Glucose Injection Research Articles

Clinical analysis of the effect of Rhodiola kirilowii Regel combined with calcium dobesilate in the treatment of early diabetic nephropathy

Objective To explore the effect of Rhodiola kirilowii Regel combined with calcium dobesilate in the treatment of early diabetic nephropathy. Methods 80 patients with early diabetic nephropathy were selected, and they were divided into treatment group and control group according to the digital table, 40 cases in each group.The two groups were given diet control and appropriate exercise and positive controlled blood sugar, blood fat, blood pressure.The control group was given calcium dobesilate, based on this, the treatment group was given Rhodiola kirilowii Regel 10mL into 5% glucose injection 250mL and 3 unit insulin to intravenous drip.The period of treatment was fifteen days.The UAER, Scr and BUN were compared between two groups before treatment and fifteen days after treatment. Results Before treatment, the Scr, BUN and UAER in the control group were (88.00±18.19)μmol/L, (5.98±1.92)mmol/L, (123.31±60.01)μg/min respectively, which in the treatment group were (85.80±18.31)μmol/L, (5.96±1.94)mmol/L, (140.21±62.92)μg/min respectively, there were no statistically significant differences between the two groups(t=-1.191, -0.016, 0.432, all P>0.05). After treatment, the Scr, BUN and UAER in the control group were (84.61±11.71)μmol/L, (6.30±1.37)mmol/L, (97.81±49.16)μg/min respectively, which in the treatment group were (75.60±11.44)μmol/L, (5.25±1.24)mmol/L, (39.81±23.43)μg/min.There were no statistically significant differences in Scr and BUN of the two groups compared with before treatment(the control group: t=0.767, -0.657; the treatment group: t=1.947, 1.219, all P>0.05). There was statistically significant difference in UAER of the two groups compared with before treatment(t=2.850, 5.402; P=0.046, 0.006), but UAER of the treatment group after treatment decreased significantly.After treatment, there were no statistically significant differences in Scr and BUN between the two groups(t=-1.229, -1.236, all P>0.05), while there was statistically significant difference in UAER between the two groups(t=-2.394, P=0.044). The effective rate in the treatment group was 87.5%, which was higher than 57.5% of the control group(χ2=9.028, P<0.05). Conclusion Rhodiola kirilowii Regel combined with calcium dobesilate can ameliorate protenuria and improve renal function of the patients with early diabetic nephropathy. Key words: Diabetic nephropathy; Rhodiola kirilowii Regel; Calcium dobesilate

Delphinidin 3‐rutinoside‐rich blackcurrant extract ameliorates glucose tolerance by increasing the release of glucagon‐like peptide‐1 secretion

Glucagon‐like peptide‐1 (GLP‐1) is an incretin that is secreted from enteroendocrine L‐cells. Dietary factor‐stimulation of endogenous GLP‐1 is a promising strategy for increasing the action of GLP‐1. Recent studies have shown that berries rich in anthocyanins improve insulin sensitivity and reduce the risk of type 2 diabetes. Our previous study found that the anthocyanin delphinidin 3‐rutinoside (D3R) significantly increases GLP‐1 secretion in GLUTag cells (enteroendocrine L cell line). Blackcurrants are berries that contain high levels of anthocyanins, particularly D3R. Pre‐administered blackcurrant extract (BCE) 5 mg/kg body weight (1 mg D3R/kg) significantly ameliorated glucose tolerance after intraperitoneal glucose injection in rats by stimulating the secretion of GLP‐1 and subsequently inducing insulin secretion. D3R did not break down significantly in the gastrointestinal tract for at least 45−60 min after BCE was administered, suggesting that BCE‐induced GLP‐1 secretion is mainly mediated by D3R and not its degradation products. These findings demonstrate the novel biological function of D3R‐rich BCE as a GLP‐1 secretagogue. An increase in endogenous GLP‐1 secretion induced by BCE may help to reduce the dosages of diabetic medicines and prevent diabetes.

Effects of Ketogenic Diet in Young Adult and Old Rats

Ketogenic diets (KD) have been promoted extensively for weight loss and health. However, their effects in aged skeletal muscle are not well‐defined. In this study, we tested the effect of a ketogenic diet in young adult (YA; 5 month old) and old (O; 28 month old) male Fisher 344 rats (n = 4–6/group). Rats were assigned to either standard chow (STD; Evigo Teklad Rodent Diet, 8604; 32% protein, 14% fat, 54% carbohydrate) or ketogenic diet (KETO; Envigo Teklad Custom Diet, TD.10911; 22.4% protein, 77.1% fat, 0.5% carbohydrate) for 4 weeks, and weighed weekly. KETO rats were pair fed isocalorically with STD chow rats within each age group with the YA rats eating 0.132 kcal/g body weigh/day, and O rats eating 0.109 kcal/g body weight/day. After 24 or 25 days glucose tolerance testing was performed by fasting the rats for 6 hours followed by an injection of 1 mg glucose/g BW. Blood glucose concentration was measured from tail blood immediately before and 15, 30, 60 and 120 minutes after the glucose injection. Ketones were also measured from tail blood immediately before the glucose injection. After the 4‐week treatment period, rats were euthanized and gastrocnemius muscle was collected for determination of mitochondrial respiration and AMP‐activated protein kinase (AMPK; an important stimulator of glucose and fatty acid metabolism) phosphorylation. We found that KETO feeding increased blood ketone levels, albeit non‐significantly (p=0.065), in YA but not O rats. KETO resulted in significant weight loss within 2 weeks in both YA and O rats. Glucose tolerance was impaired in O‐STD vs. YA‐STD rats, while KETO impaired glucose tolerance in YA, but not O rats. KETO increased mitochondrial respiration in YA, but not O rats. AMPK phosphorylation was decreased by KETO vs. STD diet in YA, but not O rats. We conclude that a KETO diet induces a significant drop in body weight and enhanced mitochondrial respiration, but impaired glucose tolerance in YA rats, suggesting a shift from glycolytic to oxidative metabolism. Somewhat surprisingly, these KETO‐induced changes in YA rats are associated with decreased AMPK activation. O rats are resistant to all of these effects of KETO diet except for weight loss, suggesting impaired metabolic plasticity with old age. Further study will be required to elucidate the exact molecular pathways underlying these shifts.Support or Funding InformationThis research was supported by Brigham Young University Mentoring Environment Grants (MEG) and Gerontology Research Grants.

Neonatal Supplemental Oxygen Exposure Promotes the Development of Metabolic Disease in Adult Rats

Premature infants frequently require supplemental oxygen to sustain life, but little is known about how supplemental oxygen administered during the critical developmental window after birth increases the risk of age‐related disease, including obesity and diabetes. We hypothesized that neonatal rats exposed to supplemental oxygen (OXY) would have impaired glucose tolerance and that they would develop a diabetes phenotype earlier than controls (CON), when offered a high fat diet. We used an established rat model of neonatal oxygen exposure (80% O2 for 8–14 days) and glucose tolerance was evaluated 14 days and 12 months post‐natally. To evaluate glucose tolerance, baseline blood glucose was measured after an overnight fast, followed by an intraperitoneal injection of concentrated glucose. Blood glucose was then measured 15, 30, 60 and 120 minutes post‐injection. In a second experiment, two month old OXY and CON rats were randomly assigned to an animal‐based fat diet (60% of calories from fat), or standard, low fat diet for ten weeks. At the beginning of the study and each subsequent week, glucose tolerance was measured. At 14 days and 12 months, OXY rats had higher blood glucose at 15 and 30 minutes compared to CON rats. OXY rats fed a high fat diet developed frank glucose intolerance after 4 weeks. Ten weeks of high fat diet had minimal effect on glucose tolerance in CON rats. Taken together, these data suggest that supplemental oxygen during the neonatal period may pre‐dispose the premature infant to the development of metabolic disease later in life.Support or Funding InformationThis work has been supported by funding from the University of Iowa's Department of Health and Human Physiology.

Developmental Exposure to Indoor Flame Retardants Produces Diabetic Phenotype in Adult Female C57BL6 Mice

Polybrominated diphenyl ethers are a group of flame‐retardant organohalogen pollutants that act as endocrine and neuroendocrine disrupting chemicals. In humans, exposure to brominated flame retardants or other environmentally persistent organic pollutants (POPs) such as polychlorinated biphenyls (PCBs) has been associated with increasing trends of diabetes and metabolic disease (Gray et al. 2013; Baker et al. 2013; Lim et al, 2008; Lee et al, 2006). POPs may disrupt metabolic homeostasis through chronic low‐level exposure and bio‐accumulation in liver, adipose tissue and brain (Zhang et al, 2016; Turyk et al, 2015). However, the effects of PBDEs on metabolic processes are poorly understood. In this study we examined the effects of gestational and lactational exposure to the industrial PBDE mixture DE‐71 on glucose tolerance test (GTT), insulin tolerance test (ITT), and liver lipid content in C57BL/6 female offspring in adulthood (128–147 days; 17.1–22 g). We also examined intestinal permeability since intestinal‐derived bacterial products entering the bloodstream may cause inflammation, liver disease that may contribute to obesity and diabetes (Turner, 2009). Mice were exposed to environmentally relevant doses of PBDEs for 10 weeks (pre‐conception: 4 weeks; gestation: 3 weeks; lactation: 3 weeks). Daily dosing consisted of low dose (0.1 mg/kg/d), high dose (0.4 mg/kg/d), or corn oil vehicle (control) via ingestion of infused corn flakes. GTT results revealed that blood glucose levels normalized to fasting levels were significantly elevated at 30 and 60 min post injection of glucose (2.0 g/kg) in LD mice relative to oil vehicle controls (p&lt;0.0001, n=20). ITT results showed a significantly decreased sensitivity to insulin (0.5 U/kg) at post‐injection time points from 15–120 min for LD and 15–90 min for HD female offspring (p&lt;0.05 to 0.0001, n=19). Mean levels of liver lipids were significantly elevated in LD female offspring compared to controls (p&lt;0.05, n= 18). To determine if PBDE‐exposed offspring showed altered intestinal permeability, mice were orally gavaged with 60 mg/kg FITC‐dextran (mol. wt. 3,000–5,000; FD‐4, Sigma) and fluorescence measured in the blood 4 hr later by fluorimetry (excitation 490 nm, emission 530 nm). PBDE at HD had an apparent effect on elevated plasma FITC levels but the effects were not significant indicating that PBDEs may not produce their effects via changes in intestinal barrier integrity. These results indicate that mice perinatally exposed to PBDEs (0.1 mg/kg dose) display abnormal glucose and lipid metabolic parameters indicative of a diabetic phenotype.Support or Funding InformationSupported by University of California COR grant and UCMEXUS.

Fasting regulates EGR1 and protects from glucose- and dexamethasone-dependent sensitization to chemotherapy.

Fasting reduces glucose levels and protects mice against chemotoxicity, yet drugs that promote hyperglycemia are widely used in cancer treatment. Here, we show that dexamethasone (Dexa) and rapamycin (Rapa), commonly administered to cancer patients, elevate glucose and sensitize cardiomyocytes and mice to the cancer drug doxorubicin (DXR). Such toxicity can be reversed by reducing circulating glucose levels by fasting or insulin. Furthermore, glucose injections alone reversed the fasting-dependent protection against DXR in mice, indicating that elevated glucose mediates, at least in part, the sensitizing effects of rapamycin and dexamethasone. In yeast, glucose activates protein kinase A (PKA) to accelerate aging by inhibiting transcription factors Msn2/4. Here, we show that fasting or glucose restriction (GR) regulate PKA and AMP-activated protein kinase (AMPK) to protect against DXR in part by activating the mammalian Msn2/4 ortholog early growth response protein 1 (EGR1). Increased expression of the EGR1-regulated cardioprotective peptides atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in heart tissue may also contribute to DXR resistance. Our findings suggest the existence of a glucose–PKA pathway that inactivates conserved zinc finger stress-resistance transcription factors to sensitize cells to toxins conserved from yeast to mammals. Our findings also describe a toxic role for drugs widely used in cancer treatment that promote hyperglycemia and identify dietary interventions that reverse these effects.

Label-free electrochemiluminescent biosensor for rapid and sensitive detection of pseudomonas aeruginosa using phage as highly specific recognition agent

A virulent phage named as PaP1 was isolated from hospital sewage based on a lambda phage isolation protocol. This phage showed a strong and highly specific binding ability to Pseudomonas aeruginosa (P. aeruginosa). Using this isolated phage as a recognition agent, a novel electrochemiluminescent (ECL) biosensor was developed for label-free detection of P. aeruginosa. The biosensor was fabricated through depositing phage-conjugated carboxyl graphene onto the surface of a glass carbon electrode. After specific binding of the host bacteria through the adsorption of P. aeruginosa cell wall by phage tail fibers and baseplate, the ECL signal of luminol suffered a decrease since the formed non-conductive biocomplex obstructed the interfacial electron transfer and blocked the diffusion of the ECL active molecules. The ECL emission declined linearly with P. aeruginosa concentration in the range of 1.4×102 −1.4×106CFUmL−1, with a very low detection limit of 56CFUmL−1. The whole detection process could be completed within 30min as a ready-for-use biosensor was adopted. This biosensor was successfully applied to quantitate P. aeruginosa in milk, glucose injection and human urine with acceptable recovery values ranging from 78.6% to 114.3%.

Glucose variability aggravates cardiac fibrosis by altering AKT signalling path.

To study the effect of blood glucose variability on cardiac fibrosis and its mechanism in a model of diabetic cardiomyopathy. A total of 45 Sprague Dawley rats were randomly divided into three groups: control, control diabetes mellitus and fluctuated blood glucose groups. Fluctuated blood glucose was induced by daily subcutaneous insulin and intraperitoneal glucose injections at different time points. Blood lipids and glycosylated haemoglobin A1c were assessed. Super oxide dismutase activity and malondialdehyde level in rat heart homogenates were determined by assay kit. Structural cardiac tissue changes were observed by haematoxylin and eosin staining and Masson's trichrome staining. Collagen type 3, fibronectin, phosphorylated Ser/Thr protein kinase, phosphorylated glycogen synthase kinase-3 beta, glycogen synthase kinase-3 beta, nuclear factor kappa-light-chain-enhancer of activated B cells, cleaved-cysteinyl aspartate-specific proteinase-3 (caspase-3) and tumour necrosis factor-α levels were determined by western blot. Compared with the control group, cardiac fibrosis and oxidative stress in heart tissue were aggravated in diabetic rats, which were more pronounced in glucose variability rats. However, the expression levels of AKT and glycogen synthase kinase-3 beta were not significantly different in three groups, but the expression levels of phosphorylated Ser/Thr protein kinase and phosphorylated glycogen synthase kinase-3 beta were significantly decreased in the control diabetes mellitus and fluctuated blood glucose groups compared to control group, and levels in the fluctuated blood glucose group were significantly less than in the control diabetes mellitus group. In addition, the expression levels of nuclear factor kappa B and caspase-3 in both the control diabetes mellitus and fluctuated blood glucose groups were higher than in the control group, with the highest levels measured in the fluctuated blood glucose group. Blood glucose variability can aggravate heart tissue fibrosis, possibly involving oxidative stress by inhibiting AKT signalling path.

Effects of ω-3 polyunsaturated fatty acids on lymphocyte apoptosis rate in rats with sepsis

To investigate the effects of ω-3 polyunsaturated fatty acids (ω-3 PUFAs) on the apoptosis of thymic and splenic lymphocytes in rats with sepsis. A total of 80 female Sprague-Dawley rats aged 7-8 weeks were randomly divided into model group, conventional lipid emulsion group (0.1 g/kg daily), low-dose ω-3 PUFAs group (0.1 g/kg daily), middle-dose ω-3 PUFAs group (0.2 g/kg daily), and high-dose ω-3 PUFAs group (0.3 g/kg daily). Cecal ligation and puncture were used to establish a rat model of sepsis. The treatment groups were then given tail vein injection of lipid emulsion or glucose diluents of ω-3 PUFAs at different doses, and the model group was given glucose injection via the tail vein at the same dose. According to the time of sacrifice, each group was further divided into 24-hour and 72-hour subgroups, with 8 rats in each subgroup. Hematoxylin and eosin staining was used to observe the pathological changes in the thymus and spleen. TUNEL was used to measure the apoptosis rates of thymic and splenic lymphocytes. In the three ω-3 PUFAs groups, the rats had a complete thymic lobular structure and clear structures of the cortex and medulla. In the model and the conventional lipid emulsion groups, the boundaries of the cortex and medulla were unclear and the number of lymphocytes was significantly reduced. In the ω-3 PUFAs groups, the structure of the red and white pulp of the spleen was maintained with the presence of splenic follicles, while in the model and the conventional lipid emulsion groups, the structure of the red and white pulp of the spleen was disordered and splenic follicles were significantly reduced or disappeared. Compared with the model and the conventional lipid emulsion groups, the ω-3 PUFAs groups showed significant reductions in the apoptosis rates of thymic and splenic lymphocytes at 24 and 72 hours (P<0.01). Compared with the low-dose ω-3 PUFAs group, the high-dose ω-3 PUFAs group had significantly reduced apoptosis rates of splenic lymphocytes at 24 and 72 hours (P<0.05). ω-3 PUFAs can reduce the apoptosis of thymic and splenic lymphocytes in rats with sepsis in a dose-dependent manner.

THE EFFECTS OF PHYSICAL EXERCISE ON THE INSULIN-DEPENDENT DIABETES MELLITUS SUBJECTS USING THE MODIFIED MINIMAL MODEL

&lt;p&gt;&lt;strong&gt;Objective: &lt;/strong&gt;In this paper, the modified minimal model (MM) with a mathematical function for describing the insulin infusion rates was used to study of the effects of physical exercise on the dynamics of glucose and insulin on the insulin dependent diabetes mellitus (IDDM), including type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) subjects.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;In an intravenous glucose tolerance test (IVGTT) procedure, a dose of glucose was administered intravenously to overnight-fasted subjects, 20 min after the glucose bolus, insulin was injected over 1-2 min either into the portal vein or into the femoral vein, and subsequently the glucose and insulin concentrations in plasma were frequently sampled (usually 30 times) over a period of 180 min. The dynamic glucose and insulin responses to glucose and insulin injection were analysed using the modified MM without and with physical exercise from IVGTT data.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Our simulation results shown physical exercise improved blood glucose control and enhanced insulin sensitivity (&lt;em&gt;S&lt;sub&gt;I&lt;/sub&gt;&lt;/em&gt;) index in subjects with T1DM and T2DM. However, the T1DM and T2DM subjects need to be aware of the basic strategies to prevent hypoglycemia and maintain reasonable glucose control. It should be noted that the putative improvement in exercise-induced peripheral &lt;em&gt;S&lt;sub&gt;I&lt;/sub&gt;&lt;/em&gt; index in subjects with T1DM and T2DM was not always coincidental with the improvement of the insulin dosage.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;The feature increased physical exercise, along with knowledge about how to modify daily insulin dosage to prevent hypoglycemia, improved blood glucose control and enhanced &lt;em&gt;S&lt;sub&gt;I&lt;/sub&gt;&lt;/em&gt; index. &lt;/p&gt;

Highly Specific Bacteriophage-Affinity Strategy for Rapid Separation and Sensitive Detection of Viable Pseudomonas aeruginosa.

A virulent bacteriophage highly specific to Pseudomonas aeruginosa (P. aeruginosa) was isolated from hospital sewage using a lambda bacteriophage isolation protocol. The bacteriophage, named as PAP1, was used to functionalize tosyl-activated magnetic beads to establish a bacteriophage-affinity strategy for separation and detection of viable P. aeruginosa. Recognition of the target bacteria by tail fibers and baseplate of the bacteriophage led to capture of P. aeruginosa onto the magnetic beads. After a replication cycle of about 100 min, the progenies lysed the target bacteria and released the intracellular adenosine triphosphate. Subsequently, firefly luciferase-adenosine triphosphate bioluminescence system was used to quantitate the amount of P. aeruginosa. This bacteriophage-affinity strategy for viable P. aeruginosa detection showed a linear range of 6.0 × 102 to 3.0 × 105 CFU mL-1, with a detection limit of 2.0 × 102 CFU mL-1. The whole process for separation and detection could be completed after bacteria capture, bacteriophage replication, and bacteria lysis within 2 h. Since the isolated bacteriophage recognized the target bacteria with very high specificity, the proposed strategy did not show any signal response to all of the tested interfering bacteria. Furthermore, it excluded the interference from inactivated P. aeruginosa because the bacteriophage could replicate only in viable cells. The proposed strategy had been applied for detection of P. aeruginosa in glucose injection, human urine, and rat plasma. In the further work, this facile bacteriophage-affinity strategy could be extended for detection of other pathogens by utilizing virulent bacteriophage specific to other targets.

Dual Role of Insulin in Spexin Regulation: Functional Link Between Food Intake and Spexin Expression in a Fish Model.

Spexin (SPX), a neuropeptide discovered by the bioinformatics approach, has been recently identified as a satiety factor in a fish model. However, the functional link between feeding and SPX expression as well as the signal transduction for SPX regulation are totally unknown. In this study, we used goldfish as a model to examine the functional role of insulin as a postprandial signal for SPX regulation in bony fish. In goldfish, feeding could elevate plasma levels of glucose, insulin, and SPX with concurrent rises in insulin and SPX messenger RNA (mRNA) expression in the liver. Similar elevation in SPX mRNA level was also observed in the liver and brain areas involved in appetite control in goldfish after intraperitoneal injection of glucose and insulin, respectively. In parallel experiments with goldfish hepatocytes and brain cell culture, insulin signal induced by glucose was shown to exert a dual role in SPX regulation, namely (1) acting as an autocrine/paracrine signal to trigger SPX mRNA expression in the liver and (2) serving as an endocrine signal to induce SPX gene expression in the brain. Apparently, the peripheral (in the liver) and central actions of insulin (in the brain) on SPX gene expression were mediated by insulin receptor (to a lesser extent by insulin-like growth factor I receptor) coupled to mitogen-activated protein kinase kinase 3/6/p38 mitogen-activated protein kinase and phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin but not mitogen-activated protein kinase kinase 1/2/extracellular signal-regulated kinase 1/2 cascades. Our findings indicate that an insulin component inducible by glucose is present in the liver of the fish model and may serve as the postprandial signal linking food intake with SPX expression both in the central as well as at the hepatic level.

Effects of Systemic Metabolic Fuels on Glucose and Lactate Levels in the Brain Extracellular Compartment of the Mouse.

Classic neuroenergetic research has emphasized the role of glucose, its transport and its metabolism in sustaining normal neural function leading to the textbook statement that it is the necessary and sole metabolic fuel of the mammalian brain. New evidence, including the Astrocyte-to-Neuron Lactate Shuttle hypothesis, suggests that the brain can use other metabolic substrates. To further study that possibility, we examined the effect of intraperitoneally administered metabolic fuels (glucose, fructose, lactate, pyruvate, ß-hydroxybutyrate, and galactose), and insulin, on blood, and extracellular brain levels of glucose and lactate in the adult male CD1 mouse. Primary motor cortex extracellular levels of glucose and lactate were monitored in freely moving mice with the use of electrochemical electrodes. Blood concentration of these same metabolites were obtained by tail vein sampling and measured with glucose and lactate meters. Blood and extracellular fluctuations of glucose and lactate were monitored for a 2-h period. We found that the systemic injections of glucose, fructose, lactate, pyruvate, and ß-hydroxybutyrate increased blood lactate levels. Apart for a small transitory rise in brain extracellular lactate levels, the main effect of the systemic injection of glucose, fructose, lactate, pyruvate, and ß-hydroxybutyrate was an increase in brain extracellular glucose levels. Systemic galactose injections produced a small rise in blood glucose and lactate but almost no change in brain extracellular lactate and glucose. Systemic insulin injections led to a decrease in blood glucose and a small rise in blood lactate; however brain extracellular glucose and lactate monotonically decreased at the same rate. Our results support the concept that the brain is able to use alternative fuels and the current experiments suggest some of the mechanisms involved.

Lethal dysregulation of energy metabolism during embryonic vitamin E deficiency

Vitamin E (α-tocopherol, VitE) was discovered in 1922 for its role in preventing embryonic mortality. We investigated the underlying mechanisms causing lethality using targeted metabolomics analyses of zebrafish VitE-deficient embryos over five days of development, which coincided with their increased morbidity and mortality. VitE deficiency resulted in peroxidation of docosahexaenoic acid (DHA), depleting DHA-containing phospholipids, especially phosphatidylcholine, which also caused choline depletion. This increased lipid peroxidation also increased NADPH oxidation, which depleted glucose by shunting it to the pentose phosphate pathway. VitE deficiency was associated with mitochondrial dysfunction with concomitant impairment of energy homeostasis. The observed morbidity and mortality outcomes could be attenuated, but not fully reversed, by glucose injection into VitE-deficient embryos at developmental day one. Thus, embryonic VitE deficiency in vertebrates leads to a metabolic reprogramming that adversely affects methyl donor status and cellular energy homeostasis with lethal outcomes.

Attenuation of obesity-induced inflammation in mice orally administered with salmon cartilage proteoglycan, a prophylactic agent

Obesity is associated with chronic inflammation of adipose tissue and causes development of type 2 diabetes. M1 macrophage population was increased in adipose tissue of obese mouse. M1 macrophages induce insulin resistance through the secretion of proinflammatory cytokines. Our previous studies demonstrated that salmon cartilage proteoglycan (PG) suppresses excess inflammation in various mouse inflammatory diseases. In this study, we examined the effect of PG on type 2 diabetes using high-fat-diet (HFD) induced obese mouse model. Oral PG administration enhanced the population of small adipocytes (area less than 1000 μm2) without body and tissue weight gain. In addition, PG administration suppressed mRNA expression of TNF-α, IL-6 and CXCL2 in adipose tissue. The proportion of M1 macrophages was decreased by PG administration. In addition, PG administration suppressed hyperglycemia after intraperitoneal glucose injection. Fasted serum insulin level was decreased in PG-administered mice. Moreover, insulin-stimulated phosphorylation of Akt was enhanced in the liver and gastrocnemius skeletal muscle of PG-administered mice. These data suggested that PG administration improves hyperglycemia and insulin sensitivity in obese mice by modulation of M1 macrophages which secrete proinflammatory cytokines in adipose tissue and activation of Akt in liver and skeletal muscle.

Response of Blood Perfusion at ST 36 Acupoint after Drinking Cold Glucose or Saline Injection.

Skin blood flux (SkBF) changes caused by drinking cold water are generally associated with vagal tone and osmotic factors in digestive system. According to acupuncture theory, change of SkBF at ST 36 might reflect the functional changes of digestive system. The aim of this study is to analyze the changes of SkBF after drinking 3°C 0.9% saline or 5% glucose injection by monitor blood flux at bilateral ST 36. The results indicated that, after drinking different cold water, the change ratio of SkBF at right side ST 36 has been different. Because all solutions have the same temperature (3°C) and both saline and glucose solution have the same osmolality, suggesting that the SkBF changes resulting from drinking cold water are not regulated just by the vagal tone and osmolality, there must have been other factors. These results have not been consistent with the frequency domain results of heart rate variability (HRV) analysis. Coherence analysis of blood flux signals at bilateral ST 36 indicated that there have been different coherence-frequency curves among different groups in special frequency bands, which suggested that coherence analysis might provide a potential tool to evaluate different status.

Influence of Infusion of Different Liquid on Changes of Blood Gas and Electrolyte of Children during the Perioperative Period

Objective To compare the effects of sodium potassium magnesium calcium and Glucose Injection, 5% Glucose Injection and 9% Sodium Chloride Injection on children with blood glucose, blood lactic acid and blood gas electrolyte during operation on children. Methods patients were randomly divided into A group(sodium potassium magnesium calcium and Glucose Injection group,n=20), B group(5% sodium chloride glucose injection, n=20)and C group(9% Sodium Chloride Injection group, n=20). Blood glucose, blood lactic acid, arterial blood Gas and electrolytes were measured and compared before infusion (T0)and on postoperative time(T1). Results blood glucose in B group increased but decreased significantly in C group(P < 0.05).;Blood lactic acid in C group significantly decreased than the other two groups(P < 0.05); Mg2+ decreased in B and C groups(P < 0.05). Conclusion Sodium Potassium Magnesium Calcium and Glucose Injection has the same efficacy and safety as commonly used 5% sodium chloride glucose injection and 9% sodium chloride injection, when infused in pediatric patients during perioperative period.

Clinical effects of Ganglioside and fructose-1, 6-diphosphate on neonatal heart and brain injuries after Asphyxia.

Objective:To study the clinical effect of ganglioside (GM) and fructose-1, 6-diphosphate (FDP) on neonatal heart and brain injuries after asphyxia.Methods:Ninety-one neonates with asphyxia neonatal heart and brain injuries were randomly divided into an observation group and a control group. Both groups were given symptomatic treatment as soon as possible. On this basis, the observation group was given 200 mL of 5% glucose injection and 20 mg of GM and 250 mg/kg·d FDP by intravenous infusion. The above two drugs were given once a day for 14 days. The control group was given 20 mL of 5% glucose injection, 2 mL of cerebrolysin and 250 mg/kg·d FDP by intravenous infusion, once a day for 14 days. Both groups were administered on the first day after admission, and the course of treatment was 14 days. The treatment outcomes of the two groups were compared by detecting the levels of glycogen phosphorylase isoenzyme BB (GPBB), cTn-I and CK-MB, MRI results and Neonatal Behavioral Neurological Assessment (NBNA) scores before and after treatment.Results:The levels of GPBB, cTn-I and CK-MB in the observation group were significantly higher than those of normal neonates. After treatment, the levels of cTn-I and CK-MB in the observation group were closer to those of normal neonates compared with the control group, with significant differences (P<0.05). There was a significant difference in the brain MRI examination between the two groups (P<0.05). The NBNA scores of the two groups were significantly different before and after treatment (P<0.05). The total effective rate of the observation group was significantly higher than that of the control group (P<0.05).Conclusion:Neonatal heart and brain injuries after asphyxia can be well treated by combining GM with FDP.

Qualitative and Quantitative Characterization of Monosaccharide Components of Salvia miltiorrhiza, Liguspyragine Hydrochloride, and Glucose Injection.

Salvia miltiorrhiza, liguspyragine hydrochloride, and glucose injection (SLGI) was made of Salvia miltiorrhiza Bge., liguspyragine hydrochloride, glucose, and glycerin. There were many kinds of monosaccharide components in SLGI, which might be from the raw material and Salvia miltiorrhiza Bge. Separation was performed on a Phenomenex Luna C18 analytical column (250 mm × 4.6 mm i.d., 5 μm, AccuStandard Inc., USA) at 30°C. The mobile phase consisted of two solvents: 0.1 mol/L phosphate-buffered saline (pH 6.7) (solvent A) and acetonitrile (solvent B) with gradient elution. The flow rate was maintained at 1.0 mL/min. Five kinds of monosaccharide components, glucose, D-mannose, L-rhamnose monohydrate, galactose, and xylose, were detected by precolumn derivatization HPLC, and their contents were compared with each other. And finally, concentrations of glucose in SLGI were determined and they were higher than the values of marked amount, which showed that one source of glucose might be from Salvia miltiorrhiza Bge. in SLGI. The average concentration of glucose was 5.18 g/100 mL, which was near the average value at 5.25 g/100 mL detected by ultraviolet spectrophotometry and also close to the marked amount (5.00 g/100 mL) on the label.

Recipient Glycemic Micro-environments Govern Therapeutic Effects of Mesenchymal Stem Cell Infusion on Osteopenia.

Therapeutic effects of mesenchymal stem cell (MSC) infusion have been revealed in various human disorders, but impacts of diseased micro-environments are only beginning to be noticed. Donor diabetic hyperglycemia is reported to impair therapeutic efficacy of stem cells. However, whether recipient diabetic condition also affects MSC-mediated therapy is unknown. We and others have previously shown that MSC infusion could cure osteopenia, particularly in ovariectomized (OVX) mice. Here, we discovered impaired MSC therapeutic effects on osteopenia in recipient type 1 diabetes (T1D). Through intensive glycemic control by daily insulin treatments, therapeutic effects of MSCs on osteopenia were maintained. Interestingly, by only transiently restoration of recipient euglycemia using single insulin injection, MSC infusion could also rescue T1D-induced osteopenia. Conversely, under recipient hyperglycemia induced by glucose injection in OVX mice, MSC-mediated therapeutic effects on osteopenia were diminished. Mechanistically, recipient hyperglycemic micro-environments reduce anti-inflammatory capacity of MSCs in osteoporotic therapy through suppressing MSC interaction with T cells via the Adenosine monophosphate-activated protein kinase (AMPK) pathway. We further revealed in diabetic micro-environments, double infusion of MSCs ameliorated osteopenia by anti-inflammation, attributed to the first transplanted MSCs which normalized the recipient glucose homeostasis. Collectively, our findings uncover a previously unrecognized role of recipient glycemic conditions controlling MSC-mediated therapy, and unravel that fulfillment of potent therapeutic effects of MSCs requires tight control of recipient micro-environments.