Increase In Blood Glucose Concentration Research Articles

Effects of crude glycerin on milk composition, nutrient digestibility and ruminal fermentation of dairy cows fed corn silage-based diets

The objective of the current study was to evaluate the effects of increasing levels of crude glycerin on dry matter intake, nutrient digestibility, ruminal parameters, blood metabolites, milk yield and composition of dairy cows fed corn silage-based diets. Twenty-four Holstein cows (16 non-cannulated and 8 rumen-cannulated; 184±50 days in milk [DIM] and 594±39kg of body weight [BW]) were assigned to a replicated 4×4 Latin square design experiment, consisting of 14 days for adaptation to diets and 7 days for sampling. Cows were assigned to receive one of the diets: 0 (Control), 70, 140 or 210g of crude glycerin/kg of diet dry matter (DM). Dry matter intake and milk yield linearly decreased with the inclusion of crude glycerin. However, crude glycerin did not affect milk composition. Total-tract digestibility of DM, crude protein (CP) and ether extract (EE) linearly increased, and neutral detergent fiber (NDF) digestibility linearly decreased according to dietary inclusion of crude glycerin. Feeding crude glycerin changed volatile fatty acid concentrations: linearly increased propionate, quadratically affected butyrate, and linearly decreased acetate concentrations, resulting in lower acetate to propionate ratio. Total volatile fatty acid was not affected by crude glycerin. Ruminal NH3-N linearly decreased according to crude glycerin dietary levels. Crude glycerin linearly increased blood glucose concentration. Inclusion of high levels of crude glycerin (210g/kg) in diets of mid-lactating cows, increased dry matter digestibility and ruminal propionate concentrations, but negatively affected dry matter intake and milk yield.

Gintonin enhances performance of mice in rotarod test: Involvement of lysophosphatidic acid receptors and catecholamine release

Ginseng has a long history of use as a tonic for restoration of vigor. One example of ginseng-derived tonic effect is that it can improve physical stamina under conditions of stress. However, the active ingredient and the underlying molecular mechanism responsible for the ergogenic effect are unknown. Recent studies show that ginseng contains a novel ingredient, gintonin, which consists of a unique class of herbal-medicine lysophosphatidic acids (LPAs). Gintonin activates G protein-coupled LPA receptors to produce a transient [Ca2+]i signal, which is coupled to diverse intra- and inter-cellular signal transduction pathways that stimulate hormone or neurotransmitter release. However, relatively little is known about how gintonin-mediated cellular modulation is linked to physical endurance. In the present study, systemic administration of gintonin, but not ginsenosides, in fasted mice increased blood glucose concentrations in a dose-dependent manner. Gintonin treatment elevated blood glucose to a maximum level after 30min. This elevation in blood glucose level could be abrogated by the LPA1/3 receptor antagonist, Ki16425, or the β-adrenergic receptor antagonist, propranolol. Furthermore, gintonin-dependent enhanced performance of fasted mice in rotarod test was likewise abrogated by Ki16425. Gintonin also elevated plasma epinephrine and norepinephrine concentrations. The present study shows that gintonin mediates catecholamine release through activation of the LPA receptor and that activation of the β-adrenergic receptor is coupled to liver glycogenolysis, thereby increasing the supply of glucose and enhancing performance in the rotarod test. Thus, gintonin acts via the LPA-catecholamine-glycogenolysis axis, representing a candidate mechanism that can explain how ginseng treatment enhances physical stamina.

Volatile anesthetics suppress glucose-stimulated insulin secretion in MIN6 cells by inhibiting glucose-induced activation of hypoxia-inducible factor 1.

Proper glycemic control is one of the most important goals in perioperative patient management. Insulin secretion from pancreatic β-cells in response to an increased blood glucose concentration plays the most critical role in glycemic control. Several animal and human studies have indicated that volatile anesthetics impair glucose-stimulated insulin secretion (GSIS). A convincing GSIS model has been established, in which the activity of ATP-dependent potassium channels (KATP) under the control of intracellular ATP plays a critical role. We previously reported that pimonidazole adduct formation and stabilization of hypoxia-inducible factor-1α (HIF-1α) were detected in response to glucose stimulation and that MIN6 cells overexpressing HIF-1α were resistant to glucose-induced hypoxia. Genetic ablation of HIF-1α or HIF-1β significantly inhibited GSIS in mice. Moreover, we previously reported that volatile anesthetics suppressed hypoxia-induced HIF activation in vitro and in vivo.To examine the direct effect of volatile anesthetics on GSIS, we used the MIN6 cell line, derived from mouse pancreatic β-cells. We performed a series of experiments to examine the effects of volatile anesthetics (sevoflurane and isoflurane) on GSIS and demonstrated that these compounds inhibited the glucose-induced ATP increase, which is dependent on intracellular hypoxia-induced HIF-1 activity, and suppressed GSIS at a clinically relevant dose in these cells.

The effect of allopurinol administration on mitochondrial respiration and gene expression of xanthine oxidoreductase, inducible nitric oxide synthase, and inflammatory cytokines in selected tissues of broiler chickens

Birds have a remarkable longevity for their body size despite an increased body temperature, higher metabolic rate, and increased blood glucose concentrations compared to most mammals. As the end-product of purine degradation, uric acid (UA) is generated in the xanthine/hypoxanthine reactions catalyzed by xanthine oxidoreductase (XOR). In the first study, Cobb × Cobb broilers (n = 12; 4 weeks old) were separated into 2 treatments (n = 6); control (CON) and allopurinol (AL) 35 mg/kg BW (ALLO). The purpose of this study was to assess mitochondrial function in broiler chickens in response to potential oxidative stress generated from the administration of AL for 1 wk. There was a significant reduction in state 3 respiration (P = 0.01) and state 4 respiration (P = 0.007) in AL-treated birds compared to the controls. The purpose of the second study was to assess the effect of AL on gene expression of inflammatory cytokines interferon-γ (IFN)-γ, IL-1β, IL-6, and IL-12p35, as well as inducible nitric oxide synthase and XOR in liver tissue. Cobb × Cobb broilers were separated into two groups at 4 wk age (n = 10); CON and ALLO. After 1 wk AL treatment, half of the birds in each group (CON 1 and ALLO 1) were euthanized while the remaining birds continued on AL treatment for an additional week (CON 2 and ALLO 2). A significant increase in gene expression of XOR, IFN-γ, IL-1β, and IL-12p35 in ALLO 2 birds as compared to birds in CON 2 was detected. Liver UA content was significantly decreased in both ALLO 1(P = 0.003) and ALLO 2 (P = 0.012) birds when compared to CON 1 and CON 2, respectively. The AL reduced liver UA concentrations and increased expression of inflammatory cytokines. Additional studies are needed to determine if AL causes a direct effect on mitochondria or if mitochondrial dysfunction observed in liver mitochondria was due indirectly through increased oxidative stress or increased inflammation.

Effects of the step-up/step-down and step-down milk feeding procedures on the performance, structural growth, and blood metabolites of Holstein dairy calves

The objective of this study was to compare the efficacy of the step-up/step-down (SUSD) and step-down (STP) methods of milk feeding on the performance, growth parameters, blood metabolites, and health of dairy calves. For this purpose, 45 Holstein male calves (3d of age and 41±3kg of body weight) were randomly assigned to one of the following milk feeding groups: (1) conventional (CONV; 4L/d milk from d 1 to 52, and 2L/d milk from d 53 to 56 of the study), (2) STP (6L/d milk from d 1 to 29, and 4L/d milk from d 30 to 45 of the study followed by feeding 2L/d milk from d 46 to 56 of the study), and (3) SUSD (6L/d milk from d 1 to 5, 8L/d milk from d 6 to 15, 10L/d milk from d 16 to 35, 8L/d milk from d 36 to 42, 6L/d milk from d 43 to 47, 4L/d milk from d 48 to 52 of the study followed by feeding 2L/d milk from d 53 to 56 of the study). Calves were weaned on d 56 and followed until d 70 of the study period. Animals had ad libitum access to the same starter ration during the entire study period (d 3 to 70). Starter intake, total dry matter intake, and average daily gain were greater in the SUSD calves than those in the CONV and STP treatments during the preweaning period. The SUSD procedure was found to increase body weight during the entire study and improved body length, wither height, heart girth, hip height, and hip width on d 56 and 70 of the study compared with the STP and CONV calves. The SUSD treatment increased blood glucose concentration on d 35 compared with CONV and STP procedures. The STP group had a higher starter intake than the CONV and SUSD animals. The STP animals exhibited a higher plasma concentration of total protein and BHBA than did the SUSD animals during the preweaning period. Neither the SUSD nor the STP procedure negatively affected the fecal score. In conclusion, the SUSD milk feeding procedure was found to improve the performance of dairy calves compared with the STP and CONV procedures. However, it appears that the STP procedure induces earlier reticulo-rumen developement in dairy calves than does the SUSD procedure.

Receptor for Advanced Glycation End-Products Signaling Interferes with the Vascular Smooth Muscle Cell Contractile Phenotype and Function.

Increased blood glucose concentrations promote reactions between glucose and proteins to form advanced glycation end-products (AGE). Circulating AGE in the blood plasma can activate the receptor for advanced end-products (RAGE), which is present on both endothelial and vascular smooth muscle cells (VSMC). RAGE exhibits a complex signaling that involves small G-proteins and mitogen activated protein kinases (MAPK), which lead to increased nuclear factor kappa B (NF-κB) activity. While RAGE signaling has been previously addressed in endothelial cells, little is known regarding its impact on the function of VSMC. Therefore, we hypothesized that RAGE signaling leads to alterations in the mechanical and functional properties of VSMC, which could contribute to complications associated with diabetes. We demonstrated that RAGE is expressed and functional in the A7r5 VSMC model, and its activation by AGE significantly increased NF-κB activity, which is known to interfere with the contractile phenotype of VSMC. The protein levels of the contraction-related transcription factor myocardin were also decreased by RAGE activation with a concomitant decrease in the mRNA and protein levels of transgelin (SM-22α), a regulator of VSMC contraction. Interestingly, we demonstrated that RAGE activation increased the overall cell rigidity, an effect that can be related to an increase in myosin activity. Finally, although RAGE stimulation amplified calcium signaling and slightly myosin activity in VSMC challenged with vasopressin, their contractile capacity was negatively affected. Overall, RAGE activation in VSMC could represent a keystone in the development of vascular diseases associated with diabetes by interfering with the contractile phenotype of VSMC through the modification of their mechanical and functional properties.

THE EFFECT OF SAUROPUS ANDROGYNUS LEAVES EXTRACT PLUS TURMERIC POWDER ON FAT DEPOSITION, CARCASS QUALITY AND BLOOD PROFILE IN BROILERS FED LOW PROTEIN DIETS

The present study was designed to evaluate the effectiveness of Sauropus androgynus leavesextract (SALE) plus turmeric powder (TP) on carcass quality and blood profile in broilers fed lowprotein diets. Sixty broilers aged 14 days were divided to 5 treatment groups as follows: 1) Broilers fed19% protein diet without SALE plus TP as control (P0); 2) Broilers fed 17% protein diet supplementedto 4.5 g SALE/kg diet plus 0.5% TP (P1); 3) Broilers fed 17% protein diet supplemented to 4.5 gSALE/kg diet plus 1% TP (P2); 4) Broilers fed 15% protein diet supplemented to 4.5 g SALE/kg dietplus 0.5% TP (P3) and; 5) Broilers fed 15% protein diet supplemented to 4.5 g SALE/kg diet plus 1%TP (P4). Supplementation of SALE plus TP significantly affected body weight gain, feed intake, proteinintake, thigh meat haemorrhage and fat deposition (P 0.05). In conclusion suplementation of SALE plus TP had no beneficial effect onreducing fat deposition in broilers fed low protein diets, but it reduced blood uric acid but increasedblood glucose concentration.

Association between dietary patterns and metabolic syndrome in individuals with normal weight: a cross-sectional study.

BackgroundThe results of several papers have confirmed the existence of correlations between an unhealthy diet and the presence of metabolic syndrome. However, relationships between eating habits and metabolic obesity with normal weight have not yet been sufficiently studied. The aim of the study is to determine which dietary patterns are present in individuals with a normal BMI and to find out whether those patterns were connected with the risk of metabolic syndrome and its features.MethodsA cross-sectional study was carried out in a group of 2479 subjects with a normal weight (BMI = 18.5–24.9 kg/m2), aged between 37–66. The study included the evaluation of eating habits, anthropometric measurements, blood pressure tests and the analysis of the collected fasting-blood samples, on the basis of which cholesterol, triglycerides and glucose levels were determined. Dietary patterns were determined by means of factor analysis.ResultsIn the group of individuals with a normal BMI, four dietary patterns were distinguished: “healthy”, “fat, meat and alcohol”, “prudent” and “coca cola, hard cheese and French fries”. After controlling for potential confounders, subjects in the highest tertile of prudent dietary pattern scores had a lower odds ratio for the metabolic obesity normal weight) (odds ratio: 0.69; 95 % CI: 0.53-0.89; p < 0.01) and low HDL cholesterol (odds ratio: 0.77; 95 % CI: 0.59-0.99; p < 0.05), in comparison to those from the lowest tertile, whereas the individuals in the second tertile had a higher odds ratio for the increased blood glucose concentration than those in the lowest tertile (odds ratio: 0.74; 95 % CI: 0.57-0.96; p < 0.05).ConclusionA dietary pattern characterized by a high consumption of fish and whole grains, and a low consumption of refined grains, sugar, sweets and cold cured meat, is connected with lower risk of metabolic obesity normal weight as well as with the lower risk of low HDL cholesterol concentration and increased glucose concentration.

Balanced hydroxyethyl starch solution and hyperglycaemia in non diabetics - a prospective, randomized and controlled study.

There are very few studies that have examined the effect of hydroxyethyl starch (HES) solutions on blood glucose level. The study was aimed to compare the effects on blood glucose levels in patients undergoing lower limb surgeries under neuraxial block, receiving HES with those receiving 0.9% saline. 160 non-diabetic ASA I or II patients, aged between 18-65 years were selected for the trial. Patients were divided into two groups; Group C (n = 80, patients received only 0.9% saline for preloading and maintenance until six hours of the end of preloading) and Group T (n = 80, patients received Tetraspan™ 10 mL kg⁻¹, for preloading and 0.9% saline for maintenance until six hours from the end of preloading). Blood glucose was recorded prior to the start of preloading and repeated at two, four and six hours after the end of HES infusion or the preloading dose of 0.9% saline. The following blood glucose levels were comparable at all times; fasting/baseline (85.3 ± 19.2 mg dL⁻¹ in group C and 95.4 ± 17.3 mg dL⁻¹ in group T); increase in blood glucose concentration at 2 hours (6.44 ± 20.59 mg dL⁻¹ in group C and 10.8 ± 18.1 mg dL⁻¹ in group T); 4 hours (4.1 ± 12.1 mg dL⁻¹ in group C and 3.5 ± 11.8 mg dL⁻¹ in group T); and at 6 hours (2.9 ± 13.4 mg dL⁻¹ in group C and 3.5 ± 10.6 mg dL⁻¹ in group T). A balanced HES solution administered intravenously did not cause an increase in blood glucose concentrations compared to those who received 0.9% saline.

Modulation of Blood Glucose Concentration by Vagal Nerve Stimulation

Chronic cervical vagal nerve stimulation (VNS) causes weight loss in obese patients and in experimental animal models of obesity. Furthermore, parasympathetic activity directed to the liver has been demonstrated to reduce hepatic glucose release. Thus, chronic cervical VNS may be particularly beneficial in obese type 2 diabetic patients. Here we tested the hypothesis that acute cervical VNS reduces blood glucose concentration in anesthetized rats. Sprague Dawley rats were instrumented with catheters in the left carotid artery, bipolar electrodes on the right cervical vagus nerve, and a novel telemetric glucose sensor (HD-XG, DSI) in the abdominal aorta, that allows for continuous monitoring of blood glucose concentration. Once stable mean blood pressure (106±14 mmHg), heart rate (322±25 bpm), and blood glucose concentration (157±21 mg/dL) was obtained (usually after 30-60 min) VNS (rectangular impulses, 3 V, 1 ms pulse width, 5 Hz) was initiated. The stimulator was turned on and off every 30 min for five complete on/off cycles. During the “on cycles” heart rate and mean blood pressure decreased (-79±5 bpm and -9±3 mmHg) while blood glucose concentration increased (+116±66 mg/dL). During the “off cycles” heart rate, mean blood pressure, and blood glucose concentration returned to baseline levels. A similar increase in blood glucose concentration was observed with efferent VNS after sectioning the vagus nerve cranial to the stimulation electrode. In summary, acute cervical VNS at an intensity that reduces heart rate elicits a glucogenic effect in anesthetized rats. Further studies are needed to understand the mechanisms by which acute and potentially also chronic cervical VNS may increase blood glucose.

TNF-α Antibody Therapy in Combination With the T-Cell-Specific Antibody Anti-TCR Reverses the Diabetic Metabolic State in the LEW.1AR1-iddm Rat.

Anti-tumor necrosis factor-α (TNF-α) therapy (5 mg/kg body weight), alone or combined with the T-cell-specific antibody anti-T-cell receptor (TCR) (0.5 mg/kg body weight), was performed over 5 days immediately after disease manifestation to reverse the diabetic metabolic state in the LEW.1AR1-iddm rat, an animal model of human type 1 diabetes. Only combination therapy starting at blood glucose concentrations below 15 mmol/L restored normoglycemia and normalized C-peptide. Increased β-cell proliferation and reduced apoptosis led to a restoration of β-cell mass along with an immune cell infiltration-free pancreas 60 days after the end of therapy. This combination of two antibodies, anti-TCR/CD3, as a cornerstone compound in anti-T-cell therapy, and anti-TNF-α, as the most prominent and effective therapeutic antibody in suppressing TNF-α action in many autoimmune diseases, was able to reverse the diabetic metabolic state. With increasing blood glucose concentrations during the disease progression, however, the proapoptotic pressure on the residual β-cell mass increased, ultimately reaching a point where the reservoir of the surviving β-cells was insufficient to allow a restoration of normal β-cell mass through regeneration. The present results may open a therapeutic window for reversal of diabetic hyperglycemia in patients, worthwhile of being tested in clinical trials.

Inhibitory effect of somatostatin on insulin secretion is not mediated via the CNS.

The inhibitory effect of somatostatin (SST) on insulin secretion in vivo is attributed to a direct effect on pancreatic beta cells, but this is inconsistent with some in vitro results in which exogenous SST is ineffective in inhibiting secretion from isolated islets. We therefore investigated whether insulin secretion from the pancreatic islets may partly be regulated by an indirect effect of SST mediated via the CNS. Islet hormone secretion was assessed in vitro by perifusion and static incubations of isolated islets and in vivo by i.v. or i.c.v. administration of the SST analogue BIM23014C with an i.v. glucose challenge to conscious, chronically catheterised rats. Hormone content of samples was assessed by ELISA or RIA and blood glucose levels using a glucose meter. Exogenous SST14/SST28 or BIM23014C did not inhibit the release of insulin from isolated rodent islets in vitro, whereas peripheral i.v. administration of BIM23014C (7.5 μg) with glucose (1 g/kg) led to decreased plasma insulin content (2.3±0.5 ng insulin/ml versus 4.5±0.5 ng/ml at t=5 min, P<0.001) and elevated blood glucose levels compared with those of the controls (29.19±1.3 mmol/l versus 23.5±1.7 mmol/l, P<0.05). In contrast, central i.c.v. injection of BIM23014C (0.75 μg) had no significant effect on either plasma insulin (3.3±0.4 ng/ml, P>0.05) or blood glucose levels (23.5±1.7 mmol/l, P>0.05) although i.v. administration of this dose increased blood glucose concentrations (32.3±0.7 mmol/l, P<0.01). BIM23014C did not measurably alter plasma glucagon, SST, GLP1 or catecholamine levels whether injected i.v. or i.c.v. These results indicate that SST does not suppress insulin secretion by a centrally mediated effect but acts peripherally on islet cells.

Antidiabetic Effects of Some Tropical Fruit Extracts in Fructose Induced Insulin Resistant Wistar Rats

Aim: Fruit extracts of Apple (Malus domestica), coconut (Cocos nucifera) and cucumber (Cucumis sativus) were tested for their antidiabetic potential in rats with fructose-induced insulin resistance for 28 days. Study Design: In-vivo antidiabetic study using fructose-induced insulin resistant rats. Place and Duration of Study: Department of Biochemistry, Lagos State University, Ojo, Lagos, Nigeria, between March and May 2014. Methodology: Wistar rats were randomized into 5 groups comprising 5 animals each. Group A (control) was fed on standard rat chow and distilled water ad libitum while Groups B-E were fed standard rat chow and 10% w/v fructose. Groups C-E were also administered 500 mg/kg body weight of apple, coconut and cucumber extracts for 28 days. At the end of the experiment, all animals were sacrificed and the serum glucose, lipid profile and electrolytes were determined. Results: The fructose-fed rats had significantly decreased weight and increased blood glucose concentration (P < 0.05), when compared to the control rats. The fructose-fed rats also witnessed significant increase (P < 0.05) in total cholesterol and low density lipoprotein cholesterol (LDLC) concentration as well as significant decrease (P < 0.05) in the high density lipoprotein (HDLC) and serum electrolytes concentration compared to control. Administration of the aqueous extracts of apple, coconut and cucumber to the fructose-fed rats significantly increase (P < 0.05) their body weights, HDLC and serum electrolytes’ concentration in the rats while significantly reducing (P < 0.05) blood glucose, total cholesterol and LDLC. Conclusions: Aqueous extracts of apple, coconut and cucumber displayed antidiabetic effect, but apple exhibited the most potent effect as it ameliorates most of the derangements observed in insulin-resistant rats.

Maternal insulin resistance and transient hyperglycemia impact the metabolic and endocrine phenotypes of offspring.

Studies in both humans and rodents suggest that maternal diabetes leads to a higher risk of the fetus developing impaired glucose tolerance and obesity during adulthood. However, the impact of hyperinsulinemia in the mother on glucose homeostasis in the offspring has not been fully explored. We aimed to determine the consequences of maternal insulin resistance on offspring metabolism and endocrine pancreas development using the LIRKO mouse model, which exhibits sustained hyperinsulinemia and transient increase in blood glucose concentrations during pregnancy. We examined control offspring born to either LIRKO or control mothers on embryonic days 13.5, 15.5, and 17.5 and postpartum days 0, 4, and 10. Control offspring born to LIRKO mothers displayed low birth weights and subsequently rapidly gained weight, and their blood glucose and plasma insulin concentrations were higher than offspring born to control mothers in early postnatal life. In addition, concentrations of plasma leptin, glucagon, and active GLP-1 were higher in control pups from LIRKO mothers. Analyses of the endocrine pancreas revealed significantly reduced β-cell area in control offspring of LIRKO mothers shortly after birth. β-Cell proliferation and total islet number were also lower in control offspring of LIRKO mothers during early postnatal days. Together, these data indicate that maternal hyperinsulinemia and the transient hyperglycemia impair endocrine pancreas development in the control offspring and induce multiple metabolic alterations in early postnatal life. The relatively smaller β-cell mass/area and β-cell proliferation in these control offspring suggest cell-autonomous epigenetic mechanisms in the regulation of islet growth and development.

The strong relation between post-hemodialysis blood methylglyoxal levels and post-hemodialysis blood glucose concentration rise.

Hemodialysis is known to decrease blood glucose concentration (BGC), insulin, and methylglyoxal levels. However, the effects of decreases in these factors on the increase in post-hemodialysis BGC remain unknown. This study identifies the effects of hemodialysis-induced changes in concentrations of these elements on post-hemodialysis BGC. Study subjects included seventeen insulin-treated diabetes patients receiving hemodialysis. The fluctuations in BGC on hemodialysis-treatment days and non-hemodialysis-treatment days were evaluated using a continuous glucose monitoring system. BGC was evaluated before breakfast, before starting hemodialysis, at the end of hemodialysis, 1 h post-hemodialysis (lunch), and 6 h post-hemodialysis (dinner). BGC, insulin, and methylglyoxal levels were measured at the start and end of hemodialysis. This study also evaluated the changes in the concentrations of glucose and insulin in the arterial line and the venous line during hemodialysis. Hemodialysis decreases BGC, insulin, and methylglyoxal levels. Concentrations of glucose and insulin in the arterial line gradually decreased during dialysis, while concentrations in the venous line approached their original concentrations in the dialysis solution. BGC rose sharply after eating lunch 1 h post-hemodialysis. The blood glucose, insulin, and methylglyoxal concentrations at the end of hemodialysis were associated with the M values and the mean amplitude of glycemic excursion values between before lunch and dinner. In particular, methylglyoxal concentration at the end of hemodialysis was strongly related to the post-hemodialysis increase in BGC. Hemodialysis-induced decreases in methylglyoxal concentrations and methylglyoxal concentration at the end of hemodialysis influence post-hemodialysis fluctuations in BGC.

Moderate intensity physical activity prevents increased blood glucose concentrations, fat pad deposition and cardiac action potential prolongation following diet-induced obesity in a juvenile-adolescent rat model.

BackgroundBoth obesity and a lack of physical activity have been associated with an elevated risk of cardiovascular disease (CVD). The incidence of obesity is increasing, especially in juvenile-adolescents. While there is limited research examining the chronic effects of obesity in adolescent humans and animal models of this condition, little is also known concerning how moderate physical activity might prevent or attenuate secondary cardiovascular complications induced by obesity during adolescence. We investigated the effects of diet-induced obesity (consisting of a high-fat, high-carbohydrate diet (HFHC)) on biometric indices, vascular and airway function, cardiovascular function, systemic oxidative stress and markers of inflammation in a juvenile-adolescent rodent model. Four groups were used: control (CON), physical activity (PA) treated, HFHC and HFHC + PA (n = 16 per group). HFHC feeding started at 4 weeks of age for a period of 12 weeks. Physical activity treatment was initiated (PA and HFHC + PA groups) when the animals were 8 weeks of age, for 8 weeks.ResultsPhysical activity in juvenile-adolescent healthy rats showed no change in comparison to the CON group in all experimental parameters except for increases in lipid peroxidation, decreases in inflammatory cytokines, improvements in vascular reactivity and decreased atrial responses to positive chronotropic agents. The HFHC animals were mildly hyperglycemic, hypertensive, displayed renal hypertrophy and showed increased retroperitoneal fat pad deposition compared to the CON group. HFHC + PA rats were also hypertensive, however showed improvements in cardiac electrophysiology, body weight, fat pad deposition and inflammatory signaling, in comparison to the HFHC fed rats and CON animals.ConclusionIn conclusion, in a juvenile-adolescent animal model of diet-induced obesity engagement in physical activity is beneficial in reducing the inflammatory effects of obesity.

Hyperglycemia 3 Days After Esophageal Cancer Surgery Is Associated with an Increased Risk of Postoperative Infection

PurposePostoperative hyperglycemia is associated with infectious complications after various types of surgery. Our objective was to determine whether postoperative blood glucose levels up to 1 week after highly invasive esophageal cancer surgery are associated with the incidence of postoperative infections (POIs). MethodsWe conducted a retrospective chart review of 109 consecutive thoracic esophageal squamous cell cancer patients who underwent invasive esophagectomy with thoracotomy and laparotomy. The incidence of postoperative POIs and risk factors for POIs, including postoperative blood glucose levels, were evaluated. ResultsOf the 109 patients, 37 (34.0 %) developed POIs. Clinically, 73.0 % of the POIs became evident on or after postoperative day 4 (median, 5.25 days; interquartile range, 3.00–9.25 days). On and after postoperative day 3, chronological changes in blood glucose levels were significantly different between two groups of patients with or without POIs, as indicated by repeated measures ANOVA (P = 0.006). Multivariate logistic regression analysis results showed that an increased blood glucose concentration on postoperative day 3 was a significant risk factor for POIs. ConclusionsOur findings suggested that postoperative hyperglycemia on postoperative day 3 was a predictive factor of POIs after highly invasive esophageal cancer surgery.

Review of studies that have used knockout mice to assess normal function of prion protein under immunological or pathophysiological stress.

Deletion of cellular isoform of prion protein (PrP(C)) increases neuronal predisposition to damage by modulating apoptosis and the negative consequences of oxidative stress. In vivo studies have demonstrated that PrP(C)-deficient mice are more prone to seizure, depression, and induction of epilepsy and experience extensive cerebral damage following ischemic challenge or viral infection. In addition, adenovirus-mediated overexpression of PrP(C) reduces brain damage in rat models of cerebral ischemia. In experimental autoimmune encephalomyelitis, PrP(C)-deficient mice reportedly have a more aggressive disease onset and less clinical improvement during the chronic phase than wild-type mice mice. In mice given oral dextran sulfate, PrP(C) has a potential protective role against inflammatory bowel disease. PrP(C)-deficient mice demonstrate significantly greater increases in blood glucose concentrations after intraperitoneal injection of glucose than wild-type mice. Further in vivo challenges to PrP gene-deficient models and conditional knockout models with siRNA and in vivo administration of PrP-ligating agents may assist in refining knowledge of the lymphoid function of PrP(C) and predicting the effects of anti-PrP treatment on the immune system. Together, these findings indicate that PrP(C) may have multiple neuroprotective and anti-inflammatory roles, which explains why this protein is so widely expressed.

Effect of feeding different levels of wheat roti on nutrient utilization and blood metabolite profile in semi-captive Asian elephants (Elephas maximus).

This experiment was conducted to study the effect of different levels of wheat roti (WR) on nutrient utilization and blood metabolites in Asian elephants fed roughages ad libitum. Nine (3M, 6F) Asian elephants (14-52years of age, 1909-3968kg BW) were used in an experiment based on replicated Latin square design. Animals in each group (n=3) were assigned to one of the three dietary treatments in a manner that animals in all the three groups were exposed to all the three treatments in three different periods. Each feeding trial comprised 30days (25days of adaptation and 5days collection period). The amount of WR fed to the elephants was 0.18, 0.12 and 0.06% of BW in groups I, II and III, respectively. They were allowed to forage in the nearby forests for 6h/day and to bathe for 2h/day. The animals had ad libitum access to cut Rohini (Mallotus philippensis) trees in their night shelter. Intake and apparent digestibility of dry matter (DM), crude protein (CP), gross energy (GE), Ca, P, Fe, Cu and Zn were measured. Feed consumption was not significantly different among the groups. Significant (p<0.01) decrease in digestibility of DM and GE and blood glucose concentration was observed with decreased level of WR in the diet. Feeding of WR at 0.06% of BW supplied adequate amount of DE, CP, Ca, P, Fe, Cu and Zn to meet requirement for adult maintenance. Feeding of WR in excess of 0.06% of BW supplied DE in excess of requirement, increased blood glucose concentration which may cause obesity and other associated health problems. It was concluded that the amount of WR should be restricted to 0.06% of BW in the diet of captive Asian elephants.

Tacrolimus reversibly reduces insulin secretion, induces insulin resistance, and causes islet cell damage in rats.

To investigate the diabetogenic effects of the immunosuppressive agent tacrolimus, the reversibility of these effects upon treatment discontinuation, and the underlying mechanisms in a rat model. 60 healthy male rats were randomly divided into three groups for intragastric administration of tacrolimus either at 4 mg/kg/d or 2 mg/kg/d or an equal volume of normal saline (control). The treatment was administered for 5 months, followed by a 5-month period of no intervention. Fasting plasma glucose and insulin levels were used to calculate the homeostasis model assessment of ß-cell function (HOMA-ß) and insulin sensitivity index (ISI). Tacrolimus treatment significantly increased blood glucose concentrations (p < 0.05) and lowered HOMA-ß and ISI (p < 0.01) in a time- and dose-dependent manner. Five months after tacrolimus treatment, significant islet cell injury was observed. However, 5 months after tacrolimus discontinuation, blood glucose concentrations significantly declined, HOMA-β and ISI levels significantly increased, and islet cell morphology noticeably improved. In conclusion, tacrolimus treatment of healthy rats increased blood glucose concentrations in a time- and concentration-dependent manner. Development of tacrolimus-induced diabetes and reversibility after tacrolimus discontinuation may involve factors of and interactions between the insulin secretion pathway, local and/or systemic insulin resistance, and islet cell damage.