-based non-enzymatic protein translational modification, affects diverse biological processes, such as spermatogenesis, tissue injury, inflammation, and neuropsychiatric diseases. Crotonylation is decreased in hepatocellular carcinomas (HCCs), but the mechanism remains unknown. In this study, we aim to describe the role of glutaryl-CoA dehydrogenase (GCDH) in tumor suppression. Three cohorts containing 40, 248 and 17 pairs of samples were used to evaluate the link between GCDH expression levels and clinical characteristics of HCC, as well as responses to anti-programmed cell death protein 1 (PD-1) treatment. Subcutaneous xenograft, orthotopic xenograft, Trp53Δhep/Δhep; MYC- and Ctnnboe; METoe-driven mouse models were adopted to validate the effects of GCDH on HCC suppression. GCDH depletion promoted HCC growth and metastasis, whereas its overexpression reversed these processes. AsGCDH converts glutaryl-CoA to crotonyl-CoA to increase crotonylation levels, we performed lysine crotonylome analysisand identified the pentose phosphate pathway (PPP) and glycolysis-related proteins PGD, TKT, and ALDOC asGCDH-induced crotonylation targets. Crotonyl-bound targets showed allosteric effects that controlled their enzymatic activities, leading to decreases in ribose 5-phosphate and lactate production, further limiting the Warburg effect. PPPblockade also stimulated peroxidation, synergizing with senescent modulators to induce senescence in GCDHhigh cells.These cells induced the infiltration of immune cells by the SASP (senescence-associated secretory cell phenotype)toshape an anti-tumor immune microenvironment. Meanwhile, the GCDHlow population was sensitized to anti-PD-1 therapy. GCDH inhibits HCC progression via crotonylation-induced suppression of the PPP and glycolysis, resulting in HCC cell senescence. The senescent cell further shapes an anti-tumor microenvironment via the SASP. The GCDHlow population is responsive to anti-PD-1 therapy because of the increased presence of PD-1+CD8+ T cells. Glutaryl-CoA dehydrogenase (GCDH) is a favorable prognostic indicator in liver, lung, and renal cancers. In addition, most GCDH depletion-induced toxic metabolites originate from the liver, accumulate locally, and cannot cross the blood-brain barrier. Herein, we show that GCDH inhibits hepatocellular carcinoma (HCC) progression via crotonylation-induced suppression of the pentose phosphate pathway and glycolysis, resulting in HCC cell senescence. We also found that more PD-1+CD8+ T cells are present in the GCDHlow population, who are thus more responsive to anti-PD-1 therapy. Given that the GCDHlow and GCDHhigh HCC population can be distinguished based on serum glucose and ammonia levels, it will be worthwhile to evaluate the curative effects of pro-senescent and immune-therapeutic strategies based on the expression levels of GCDH.