Sucrose Diet Research Articles

Independent and combined effects of obesity and traumatic joint injury to the structure and composition of rat knee cartilage

ABSTRACT Osteoarthritis (OA) is a multifactorial joint disease characterized by articular cartilage degradation. Risk factors for OA include joint trauma, obesity, and inflammation, each of which can affect joint health independently, but their interaction and the associated consequences of such interaction were largely unexplored. Here, we studied compositional and structural alterations in knee joint cartilages of Sprague-Dawley rats exposed to two OA risk factors: joint injury and diet-induced obesity. Joint injury was imposed by surgical transection of anterior cruciate ligaments (ACLx), and obesity was induced by a high fat/high sucrose diet. Depth-dependent proteoglycan (PG) content and collagen structural network of cartilage were measured from histological sections collected previously in Collins et al.. (2015). We found that ACLx primarily affected the superficial cartilages. Compositionally, ACLx led to reduced PG content in lean animals, but increased PG content in obese rats. Structurally, ACLx caused disorganization of collagenous network in both lean and obese animals through increased collagen orientation in the superficial tissues and a change in the degree of fibrous alignment. However, the cartilage degradation attributed to joint injury and obesity was not necessarily additive when the two risk factors were present simultaneously, particularly for PG content and collagen orientation in the superficial tissues. Interestingly, sham surgeries caused a through-thickness disorganization of collagen network in lean and obese animals. We conclude that the interactions of multiple OA risk factors are complex and their combined effects cannot be understood by superposition principle. Further research is required to elucidate the interactive mechanism between OA subtypes.

ANTIBACTERIAL ACTIVITY TEST OF CUCUMBER PEEL EXTRACT (Cucumis sativus L.) AGAINST Streptococcus mutans BACTERIA

Background: Dental caries is a process of tooth demineralization caused by acids produced from food metabolism in bacteria. One of the main etiological factors of dental caries is the microorganisms known as Streptococcus mutans bacteria. S. mutans is one of the components of human dental plaque that is associated with sucrose diet and high caries activity. Cucumber peel extract (Cucumis sativus L.) is known to have an antibacterial activity due to the presence of secondary metabolites such as flavonoids, steroids, alkaloids, saponins and phenols found in cucumber peel. Purpose: This study aimed to determine the antibacterial activity at the lowest concentration of cucumber peel extract (Cucumis sativus L.) against Streptococcus mutans bacteria. Method: This study employed the disc diffusion method with a post-test only control group design. Streptococcus mutans bacteria were cultured on Mueller Hinton Agar media, and cucumber peel extract (Cucumis sativus L.) was applied as the antibacterial agent at concentrations of 0.01 g/ml, 0.05 g/ml, 0.1 g/ml, 0.2 g/ml, 0.4 g/ml and 0.5 g/ml with seven repetitions. Results: The results of the study showed that cucumber peel extract (Cucumis sativus L.) formed inhibition zones around the paper discs against the growth of Streptococcus mutans bacteria at concentrations of 0.4 g/ml and 0.5 g/ml. Conclusion: The concentrations of 0,4 g/ml and 0,5 g/ml are the lowest concentrations of cucumber peel extract (Cucumis sativus L.) that can inhibit the growth of Streptococcus mutans bacteria. Keywords : Antibacterial, Cucumber peel, Dental Caries, Streptococcus mutans

VCD-induced menopause mouse model reveals reprogramming of hepatic metabolism

ObjectiveMenopause adversely impacts systemic energy metabolism and increases the risk of metabolic disease(s) including hepatic steatosis, but the mechanisms are largely unknown. Dosing female mice with vinyl cyclohexene dioxide (VCD) selectively causes follicular atresia in ovaries, leading to a murine menopause-like phenotype. MethodsIn this study, we treated female C57BL6/J mice with VCD (160 mg/kg i.p. for 20 consecutive days followed by verification of the lack of estrous cycling) to investigate changes in body composition, energy expenditure (EE), hepatic mitochondrial function, and hepatic steatosis across different dietary conditions. ResultsVCD treatment induced ovarian follicular loss and increased follicle-stimulating hormone (FSH) levels in female mice, mimicking a menopause-like phenotype. VCD treatment did not affect body composition, or EE in mice on a low-fat diet (LFD) or in response to a short-term (1-week) high-fat, high sucrose diet (HFHS). However, the transition to a HFHS lowered cage activity in VCD mice. A chronic HFHS diet (16 weeks) significantly increased weight gain, fat mass, and hepatic steatosis in VCD-treated mice compared to HFHS-fed controls. In the liver, VCD mice showed suppressed hepatic mitochondrial respiration on LFD, while chronic HFHS resulted in compensatory increases in hepatic mitochondrial respiration. Also, liver RNA sequencing revealed that VCD promoted global upregulation of hepatic lipid/cholesterol synthesis pathways. ConclusionOur findings suggest that the VCD-induced menopause model compromises hepatic mitochondrial function and lipid/cholesterol homeostasis that sets the stage for HFHS diet-induced steatosis while also increasing susceptibility to obesity.

Antidiabetic and Antioxidant Effect of Ethanolic Extract of Propolis from Meiganga (Cameroon) on Type 2 Diabetes in Rats

Diabetes mellitus is a metabolic disorder characterized by chronic hyperglycemia. In Cameroon, the traditional treatment of this pathology is based on the use of Propolis. The present study aims to evaluate the antidiabetic and antioxidant properties of the ethanoic extract of Meiganga propolis (Adamawa Region, Cameroon). To confirm the different properties of this extract, the glycaemia, lipid profile and oxidative stress parameters of different groups of animals were assessed in a type 2 diabetes model induced by the Hypercaloric Sucrose Diet combined with dexamethasone. Simultaneous administration of the ethanolic extract of Meiganga propolis (EEMP 300 mg/kg) and the hypercaloric sucrose diet to rats for 30 days prevented a significant increase in fasting blood glucose levels compared with animals in the diabetic control group, whose fasting blood glucose levels were 78.25 ± 2.29 and 156.5 ± 2.75 mg/dL respectively on day 30. In terms of lipid profile, the administration of propolis extract (300 mg/kg) prevented a significant increase in LDL-cholesterol and triglyceride levels compared with animals in the diabetic control groups. The values were 27±2.71 mg/dL and 97.8±2.92 mg/dL for LDL-cholesterol. In terms of oxidative stress, simultaneous administration of propolis extract (300 mg/kg) and a high calorie diet to rats for 30 days prevented a significant increase in malondialdehyde (MDA) and increased superoxide dismutase (SOD) levels compared with animals in the diabetic control group. Values for this superoxide dismutase in the liver were 81.72 U/g of organ for EEMP 300 mg/kg and 58.6 U/g of organ in the liver of diabetic rats. These results justify the use of ethanoic extract of Meiganga propolis in the prevention of type 2 diabetes in Cameroon.

Blighia welwitschii (Hiern) leaf solvent fractions ameliorate diabetes in Drosophila melanogaster induced by high–sucrose diet

The therapeutic potential of Blighia welwitschii in insulin resistant disorder is poorly understood. Herein, the antioxidant and anti-diabetes potentials of solvent fractions of B. welwitschii leaf was performed using various experimental approaches in Drosophila melanogaster model. In vitro antioxidant and alpha amylase inhibitory assay were carried out on successive fractions of aqueous, butanol, ethylacetate and hexane using standard procedures. The most active fraction was subjected to HPLC analysis and the bioactive compounds identified were virtually screened against D. melanogaster α-amylase (2QV4) binding site using Schrodinger suite (2017 v 1). The butanol and ethylacetate fractions were fed to diabetes and non-diabetes flies to study their anti-diabetes and anti-oxidant properties followed by ILP-2, InR and IMPL2 mRNA expression using standard procedures. The findings from this study showed that, ethylacetate and butanol fractions possess high percentage hydroxyl radical inhibiting capacity and appreciable ferric reducing antioxidant potential. The phenolics and flavonoids contents were appreciably high compared with other fractions. These fractions also restored glucose imbalance and thiol homeostasis in diabetes flies. The in silico and in vitro anti-diabetes analyses suggested that, the active compounds possess inhibitory efficacy against α-amylase with cyanidin-3-o-rutinoside having the highest binding affinity (−12.8 kcal/mol). The EBW showed non-significant down-regulation of IMPL2 and InR mRNA expression in diabetes flies compared with diabetes untreated flies. Overall, butanol and ethylacetate fractions of B. welwitschii leaf ameliorate insulin resistant diabetes and therefore might be useful for the management of diabetes. However, further anti-diabetes study in other animal model is proposed to compliment this finding.

ACAD10 is not required for metformin's metabolic actions or for maintenance of whole-body metabolism in C57BL/6J mice.

Acyl-coenzyme A dehydrogenase family member 10 (ACAD10) is a mitochondrial protein purported to be involved in the fatty acid oxidation pathway. Metformin is the most prescribed therapy for type 2 diabetes; however, its precise mechanisms of action(s) are still being uncovered. Upregulation of ACAD10 is a requirement for metformin's ability to inhibit growth in cancer cells and extend lifespan in Caenorhabditis elegans. However, it is unknown whether ACAD10 plays a role in metformin's metabolic actions. We assessed the role for ACAD10 on whole-body metabolism and metformin action by generating ACAD10KO mice on a C57BL/6J background via CRISPR-Cas9 technology. In-depth metabolic phenotyping was conducted in both sexes on a normal chow and high fat-high sucrose diet. Compared with wildtype mice, we detected no difference in body composition, energy expenditure or glucose tolerance in male or female ACAD10KO mice, on a chow diet or high-fat, high-sucrose diet (p ≥ .05). Hepatic mitochondrial function and insulin signalling was not different between genotypes under basal or insulin-stimulated conditions (p ≥ .05). Glucose excursions following acute administration of metformin before a glucose tolerance test were not different between genotypes nor was body composition or energy expenditure altered after 4 weeks of daily metformin treatment (p ≥ .05). Despite the lack of a metabolic phenotype, liver lipidomic analysis suggests ACAD10 depletion influences the abundance of specific ceramide species containing very long chain fatty acids, while metformin treatment altered clusters of cholesterol ester, plasmalogen, phosphatidylcholine and ceramide species. Loss of ACAD10 does not alter whole-body metabolism or impact the acute or chronic metabolic actions of metformin in this model.

Dominant lignan profiles and antidiabetic activity of thermally treated and non-treated burdock seeds

Burdock seeds (Fructus arctii) are used as a traditional medicine for cough, inflammation, detoxification, cancer and diabetes, usually as decoction obtained with seeds subjected to thermal pre-treatment. The present work aimed to perform the phytochemical characterization of the stir-baked and non-baked seeds of various Arctium lappa populations from nine localities. Arctiin was dominant compound in non-baked seeds ranging from 40.6–92.6 mg/g. Thermal treatment resulted in a significant transformation of phenolic compounds and arctigenin was prevalent in the baked samples with the content from 25.2–57.4 mg/g. The antidiabetic potential of baked and non-baked burdock seed extracts was further evaluated in vitro by inhibition of α-amylase and α-glucosidase activity, while molecular docking analysis was used to reveal the main molecular interactions underlying the inhibitory effects on these enzymes. In vitro study showed that stir-baked burdock seed extracts were stronger inhibitors of both enzymes compared to non-baked. The several extracts showed strong inhibition of both enzymes by almost or more than 60%, which was lower compared to acarbose (82.99% at a concentration of 1 mg/mL). Arctin and arctigenin were individually significantly stronger inhibitors of α-amylase and particularly α-glucosidase compared to burdock extracts and acarbose, and their activity was concentration dependent. Moreover, antidiabetic activity for the most active sample was determined in vivo using animals on high-fat and sucrose diet, where promising results were obtained. Briefly, after three months of administration of the stir-baked seed extract (100 mg/kg body weight), complete recovery from a hyperglycemic state was achieved. According to the obtained results A. lappa stir-baked seed extract is a potential drug with hypoglycemic action as indicated by in vitro, in vivo and in silico studies.

Genetic and acquired sucrase-isomaltase deficiency: A clinical review.

Genetic sucrase-isomaltase deficiency (GSID) is an inherited deficiency in the ability to digest sucrose and potentially starch due to mutations in the sucrase-isomaltase (SI) gene. Congenital sucrase-isomaltase deficiency is historically considered to be a rare condition affecting infants with chronic diarrhea as exposure to dietary sucrose begins. Growing evidence suggests that individuals with SI variants may present later in life, with symptoms overlapping with those of irritable bowel syndrome. The presence of SI genetic variants may, either alone or in combination, affect enzyme activity and lead to symptoms of different severity. As such, a more appropriate term for this inherited condition is GSID, with a recognition of a spectrum of severity and onset of presentation. Currently, disaccharidase assay on duodenal mucosal tissue homogenates is the gold standard in diagnosing SI deficiency. A deficiency in the SI enzyme can be present at birth (genetic) or acquired later, often in association with damage to the enteric brush-border membrane. Other noninvasive diagnostic alternatives such as sucrose breath tests may be useful but require further validation. Management of GSID is based on sucrose and potentially starch restriction tailored to the individual patients' tolerance and symptoms. As this approach may be challenging, additional treatment with commercially available sacrosidase is available. However, some patients may require continued starch restriction. Further research is needed to clarify the true prevalence of SI deficiency, the pathobiology of single SI heterozygous mutations, and to define optimal diagnostic and treatment algorithms in the pediatric population.

Активність ензимів поліольного шляху у нирках щурів за умов різної забезпеченості раціону протеїном і сахарозою

The study examined the activity of enzymes in the polyol pathway and the status of free radical processes in the kidneys of rats subjected to different dietary protein and sucrose levels. It was found that the kidneys of animals consuming a highsucrose diet, irrespective of protein content, exhibited the highest increase in the activity of polyol pathway enzymes, namely aldose reductase and sorbitol dehydrogenase. Consumption of a high-sucrose diet enhances the generation of O2 •- in the kidneys by almost twofold, and hydroxyl radical by over fourfold compared to control indicators. This is accompanied by a twofold increase in the content of TBARS-active products and a threefold increase in the content of carbonyl derivatives of proteins, against the background of a decrease in the content of free thiol groups in proteins. The pronounced generation of hydroxyl radicals, accumulation of TBARS-active products, and reduction in the content of free SH-groups in proteins are characteristic of animals that consumed a high-sucrose diet in the context of dietary protein deficiency. It has been demonstrated that excessive sucrose consumption is a critical factor, influencing the activity of enzymes in the polyol pathway and the intensity of free radical processes. The obtained results may be considered as predisposing factors for disruptions in the structural and functional organization of the kidneys under conditions of nutrient imbalance.

Cross-sectional association between blood cholesterol and calcium levels in genetically diverse strains of mice.

Genetically diverse outbred mice allow for the study of genetic variation in the context of high dietary and environmental control. Using a machine learning approach, we investigated clinical and morphometric factors that associate with serum cholesterol levels in 840 genetically unique Diversity Outbred mice of both sexes (n = 417 male and 423 female), and on both acontrol chow (% kcals in diet: protein 22%, carbohydrate 62%, fat 16%,no cholesterol) and high fat high sucrose (%kcals in diet: protein 15%, carbohydrate 41%, fat 45%, 0.05% cholesterol). We find expected elevations of cholesterol in male mice, as well as in mice with elevated serum triglycerides and/or fed a high fat high sucrose diet. The third strongest predictor was serum calcium which correlated with serum cholesterol across both diets and sexes (r = 0.39-0.48) in both Diversity Outbred (P = 3.0 × 10-43 ) and BXD (P = 0.005) mice. This is in-line with several human cohort studies which show associations between calcium and cholesterol, and calcium as an independent predictor of cardiovascular events.

Influence of Stachys sieboldii Miq. root powder on changes in neural system parameters in growing male rats on a high fat and sucrose diet

Influence of Stachys sieboldii Miq. root powder on changes in neural system parameters in growing male rats on a high fat and sucrose diet

Enhanced Airway Hyperresponsiveness by Up-Regulation of Tumor Necrosis Factor Αlpha Pathway in Long-Term High-Fat and Sucrose Diet in Bama Mini Pigs

Enhanced Airway Hyperresponsiveness by Up-Regulation of Tumor Necrosis Factor Αlpha Pathway in Long-Term High-Fat and Sucrose Diet in Bama Mini Pigs

THE LEVEL OF LIPID PEROXIDATION IN APIS MELLIFERA L. DURING THEIR SHORT-TERM MAINTENANCE ON DIFFERENT CARBOHYDRATE DIETS

The honey bee (Apis mellifera L.), the main pollinator of entomophilous plants, is one of the most important insects of natural ecosystems and a producer of such important products as honey, perga, royal jelly, wax, propolis etc. The efficiency of beekeeping is limited by many factors, the main of which is the survival of colonies in critical periods of development, especially in the conditions of widespread use of artificial feed. Diets that do not meet the vital needs of honey bees in full nutrition negatively affect their health. The aim of the study was to evaluate the level of lipid peroxidation (LPO), as a marker of the development of stress, in foraging bees Apis mellifera carnica, which consumed different carbohydrate diets in laboratory conditions for 14 hours. Bees were selected from the outermost combs in July, 40-50 individuals into feeder boxes, transported to the laboratory and kept for 14 hours at 25°С in a thermostat on the following diets: Group I – 30% sucrose solution; II – 30% sugar solution; III – 60% sucrose solution; IV – 60% sugar solution; V – 30% glucose solution; VI – 30% fructose solution; VII – 30% glucose solution + 30% fructose solution (1:1); VIII – 15% glucose solution + 15% fructose solution (1:1); IX – 32% honey solution. The insects of the control group were frozen with liquid nitrogen, in the apiary, the insects of the experimental groups - after the end of the experiment; stored at minus 70 °C until biochemical studies. The level of LPO was determined in separate tags (head, thorax, abdomen) according to Placer's method with modifications. It was found that the transfer into feeder boxes, transportation and keeping for 14 hours of a small cluster of forager bees is a significant stress factor for them, as evidenced by the increase in the level of LPO in the tissues of the insects' heads. The lowest level of LPO was observed in the tissues of the head and abdomen in bees that were kept in feeder boxes for fourteen hours on a 30% glucose diet compared to bees that consumed fructose (30%), sucrose (30 % and 60%) diets, a mixture of monosugars (15% + 15% and 30% + 30%) and honey. Keywords Apis mellifera, carbohydrate diet, lipid peroxidation, 14 hour stress, foraging bees

Chronic Metabolic Syndrome develops a frailty of cardiac rhythm similar to aging in rats

Heart rhythm decreases and alterations depend on aging and correlate with lifestyle and metabolic alterations like obesity, dyslipidemia, and chronic inflammation; these alterations may also produce ventricular hypertrophy and atrial fibrillation, increasing lethal arrhythmias. The high sucrose diet in young adult Wistar rats produces metabolic syndrome from the eighth week that continues twenty-six weeks later. In this work, we analyzed the changes presented by the heart during six months of metabolic syndrome. After this period, the rats were anesthetized, and the electrocardiogram was recorded. We observed that metabolic syndrome produced bradycardia and arrhythmias. The electrocardiogram showed an 18 % decrease in the heart rate in rats with metabolic syndrome and a decreased ability to regulate heart rate variability using the p-p interval Poincare graph. The electrical activity recorded in the sinus node showed alteration in the morphology and propagation of the action potential, therefore, a dysfunction in the pacemaker and supraventricular arrhythmias. This data correlated with the increase in the collagen and lipid area in the pacemaker that produced unexcitable segments, which induced lethal arrhythmias by alterations in electrical activity and premature aging and frailty, like those described in humans. We proposed that the changes in electrical and morphological alterations in the sinus node that are associated with metabolic syndrome are the cause of cardiovascular frailty and premature aging of the heart.

Exposure to early-life stress impairs weight-loss maintenance success in mice.

The impact of early-life stress on weight-loss maintenance is unknown. Mice underwent neonatal maternal separation (NMS) from 0 to 3 weeks and were weaned onto a high-fat sucrose diet (HFSD) from 3 to 20 weeks. Calorie-restricted weight loss on a low-fat sucrose diet (LFSD) occurred over 2 weeks to induce a 20% loss in body weight, which was maintained for 6 weeks. After weight loss, half of the mice received running wheels, and the other half remained sedentary. Mice were then fed ad libitum on an HFSD or LFSD for 10 weeks and were allowed to regain body weight. NMS mice had greater weight regain, total body weight, and adiposity compared with naïve mice. During the first week of refeeding, NMS mice had increased food intake and were in a greater positive energy balance than naïve mice. Female mice were more susceptible to NMS-induced effects, including increases in adiposity. NMS and naïve females were more susceptible to HFSD-induced weight regain. Exercise was beneficial in the first week of regain in male mice, but, long-term, only those on the LFSD benefited from exercise. As expected, HFSD led to greater weight regain than LFSD. Early-life stress increases weight regain in mice.

High Sucrose Diet-Induced Subunit I Tyrosine 304 Phosphorylation of Cytochrome c Oxidase Leads to Liver Mitochondrial Respiratory Dysfunction in the Cohen Diabetic Rat Model.

The mitochondrial oxidative phosphorylation process generates most of the cellular energy and free radicals in mammalian tissues. Both factors play a critical role in numerous human diseases that could be affected by reversible phosphorylation events that regulate the function and activity of the oxidative phosphorylation complexes. In this study, we analyzed liver mitochondria of Cohen diabetes-sensitive (CDs) and Cohen diabetes-resistant (CDr) rats, using blue native gel electrophoresis (BN-PAGE) in combination with mitochondrial activity measurements and a site-specific tyrosine phosphorylation implicated in inflammation, a known driver of diabetes pathology. We uncovered the presence of a specific inhibitory phosphorylation on tyrosine 304 of catalytic subunit I of dimeric cytochrome c oxidase (CcO, complex IV). Driven by a high sucrose diet in both CDr and CDs rats, Y304 phosphorylation, which occurs close to the catalytic oxygen binding site, correlates with a decrease in CcO activity and respiratory dysfunction in rat liver tissue under hyperglycemic conditions. We propose that this phosphorylation, specifically seen in dimeric CcO and induced by high sucrose diet-mediated inflammatory signaling, triggers enzymatic activity decline of complex IV dimers and the assembly of supercomplexes in liver tissue as a molecular mechanism underlying a (pre-)diabetic phenotype.

Genetics and diet explain sex differences in glucose metabolism and cognitive function

AbstractBackgroundDiabetes and cognitive impairment occur together more often than would be expected by chance [1–6]. Individuals diagnosed with type 2 diabetes have a 1.4–2.2‐fold higher risk of dementia than those without diabetes [2,6,7]. Epidemiological research has demonstrated shared risk factors, metabolic disorders, and comorbidities[5,8], shared genetics[9], and evidence of causality assessing glycemic traits [4,10–12]. We set out to determine how glucose metabolism modifies normal aging‐related cognitive decline in comparison to Alzheimer’s Disease (AD)‐related decline, given genetic diversity and controlled diet (GxD).MethodWe studied an innovative, genetically diverse mouse population (AD‐BXDs, Fig. 1) to determine GxD effects on metabolic function and the transition to cognitive impairment [13]. The data were collected longitudinally from a cohort of ∼650 AD‐BXD mice (39 unique strains) fed either a low‐fat chow diet or a high‐fat, high sucrose diet (HFD:45% fat,17.5% sucrose). Glucose metabolism was assessed by measuring the area under the curve of an intraperitoneal glucose tolerance test (IPGTT). In general, faster clearance of glucose (smaller area under the curve) reflects better glycemic control. Contextual fear memory (CFM) at 6 and 14 months of age was the measure of cognitive function. We used multivariable linear regression to model the relationship between overall CFM and an IPGTT by strain effect.ResultWe found that there was heterogeneity in IPGTT by sex, strain, and diet, accounting for more than 50% of the variation explained (Fig. 2). Females generally exhibit faster glucose metabolism than males (Fig.2, left), while the magnitude of the effect of sex and diet on IPGTT differs by strain (Fig. 2, x‐axis). For our research question of how glucose metabolism affects cognitive function, we identified strains that exhibited resilience to cognitive dysfunction as predicted by their glucose metabolism, with a broad‐sense heritability of 0.81 (Fig. 3). These early findings establish a foundation to identify quantitative trait loci (QTLs) and GxD‐type QTLS based on glucose tolerance and cognitive function associations.ConclusionBy examining the effect of diet on AD‐BXD strains and incorporating metabolic measures associated with diabetes, we will be able to evaluate and validate cause in these relationships for the first time.

Sugar Substitute Stevia Inhibits Biofilm Formation, Exopolysaccharide Production, and Downregulates the Expression of Streptococcal Genes Involved in Exopolysaccharide Synthesis.

Acid production by sucrose fermentation disturbs the balance in dental plaque by lowering the oral pH. As a consequence of the profound effect of sucrose on caries initiation and progression, many studies have been directed towards finding non-cariogenic artificial sweeteners that can be used as a substitute to sucrose. Existing literature shows that dietary sucrose upregulates the expression of biofilm associated genes involved in exopolysaccharide (EPS) production. In this study, we aimed to investigate the effect of the sugar substitute stevia on biofilm formation, EPS secretion, and streptococcal genes encoding glucan-binding proteins (Gbps) and glucosyltransferases (Gtfs), which are essential for the synthesis of EPS. Streptococcus mutans and Streptococcus gordonii were grown as biofilm cultures with or without stevia and sucrose. Biomass was quantified for biofilm and EPS production by crystal violet staining and the phenol-sulfuric acid method, respectively. Expression of gtfB and gbpB genes was studied by RT-PCR. The quantities of biofilm were significantly lower when grown in the presence of stevia compared to sucrose in both species (p < 0.05). The proportion of EPS in the biofilm pellet decreased with increasing concentrations of stevia in both species but remained nearly unchanged with sucrose with respect to the control. In both streptococcal species, exposure of stevia decreased the expression of gtfB and gbpB genes compared to sucrose (p < 0.05). In comparison to the untreated control, the expression was decreased in the presence of stevia in both species, while it increased 2.5- to 4-fold in S. mutans and 1.5- to 2.5-fold in S. gordonii in the presence of sucrose. The ability of stevia to inhibit biofilm formation, reduce EPS production, and downregulate the expression of gtfB and gbpB genes in S. mutans and S. gordonii may have potential therapeutic applications in controlling dental plaques and caries.

Abstract 18076: MicroRNA-342-3p Rescues Post-Ischemic Cardiac Function in Diabetic Mice via HGF-MET Pathway Activation

Introduction: - Patients with diabetes have a poorer prognosis following myocardial infarction compared to healthy controls. This is partly due to impaired post-ischemic angiogenesis in the diabetic heart. The role of microRNAs (miRs) in angiogenesis is relatively unexplored. miR expression is responsive to stimuli such as hypoxia, metabolic environment, growth factors, etc. Here, we describe how miR-342-3p, a hypoxia-responsive miR, regulates angiogenesis under physiologic and diabetic conditions. Methods: - miR-342-3p or control mimic was injected into the border zone of hearts post-ischemia/reperfusion in male Ldlr -/- mice on a high fat and high sucrose (HFSC) diet. Echocardiography, histology, immunofluorescence, RNA FISH and in vitro assays were used to elucidate the mechanism of action of this miR. Results: - Ejection fraction (EF) and fractional shortening (FS) of miR-342-3p injected hearts were significantly higher by 145% and 173%, respectively, at day 14 compared to controls (p = 0.0204 and p = 0.0095). Capillary density as well as ki67+ endothelial cells were more abundant by 107% and 154%, respectively (p = 0.0371 and p = 0.0242) vs control. RNA sequencing of miR-342-3p overexpressing endothelial cells implicated HGF-MET signaling as one of the top upregulated pathways. Western blots (WB) revealed an increase in MET expression (p = 0.0255) in miR-342-3p overexpressing cells vs control. Decorin (DCN) was identified as a direct target of miR-342-3p and validated by WB and luciferase reporter assays. Hypoxia (2% O 2 ) induced miR-342-3p expression (p = 0.0023) while suppressing DCN levels. However, both high glucose (25 mM) and palmitate (100 μM) treatments blunted the miR-342-3p induction while increasing Decorin levels. Co-IP and microscopy were used to show Decorin-MET co-localization. Lastly, miR-342-3p and DCN were inversely expressed (p = 0.0188 and p = 0.0015 respectively) in diabetic and healthy ECs obtained from patients. Conclusion: - These findings establish a critical role for miR-342-3p in regulating cardiac angiogenesis post-ischemic injury in diabetic mice. Under diabetic conditions, the hypoxia induced expression of miR-342-3p is blunted, leading to Decorin mediated degradation of MET receptors, which impairs angiogenesis.

Effect of high-sucrose diet on liver enzymes and serum protein levels of Wistar albino rats

A global change in dietary habits has led to the introduction of sweeteners in foods. This study investigated the effect of concentrations of sucrose on liver enzymes and serum protein levels in Wistar rats. Thirty-five (35) Wistar rats were equally randomized into seven groups and fed with a rat diet mixed with sucrose at concentrations of 10, 20, 40, 60, 80, and 100% w/w, while the control group was fed on a normal diet without sucrose. Their blood samples were analyzed for total protein, albumin, ALT, AST, ALK phosphatase, and gamma-glutamyl transpeptidase (ƔGT) levels. The results indicated that there was a significant (p&lt;0.05) increase in AST (16.00-82.00 µ/L), ALT (44.00-90.80 µ/L), ALK Phos (44.00-90.80 µ/L), and a corresponding decrease in total proteins (69.80-61.39 g/L), albumin (36.00-34.00 g/L) and ƔGT (493.00-191.00 µ/L) levels as the concentration of sucrose increased. Rats fed with sucrose diets had higher levels of AST (39.27 µ/L), ALT (14.50 µ/L), and ALK Phos (68.47 µ/L) than rats fed with normal diets. Therefore, high doses of sucrose can cause increases in serum liver enzymes and total proteins that are suggestive of liver necrosis. Hence, by decreasing the concentrations of sucrose, the liver may be protected.