Increase In Fasting Blood Glucose Research Articles

Oral L-glutamine rescues fructose-induced poor fetal outcome by preventing placental triglyceride and uric acid accumulation in Wistar rats

BackgroundMetabolic adaptation of pregnant mothers is crucial for placental development and fetal growth/survival. However, evidence exists that indiscriminate consumption of fructose-enriched drink (FED) during pregnancy disrupts maternal-fetal metabolic tolerance with attendant adverse fetal outcomes. Glutamine supplementation (GLN) has been shown to exert a modulatory effect in metabolic disorders. Nevertheless, the effects of GLN on FED-induced poor fetal outcome, and in particular the impacts on placental uric acid/lipid accumulation are unknown. The present study was conducted to test the hypothesis that oral GLN improves fetal outcome by attenuating placental lipid accumulation and uric acid synthesis in pregnant rats exposed to FED. Materials and methodsPregnant Wistar rats (160–180 g) were randomly allotted to control, GLN, FED and FED + GLN groups (6 rats/group). The groups received vehicle by oral gavage, glutamine (1 g/kg) by oral gavage, fructose (10%; w/v) and fructose + glutamine, respectively, through gestation. ResultsData showed that FED during pregnancy caused placental inefficiency, reduced fetal growth, and caused insulin resistance with correspondent increase in fasting blood glucose and plasma insulin. FED also resulted in an increased placental triglyceride, total cholesterol and de novo uric acid synthesis by activating adenosine deaminase and xanthine oxidase activities. Moreover, FED during pregnancy led to increased lipid peroxidation, lactate production with correspondent decreased adenosine and glucose-6-phosphate dehydrogenase-dependent antioxidant defense. These alterations were abrogated by GLN supplementation. ConclusionThese findings implicate that high FED intake during pregnancy causes poor fetal outcome via defective placental uric acid/triglyceride-dependent mechanism. The findings also suggest that oral GLN improves fetal outcome by ameliorating placental defects through suppression of uric acid/triglyceride accumulation.

Brazil nut prevents oxidative DNA damage in type 2 diabetes patients

The Brazil nut (Bertholletia excelsa, H.B.K.) originating from the Amazon region is one of the richest known sources of selenium (Se), a micronutrient that is essential and required for optimal physiological functioning. This mineral presents several health benefits, including improvement of the redox cellular status and maintenance of genomic stability. Knowing that type 2 diabetes mellitus (T2D) is strongly linked to oxidative stress and consequently DNA damage, the aim of this study was to assess the ex vivo antioxidative effects of Se through Brazil nut consumption and its potential in preventing oxidative DNA damage induced by H2O2. In order to accomplish this, the Comet assay (single-cell gel electrophoresis) was used to measure DNA damage in peripheral blood cells harvested before and after supplementation with Brazil nut. Comet assay was also applied ex vivo to measure the potential of Se to prevent oxidative damage to DNA induced by H2O2 in blood of type 2 diabetes patients collected before and after six months of supplementation with Brazil nut. We found that supplementation with Brazil nuts significantly increased serum Se levels. Furthermore, we observed a significant increase in fasting blood glucose after six months of consuming Brazil nuts; however, no significant effect was observed on the levels of glycated hemoglobin. Finally, we noticed that the cells were more resistant to H2O2-induced DNA damage after six months of supplementation with Brazil nut. Thus, consumption of Brazil nuts could decrease oxidative DNA damage in T2D patients, probably through the antioxidative effects of Se.

Glycemic Index and Glycemic Load to the Biochemical Profile of Dyslipidemic Patients

Background: The positive and negative health effects of dietary carbohydrates are of interest to both researchers and consumers. Low glycemic index (GI) and glycemic load (GL) carbohydrates have been shown to have favourable effects on blood lipid parameters. Objective: This study aims to investigate whether the GI and GL diet in dyslipidemic individuals. Methods: The subjects, 15 men and 15 women, dyslipidemic patients followed up at Hospital de Coari, were invited to answer a self-administered questionnaire for 3 days about food intake. The fasting biochemical profile was analyzed, such as total cholesterol, triglycerides and blood glucose. Results: Low GI diet daily value were observed in women and men and GL diet daily value below the minimum low line for both. A correlation was found between GI and GL diet with triglycerides levels and woman and not in men. Lunch GL value were associated with blood triglycerides parameters. Biochemical profile showed an increase in fasting blood glucose only in men and in lipid levels for both. Conclusion: Dyslipidemic individuals might be potential influencing factors in the associations between GI and GL diet and dyslipidemia, suggesting such modifications could potentially be a useful public health recommendation.

Effect of consumption of ancient grain bread leavened with sourdough or with baker’s yeast on cardio-metabolic risk parameters: a dietary intervention trial

The aim of this study was to compare the effect of consumption of ancient grain “Verna” bread obtained by two different leavening agents, sourdough (SD) and baker’s yeast (BY), on inflammatory parameters and cardiometabolic risk factors. Seventeen clinically healthy subjects were included to consume SD or BY bread for 4 weeks each, and blood analyses were carried out. The consumption of “Verna” bread obtained with both leavening agents led to a significant improvement of LDL cholesterol. A reduction of −10.6% and −8.53% was observed after replacement with SD and BY bread, respectively. A significant increase in fasting blood glucose (+6%) was observed only after the intervention with BY bread. A 10.7% decrease of vascular endothelial growth factor was found after the SD bread replacement period. The consumption of “Verna” bread resulted significantly associated with an improvement in the cardiometabolic and inflammatory profile. However, only consumption of BY bread determined a significant increase in blood glucose levels.

Pharmacological and metagenomics evidence of polysaccharide from Polygonum multiflorum in the alleviation of insulin resistance

Total polysaccharide from Polygonum multiflorum (PS) and 2,3,5,4′-tetrahydroxy-stilbene-2-O-β-D-glucoside (TSG) could relieve high-fat and high-sugar diet (HF-HSD) induced rats' insulin resistance (IR) by gut microbiota and host regulation. We found that PS and TSG significantly reversed the increase of fasting blood glucose and the decrease of glucose tolerance in HF-HSD induced IR rats. PS and TSG effectively reversed the imbalance of Firmicutes/Bacteroides caused by an HF-HSD, and significantly reduced the relative abundance of Proteobacteria. It also affected the functional genes of gut microbiota and regulated short-chain fatty acids (SCFAs) and its downstream signal protein molecules. Together, these results indicated that PS and TSG alleviated HF-HSD induced IR by promoting gut microbiota and host function. Thus, PS and TSG may be promising lead substances for developing IR inhibitors that could regulate gut microbiota and its molecular messenger SCFAs to remedy IR.

Preparation and Characterization of Chitosan-Stabilized Selenium Nanoparticles for Ameliorating Experimentally Induced Diabetic Nephropathy in Rats

Chitosan-stabilized selenium nanoparticles (CTS-SeNPs) were prepared by reduction technique. Single phase structure of the SeNPs was confirmed using X-ray diffraction (XRD). Transmission Electron Microscope (TEM) showed that the particle size of the samples in the range of 15 nm. This experiment aimed to study the potential effect of (CTS-SeNPs) as a therapeutic factor in diabetic nephropathy in rats. Streptozotocin (STZ) was used to induce diabetes in rats; thirty-six numbers were divided into three groups; control, STZ-induced diabetic, and STZ-induced diabetic rats taken CTS-SeNPs groups at a dose (2 mg Se/kg/d). All groups were given respective treatment orally via gastric tube for 2 month. The obtained data showed that, the diabetic group revealed presence of Microalbuminurea, the indicator of diabetic nephropathy and showed a significant increase in fasting blood glucose, urea, creatinine, TAC and MDA, it is significant that high expression level of TGF-β1 and aldose reductase while the group treated with CTS-SeNPs revealed significant decline in all values compared to the diabetic group. Diabetic group showed a significant decrease in insulin level, GPx and SOD activity while, the treated group showed significant increase in these values compared to the diabetic group. Kidney tissue showed normal histological picture except for mild vascular and glomerular congestion in treated group when compared with diabetic one. Our experiment suggests that CTS-SeNPs can moderate diabetic nephropathy in streptozotocin-induced diabetic rats.

A moderate physiological dose of benzyl butyl phthalate exacerbates the high fat diet-induced diabesity in male mice.

Exposure to endocrine disrupting chemicals (EDCs) used in plastic manufacturing processes may be contributing to the current increase in metabolic disorders. Here, we determined that benzyl butyl phthalate (BBP), a common EDC and food packaging plasticizer, mixed into chow diet (CD) and high fat diets (HFD) at varying concentrations (4μg/kg body weight (bw)/day, 169μg/kg bw/day, 3mg/kg bw/day, 50mg/kg bw/day) produced a number of detrimental and sex-specific metabolic effects in C57BL/6 male and female mice after 16weeks. Male mice exposed to moderate (3mg/kg bw/day) concentrations of BBP in an HFD were especially affected, with significant increases in body weight due to significant increases in weight of liver and adipose tissue. Other doses did not show any significant changes when compared to only CD or HFD alone. HFD in the presence of 3mg/kg bw/day BBP showed significant increases in fasting blood glucose, glucose intolerance, and insulin intolerance when compared to HFD alone. Furthermore, this group significantly alters transcriptional regulators involved in hepatic lipid synthesis and its downstream pathway. Interestingly, most of the BBP doses had no phenotypic effect when mixed with CD and compared to CD alone. The female mice did not show a similar response as the male population even though they consumed a similar amount of food. Overall, these data establish a dose which can be used for a BBP-induced metabolic research model and suggest that a moderate dosage level of EDC exposure can contribute to widely ranging metabolic effects.

1969-P: Moderate Dosage of Benzyl Butyl Phthalate Synergizes the High-Fat Diet Induced Diabesity in Male Mice

There has been a sudden and rapid degradation in global metabolic health over the last decade, due to the progression of the obesity and diabetes epidemic. Exposure to endocrine disrupting chemicals (EDCs) used in plastic manufacturing may be contributing to this increase in metabolic disorders. Previous studies are concentrated on evaluating toxicity of these EDCs in the context of reproductive biology. However, virtually none have been performed with a range of exposure levels in both genders, especially in the context of an obesity-causing Western diet. In this study, we determined that butyl benzyl phthalate (BBP), a common EDC and food packaging plasticizer, mixed into chow (CD) (4% kcal from fat) and high fat diets (HFD) (60% kcal from fat) at varying concentrations (4 µg/kg body weight/day, 169 µg/kg body weight/day, 3 mg/kg body weight/day, 50 mg/kg body weight/day) produced a number of detrimental and sex-specific metabolic effects in C57Bl/6 male and female mouse populations after 16 weeks. Males exposed to moderate (3 mg/kg body weight/day) concentrations of BBP in an HFD were especially affected, with significant increases in body weight due to increases in liver, adipose tissue, kidney, and testes size. Other doses did not show any significant changes when compared to only CD or HFD alone. Furthermore, moderate dosage in HFD showed significant increases in fasting blood glucose, glucose tolerance, and insulin tolerance when compared to HFD alone. This group alters several molecular markers, which regulate hepatic gluconeogenesis and their transcriptional regulators, lipid metabolism, hepatic lipid synthesis, insulin signaling pathways, and inflammation. The female population did not show an intense effect as males even though they consumed similar amounts of food. Overall, these data establish a dose which can be used for a BBP induced metabolic research model, suggesting that a moderate dosage level of EDC exposure can contribute to widely ranging metabolic effects. Disclosure M.K. Kay: None. J. Zhang: None. C. Powell: None. M. Park: None. R. Sonkar: None. S. Meruvu: None. M. Choudhury: None.

Effects of low glycemic index/high-fat, high-calorie diet on glycemic control and lipid profiles of children and adolescence with cystic fibrosis: A randomized double-blind controlled clinical trial

PurposeLow glycemic index diets seem to be potentially effective to improve glycemic control and reduce lipid profiles. Hence, this study aimed to evaluate the effect of a low glycemic index/high fat, high-calorie diet on glycemic status and lipid profiles of patients with cystic fibrosis. MethodsIn this randomized clinical trial, 44 children and adolescents with cystic fibrosis were randomized to receive for three months either a high fat, high-calorie diet (n = 22) or a low glycemic index/high fat, high-calorie diet (n = 22) with similar calorie and macronutrients composition. Patients in high fat, high-calorie diet arm were allowed to use all sources of carbohydrates with different glycaemic indices; whereas those in another arm consumed carbohydrates from low glycemic index sources. Serum levels of lipid profiles (triglyceride, total cholesterol, HDL cholesterol, LDL cholesterol), insulin, fasting blood glucose, and glycated hemoglobin were measured at baseline and after the intervention. ResultsBetween-group differences were significant only for fasting blood glucose (P < 0.001). However, fasting blood glucose (P = 0.003) and glycated hemoglobin (P = 0.002) significantly decreased after the intervention in the low glycemic index group, while in another group a significant increase in fasting blood glucose (P = 0.038) and triglyceride (P = 0.004) was found. No significant within-group differences were observed in other variables in both groups. ConclusionsIt seems that adherence to a low glycemic index/high fat, high-calorie diet can improve glycemic indices in children and adolescents with cystic fibrosis compared to the high fat, high-calorie diet. Trial registrationIRCT2017102325267N5.

Change in baseline characteristics over 20 years of adults with growth hormone (GH) deficiency on GH replacement therapy.

Clinical observations over time of adults with growth hormone (GH) deficiency (GHD) have indicated a shift in patient characteristics at diagnosis. The objective of this study was to compare baseline characteristics of patients diagnosed with adult-onset GHD naive to GH replacement during three study periods (1994-1999 (P1), 2000-2004 (P2), and 2005-2012 (P3)) using the KIMS (Pfizer's International Metabolic) database. Data were retrieved for a total of 6069 patients with adult-onset GHD from six countries (Belgium, Germany, Netherlands, Spain, Sweden, and UK): P1 (n = 1705), P2 (n = 2397), and P3 (n = 1967). The proportions of patients with pituitary/hypothalamic tumors and patients with multiple pituitary hormone deficiencies decreased per entry year period, while the proportions with hypertension and diabetes increased. The lag time from diagnosis of pituitary disease to start of GH treatment decreased by 2.9 years over the entry year periods. IGF-1 increased by 0.1 standard deviation score per entry year period. Maximum GH following various stimulation tests, BMI, and waist circumference increased. The use of radiotherapy, glucocorticoid replacement doses, and the proportion of women >50 years on estrogen replacement therapy decreased. The effects of 1 year of GH replacement were similar over the entry year periods despite changes in the patients' baseline characteristics. An expected increase in fasting blood glucose was seen after 1 year of GH treatment. The degree of confirmed GHD became less pronounced and more patients with co-morbidities and diabetes were considered for GH replacement therapy, possibly reflecting increased knowledge and confidence in GH therapy gained with time.

Chronic Light Cycle Disruption Alters Central Insulin and Leptin Signaling as well as Metabolic Markers in Male Mice.

Recent evidence suggests that the circadian timing system plays a role in energy and glucose homeostasis, and disruptions to this system are a risk factor for the development of metabolic disorders. We exposed animals to a constantly shifting lighting environment comprised of a 6-hour advance, occurring every 6 days, to chronically disrupt their circadian timing system. This treatment caused a gradual increase in body weight of 12 ± 2% after 12 phase shifts, compared with a 6 ± 1% increase in mice under control lighting conditions. Additionally, after the fifth phase shift, light cycle-disrupted (CD) animals showed a reversal in their diurnal pattern of energy homeostasis and locomotor activity, followed by a subsequent loss of this rhythm. To investigate potential molecular mechanisms mediating these metabolic alterations, we assessed central leptin and insulin sensitivity. We discovered that CD mice had a decrease in central leptin signaling, as indicated by a reduction in the number of phosphorylated signal transducer and activator of transcription 3 immunoreactive cells in the arcuate nucleus of the hypothalamus. Furthermore, CD animals exhibited a marked increase in fasting blood glucose (269.4 ± 21.1 mg/dL) compared with controls (108.8 ± 21.3 mg/dL). This dramatic increase in fasting glucose levels was not associated with an increase in insulin levels, suggesting impairments in pancreatic insulin release. Peripheral hyperglycemia was accompanied by central alterations in insulin signaling at the level of phospho Akt and insulin receptor substrate 1, suggesting that light cycle disruption alters central insulin signaling. These results provide mechanistic insights into the association between light cycle disruption and metabolic disease.

Exposure to Aroclor 1254 persistently suppresses the functions of pancreatic β-cells and deteriorates glucose homeostasis in male mice

Polychlorinated biphenyls (PCBs) are a class of persistent organic pollutants that have been shown to be related to the occurrence of type 2 diabetes mellitus (T2DM). Nevertheless, it is necessary to further explore the development of T2DM caused by PCBs and its underlying mechanisms. In the present study, 21-day-old C57BL/6 male mice were orally treated with Aroclor 1254 (0.5, 5, 50 or 500 μg kg−1) once every three days. After exposure for 66 d, the mice showed impaired glucose tolerance, 13% and 14% increased fasting serum insulin levels (FSIL), and 63% and 69% increases of the pancreatic β-cell mass in the 50 and 500 μg kg−1 groups, respectively. After stopping exposure for 90 d, treated mice returned to normoglycemia and normal FSIL. After re-exposure of these recovered mice to Aroclor 1254 for 30 d, fasting plasma glucose showed 15%, 28% and 16% increase in the 5, 50 and 500 μg kg−1 treatments, FSIL exhibited 35%, 27%, 30% and 32% decrease in the 0.5, 5, 50 or 500 μg kg−1 groups respectively, and there was no change in pancreatic β-cell mass. Transcription of the pancreatic insulin gene (Ins2) was significantly down-regulated in the 50 and 500 μg kg−1 groups, while DNA-methylation levels were simultaneously increased in the Ins2 promoter during the course of exposure, recovery and re-exposure. Reduced insulin levels were initially rescued by a compensative increase in β-cell mass. However, β-cell mass eventually failed to make sufficient levels of insulin, resulting in significant increases in fasting blood glucose, and indicating the development of T2DM.

Inadequate serum hepcidin levels in chronic hepatitis C infection-induced type 2 diabetes mellitus

Background Hepatitis C virus (HCV) is a major cause of chronic liver disease worldwide. In addition to established liver injury, type 2 diabetes mellitus (T2DM) is one of the most important extrahepatic metabolic disorders that are attributed to HCV infection. Aim The aim of this study is to investigate the impact of HCV infection in the development of T2DM through the assessment of serum hepcidin levels. Patients and methods The study included 60 Egyptian patients with chronic HCV infection who were divided according to the presence and absence of diabetes into two groups: 30 HCV-positive patients who developed diabetes mellitus during the course of HCV infection (HCV-T2DM patients) and 30 HCV-positive patients without T2DM (HCV patients) and 20 healthy individuals as a control group (age and sex matched). They were subjected to a full assessment of medical history, clinical examination, abdominal ultrasound, and laboratory investigations including complete blood count, liver function tests, fasting blood sugar (FBS), glycosylated hemoglobin, fasting insulin, serum hepcidin, serum ferritin, serum iron, and transferrin saturation. Serum hepcidin, ferritin, and insulin were measured using an enzyme-linked immunosorbent assay. Results We found that serum hepcidin was statistically significantly lower in HCV patients than in controls (P&lt;0.0001). Also, serum hepcidin in HCV-T2DM patients was statistically significantly lower than that in HCV-positive patients (P&lt;0.05). Serum ferritin was statistically significantly higher in HCV-positive patients than in controls (P&lt;0.0001). Also, serum ferritin was statistically significantly higher in HCV-T2DM patients than in HCV patients (P&lt;0.0001). Serum iron and serum transferrin saturation were statistically significantly higher in HCV-T2DM patients than HCV-positive patients (P&lt;0.0001 and &lt;0.0001, respectively). There was a statistically significant increase in fasting blood glucose, glycosylated hemoglobin, and fasting insulin in HCV-T2DM patients compared with HCV nondiabetic patients (P&lt;0.0001 for all). Also, we found that the serum albumin was statistically significantly lower in HCV-T2DM patients compared with HCV-positive patients (P&lt;0.0001). Conclusion HCV infection is associated with a decreased level of hepcidin in relation to body iron store, which plays a crucial role in the development of T2DM in chronic HCV infection patients.

Supplementation with beta-hydroxy-beta-methylbutyrate impacts glucose homeostasis and increases liver size in trained mice.

β-hydroxy-β-methyl butyrate (HMB) is a bioactive metabolite derived from the amino acid leucine, usually applied for muscle mass increase during physical training, as well as for muscle mass maintenance in debilitating chronic diseases. The hypothesis of the present study is that HMB is a safe supplement for muscle mass gain by strength training. Based on this, the objective was to measure changes in body composition, glucose homeostasis and hepatic metabolism of HMB supplemented mice during strength training. Two of four groups of male mice (n=6/group) underwent an 8-week training period session (climbing stairs) with or without HMB supplementation (190mg/kgBW per day). We observed lower body mass gain (4.9±0.43% versus 1.2±0.43, p<0.001) and increased liver mass (40.9±0.9mg/gBW versus 44.8±1.3, p<0.001) in the supplemented trained group compared with the non-supplemented groups. The supplemented trained group had an increase in relative adipose tissue mass (12.4±0.63mg/gBW versus 16.1±0.88, P<0.01) compared to the non-supplemented untrained group, and an increase in fasting blood glucose (111±4.58mg/dL versus 122±3.70, P<0.05) and insulin resistance (3.79±0.19 % glucose decay/min versus 2.45±0.28, P<0.05) comparing with non-supplemented trained group. Adaptive heart hypertrophy was observed only in the non-supplemented trained group (4.82±0.05mg/gBW versus 5.12±0.13, P<0.05). There was a higher hepatic insulin-like growth factor-1 expression (P=0.002) in supplemented untrained comparing with non-supplemented untrained group. Gene expression of gluconeogenesis regulatory factors was increased by training and reduced by HMB supplementation. These results confirm that HMB supplementation associated with intensive training protocol drives changes in glucose homeostasis and liver metabolism in mice.

Supplementation of Abelmoschus manihot Ameliorates Diabetic Nephropathy and Hepatic Steatosis by Activating Autophagy in Mice.

Diabetic nephropathy (DN) is a diabetic complication marked by albuminuria and a decline of the glomerular filtration rate. Diabetic kidneys are defective in the autophagy process and mitochondrial function and their enhancement of activity alleviates the pathology. In this paper, we developed a mouse model of DN by a combined treatment of a high-fat diet and streptozotocin after unilateral nephrectomy and supplementation with flower or leaf extracts of Abelmoschus manihot (AM) were tested. The preventive effects of the extracts on DN pathology and changes on autophagy and mitochondrial proteins were investigated. DN mice showed a significant increase in fasting blood glucose, plasma creatinine, blood urea nitrogen, and urinary albumin levels. Periodic acid–Schiff and Sirius red staining of the diabetic kidney presented a significant change in glomerular and tubular structures that was associated with podocyte loss and fibrotic protein accumulation. These changes were attenuated by AM extract treatment in DN mice. In addition, hepatic injury, proinflammatory cytokines, and lipid accumulation were decreased by AM extracts in DN mice. As a protective mechanism, AM extracts significantly increased the expression of proteins by regulating autophagy and mitochondrial dynamics, which potentially prevented the kidney and liver from accumulating pathogenic proteins and dysfunctional mitochondria, which alleviated the progression of DN.

Effect of Calcineurin Inhibitor on Blood Glucose Level in Non-Diabetic Kidney Transplant Patients

Background Calcineurin inhibitor (CNI) is a class of immunosuppressant agent used in kidney transplant management, known to pose risk for new-onset diabe­tes after transplant (NODAT). Tacrolimus and cyclo­sporine cause NODAT through multiple mechanisms, such as decreasing insulin secretion, increasing in­sulin resistance, and a direct effect on the pancreatic beta cell. Method This is a retrospective study on pa­tients receiving immunosuppressant agents for kidney transplant patients in Surabaya. The immunosuppres­sant agents studied were CNI (tacrolimus and cyclo­sporine) in combination with mycophenolate mofetil (MMF) or azathioprine (Aza) and steroid. The blood glucose measured were fasting blood glucose (FBD) and 2-hour postprandial blood glucose (2PPBG). Ob­jective Aim of this study is to determine the effect of calcineurin inhibitor (CNI) on glucose regulation in the nondiabetic renal transplant patient. Result Fifty-six subjects were included in the study, divided into two groups. One group of 28 patients (50%) received tac­rolimus-MMF-MP and the other group received cyc­losporine-MMF-MP. A significant increase in fasting blood glucose (pre-intervention level 86 ± 6 mg/dl vs post-intervention level 109 ± 34 mg/dl with p = 0.01) and 2-hour postprandial blood glucose (pre-interven­tion level 117 ± 20 mg/dl vs post-intervention level 150 ± 43 mg/dl with p &lt; 0.001) was found in the tacro­limus group. A significant increase was also found in the cyclosporine group, both in fasting blood glucose (pre-intervention value 85 ± 7 mg/dl vs post-interven­tion value 97 ± 22 mg/dl with p = 0.002) and 2-hour postprandial blood glucose (pre-intervention value 119 ± 18 mg/dl vs post-intervention value 148 ± 55 mg/dl with p = 0.001). Tacrolimus was found to have a relative risk of NODAT up to 1.2 fold compared to cy­closporine. Conclusion Tacrolimus poses 1.29 relative risk of NODAT compared to cyclosporine. However, both drugs significantly increase fasting blood glucose and 2-hour postprandial blood glucose in non-diabetic patients receiving kidney transplantation.

Gut microbiota mediates the anti-obesity effect of calorie restriction in mice

Calorie restriction (CR) extends lifespan and elicits numerous effects beneficial to health and metabolism in various model organisms, but the underlying mechanisms are not completely understood. Gut microbiota has been reported to be associated with the beneficial effects of CR; however, it is unknown whether these effects of CR are causally mediated by gut microbiota. In this study, we employed an antibiotic-induced microbiota-depleted mouse model to investigate the functional role of gut microbiota in CR. Depletion of gut microbiota rendered mice resistant to CR-induced loss of body weight, accompanied by the increase in fat mass, the reduction in lean mass and the decline in metabolic rate. Depletion of gut microbiota led to increases in fasting blood glucose and cholesterol levels independent of CR. A few metabolism-modulating hormones including leptin and insulin were altered by CR and/or gut microbiota depletion. In addition, CR altered the composition of gut microbiota with significant increases in major probiotic genera such as Lactobacillus and Bifidobacterium, together with the decrease of Helicobacter. In addition, we performed fecal microbiota transplantation in mice fed with high-fat diet. Mice with transferred microbiota from calorie-restricted mice resisted high fat diet-induced obesity and exhibited metabolic improvement such as alleviated hepatic lipid accumulation. Collectively, these data indicate that CR-induced metabolic improvement especially in body weight reduction is mediated by intestinal microbiota to a certain extent.

Impact of Variation of Corticosteroid Dose, Injection Site, and Multiple Injections on Blood Glucose Measurement in Diabetic Patients.

This study examined how corticosteroid dose, injection site location, and patient demographics affect blood glucose level after corticosteroid injection in diabetic patients. We prospectively enrolled 70 patients with diabetes mellitus requiring upper- and/or lower-extremity corticosteroid injections. Patients measured fasting and postprandial blood glucose for 14 days after the injection. Blood glucose from days 1 through 7 was compared with the average of days 10 through 14, acting as control. Changes in blood glucose were compared by corticosteroid dose, injection location, patient demographics, and insulin use. Patients who underwent shoulder, wrist, or hand injections and patients who received multiple injections had no significant elevations in fasting or postprandial blood glucose, whereas those with knee injections had a significant increase in fasting blood glucose on postinjection days 1 and 2. Preinjection hemoglobin A1C had a significant effect on postinjection blood glucose whereas corticosteroid dose, body mass index, insulin use, and the number of injections had no significant effect on the elevation of blood glucose. There were no cases of diabetic ketoacidosis in any subjects. Patients receiving corticosteroid injections in the upper extremity did not experience significant increases in blood glucose whereas those undergoing knee corticosteroid injections demonstrated elevated blood glucose levels. Because poorer glucose control was associated with greater elevations in blood glucose after injection, patients with higher hemoglobin A1C should be counseled to monitor postinjection glucose more closely. Therapeutic II.

A case study wistar rats by implementing Metformin on Clozapine

The medical studies in beyond decade has reported that maximum 2nd-era antipsychotics (SGAs) can reason severe metabolic derangement, which significantly upsurges the danger for type II diabetes mellitus. Numerous retrospective studies have proven multiplied in serum triglyceride in sufferers handled with Clozapine. SGAs triggered metabolic syndrome is characterized via hypertension, weight gain, hyperglycaemia, hyperlipidaemia, glucose intolerance and insulin resistance. Metformin is presently used to extravagance metabolic syndrome and type II diabetes mellitus. It is consequently essential to decide whether Metformin is effective in discussing Clozapine-brought on metabolic derangement like dyslipidaemia. To appraise the impact of Metformin in minimizing Clozapine caused metabolic irrationality like dyslipidaemia. Methodology: Wistar rats weighing a hundred and eighty-240g both intercourse had been divided into three corporations of 6 rats every. Group 1 attended as manipulate, Group 2 Preserved with Clozapine 25mg/kg frame weight and Group 3 Treated with Clozapine 25mg + Metformin 100mg/kg body weight for 30 days P.O. Group 2 and group three were preserved for 30 days. Lipid profile of institution 2 rats handled with Clozapine showed dyslipidaemia (TG 103.3±1.7mg/dl, Tc 113.7±1.6mg/dl). Whereas organization 3 rats treated with Clozapine 25mg + Metformin confirmed ordinary lipid levels (TG ninety four.7±1.7mg/dl, TC 102.Eight±0.Eight mg/dl) similar to institution 1(TG ninety three.0±2.6mg/dl, TC 103.7±1.5mg/dl). This study focuses a non-substantial increase in fasting blood glucose in SD rodents managed with clozapine that was in part checked by utilizing simultaneous organization of metformin. Rodents controlled clozapine affirmed the anticipated abatement in the statement of GLUT2, anyway simultaneous administration of metformin and clozapine for 30 days didn't show the anticipated standardization of the articulation degrees of GLUT2. This look at investigating the use of Metformin to forestall metabolic unsettling like dyslipidaemias in patients of schizophrenia managed with Clozapine.

Maternal lipopolysaccharide exposure results in glucose metabolism disorders and sex hormone imbalance in male offspring.

An adverse intrauterine environment may be an important factor contributing to the development of type 2 diabetes in later life. The present study investigated the longitudinal effects of maternal lipopolysaccharide (LPS) exposure during the third trimester on glucose metabolism and sex hormone balance in the offspring. Pregnant mice were intraperitoneally injected with LPS (50 μg/kg) daily from gestational day (GD) 15 to GD17. Glucose tolerance test (GTT) and insulin tolerance test (ITT) were assessed at postnatal day (PND) 60 and PND120. Sex hormones, their receptors, and metabolic enzymes (aromatase) were measured in male offspring at different phases of development (PND14: juvenile; PND35: adolescence; PND60: adulthood; and PND120: middle age). LPS-exposed male offspring exhibited glucose intolerance and insulin resistance by GTT and ITT at middle age, accompanied by an increase in fasting blood glucose and reductions in serum insulin levels and hepatic phosphorylated (p) -AKT/AKT ratio. However, glucose intolerance and insulin resistance were not observed in LPS-exposed female offspring. Maternal LPS exposure upregulated hepatic aromatase proteins and mRNA levels in male offspring at all time points. At adolescence, the testosterone/estradiol ratio (T/E2) was markedly reduced in LPS-exposed male offspring. Moreover, maternal LPS exposure significantly increased hepatic estrogen receptor (ER) α expressions and decreased hepatic androgen receptor (AR) expressions in male offspring. At adulthood, maternal LPS exposure increased serum estradiol levels, decreased serum testosterone levels and elevated hepatic ERβ expressions in male offspring. In conclusion, maternal LPS exposure upregulated aromatase expressions, followed by a reduction in the T/E2 ratio and an alteration in sex hormone receptor activity, which might be involved in the development of glucose metabolism disorders in middle-aged male offspring. This study provides a novel clue and direction to clarify the pathogenesis of maternal infection-related diabetes in male offspring.