Glucose Ingestion Research Articles

Effect Of Anting-Anting Leaf Extract (Acalypha Indica L.) On Lowering Blood Glucose Rats (Rattus Norvegicus) Induced By Sukrosa

Anting-anting leaves (Acalypha indica L.) are weeds that have various properties, one of which is as a lowering blood glucose levels. The chemical content contained in the form of flavonoids that function as inhibitors of α-glucosidase, maltase, α-amylase enzymes, tannin substances are also known to function as astrigents that can inhibit glucose intake is not excessive. The purpose of this study is to determine whether there is an effect of anting-anting leaf extract (Acalypha indica L.) on reducing blood glucose levels in rats (Rattus norvegicus) induced by sucrose. This research used 20 rats (Rattus norvegicus) as test animals which were divided into 5 groups. The group consisted of negative control group, positive control and 3 dose groups. The doses used were 500 mg/kgBB, 1000 mg/kgBB and 1200 mg/kgBB. Mice were made hyperglycemia with sucrose induction which was then given anting-anting leaf extract (Acalypha indica L.) according to lower glucose levels in mice. The results obtained were continued with the two-way ANOVA test and obtained significant results indicated by p < 0.05 (0.005) which showed there was a significant effect of anting-anting leaf extract (Acalypha indica L.) on reducing blood glucose levels in sucrose-induced rats (Rattus norvegicus). Significant results were continued with the post hoc test and obtained significant results.

Intake of Sugar and Food Sources of Sugar and Colorectal Cancer Risk in the Multiethnic Cohort Study

BackgroundThe influence of sugar intake on the risk of colorectal cancer (CRC) remains controversial, and there is a need to investigate the heterogeneity of effects among racial and ethnic groups. ObjectivesTo examine the association of intake of simple sugars and their food sources with CRC risk according to race/ethnicity in a multiethnic cohort study. MethodsWe analyzed data from 192,651 participants who participated in the Multiethnic Cohort Study comprising African American, Japanese American, Latino, Native Hawaiian, and White older adults living in Hawaii and California with an average follow-up of 19 y. Intakes of total and specific types of sugars and sugary foods were estimated from a quantitative food frequency questionnaire completed by the participants in 1993–1996. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for CRC risk according to quintiles (Q) of sugar and food intakes using Cox models adjusted for potential confounders. ResultsAs of December 2017, 4403 incident CRC cases were identified. Among all participants, multivariable-adjusted CRC HRs for Q2, Q3, Q4, and Q5 compared with Q1 for total sugars were 1.03 (95% CI: 0.94, 1.13), 1.05 (95% CI: 0.96, 1.16), 1.12 (95% CI: 1.01, 1.24), and 1.13 (95% CI: 1.01, 1.27), respectively. A similar positive association was observed for total fructose, glucose, fructose, and maltose but not for added sugars and sugary foods. The increased risk appeared to be limited to colon cancer and to be strongest among younger participants (i.e., 45–54 y at baseline); an association with CRC was observed for sugar-sweetened beverages in the latter group. Among racial and ethnic groups, increased risk of CRC was most apparent in Latinos. ConclusionsIn this diverse cohort, intakes of total sugar, total fructose, glucose, fructose, and maltose were associated with an increased risk of CRC, and the association was strongest for colon cancer, younger participants, and Latinos.

#1206 Combination therapy with Lisinopril and Dapagliflozin rescues GFR decline and glomerular damage in the KKAy mouse model of diabetic kidney disease

Abstract Background and Aims Male KKAy mice develop diabetic kidney disease (DKD) with progressive decline of GFR upon high fat diet feeding which is accelerated by the vasoconstrictor LNNA. In this study, efficacy of combination therapy with clinical relevant therapeutics in the form of an ACE-inhibitor (Lisinopril) and SGLT2-inhibitor (Dapagliflozin) on renal function and histopathology was investigated. Method Male KKAy mice underwent uninephrectomy (UNX). After recovery mice received high fat diet (45% LARD) and 50 mg/L LNNA in drinking water (wk0). At week 4, Lisinopril (2.5 mg/kg/day in drinking water) and at week 8 Dapagliflozin (5 and 20 mg/kg/day in diet) were started. Body weight, blood glucose, food and water intake and albuminuria were determined regularly. GFR was measured transdermally by FITC-sinistrin clearance. Mice were terminated at week 16 and renal histology was scored by a team of renal histopathologists. Non-induced and induced non-treated mice were used as controls. Results Treatment of KKAy mice on HFD+LNNA with Dapagliflozin reduced blood glucose immediately. Combination therapy with Lisinopril and Dapagliflozin (5 mg/kg/day) rescued the progressive GFR decline to levels seen in non-induced chow-controls (p < 0.05 vs UNX+HFD+LNNA). Pathology showed that the percentage of healthy glomeruli increased from 14% to 26% after combination therapy (Dapa 5). Interstitial fibrosis and tubular atrophy were significantly reduced by combination therapy (p < 0.05 vs UNX+HFD+LNNA). Conclusion Male KKAy mice on a HFD and LNNA developed DKD resulting in CKD. Combination therapy with Lisinopril and Dapagliflozin rescued GFR decline and reduced glomerular damage and interstitial fibrosis and tubular atrophy This indicates the clinical relevance of the model which can be used to study compound efficacy in both early and more advanced stages of DKD.

Glucose ingestion does not lower testosterone concentrations in men on testosterone therapy.

Oral calorie intake causes an acute and transient decline in serum testosterone concentrations. It is not known whether this decline occurs in men on testosterone therapy. In this study, we evaluated the change in testosterone concentrations following oral glucose ingestion in hypogonadal men before and after treatment with testosterone therapy. This is a secondary analysis of samples previously collected from a study of hypogonadal men with type 2 diabetes who received testosterone therapy. Study participants (n = 14) ingested 75 grams of oral glucose, and blood samples were collected over 2 h. The test was repeated after 23 weeks of intramuscular testosterone therapy. The mean age and body mass index of study volunteers were 53 ± 8 years and 38 ± 7 kg/m2, respectively. Following glucose intake, testosterone concentrations fell significantly prior to testosterone therapy (week 0, p = 0.04). The nadir of testosterone concentration was at 1 h, followed by recovery to baseline by 2 h. In contrast, there was no change in testosterone concentrations at week 23. The change in serum testosterone concentrations at 60 min was significantly more at week 0 than week 23 (-11 ± 10% vs 0 ± 16%, p = 0.05). We conclude that oral glucose intake has no impact on testosterone concentrations in men on testosterone therapy. Endocrinology societies should consider clarifying in their recommendations that fasting testosterone concentrations are required for the diagnosis of hypogonadism, but not for monitoring testosterone therapy.

Salivary testosterone changes during oral glucose tolerance tests in overweight and obese men - postprandial or circadian variation?

Serum total testosterone (T) decreases postprandially. Postprandial salivary testosterone (SalT) responses, however, have not been studied. We report on the effect of glucose ingestion on fasting SalT concentrations. To investigate the effect of oral glucose ingestion on fasting SalT. Salivary and blood samples were collected between 09.00 and 09.30 and two hours after a 75g oral glucose load in 32 men with mean (standard deviation) age of 52 (5.7) years and body mass index of 32.6 (5.56) kg/m2. Free T and bioavailable testosterone (BAT) were calculated using the Vermeulen equation. Two hours following oral glucose, there was a decrease in fasting mean (standard deviation) SalT [178.2 (56.6) vs 146.0 (42.2) pmol/L; p = 0.0003], serum cortisol [332 (105.0) vs 239 (75.3) nmol/L; p = <0.0001], prolactin [193 (75.0) vs 127 (55.9) mIU/L; p = <0.0001] and TSH [1.60 (0.801) vs 1.16 (0.584) mIU/L; p = <0.0001]. Plasma glucose increased [6.2 (0.72) vs 8.1 (3.71) mmol/L; p = 0.0029]. Serum total T, SHBG, albumin, Free T, BAT, gonadotrophins and FT4 remained unchanged. SalT decreased postprandially. A concomitant decrease in serum cortisol, prolactin and TSH reflecting diurnal variation offers an alternative explanation for the decrease in SalT independent of food consumption. Further studies are required to determine whether morning temporal changes in SalT are related to food consumption or circadian rhythm or both.

Effects of chronic inspiratory muscle strength training on metabolic and cardiovascular measures during a glucose tolerance test

Previous work has shown that both a single session of aerobic exercise and chronic exercise training improve glucose homeostasis. Similarly, a single bout of inspiratory muscle strength training (IMST) has been shown to facilitate a greater degree of glycemic control. However, less is known about the chronic effects of IMST, particularly with respect to metabolic and cardiovascular responses to an oral glucose tolerance test (OGTT). We hypothesized that 6 weeks of IMST would promote a greater degree of glycemic control, via a reduction in fasting and peak glucose during an OGTT. To test this hypothesis, participants (n=14, 57% female, average age=21.9) completed 6 weeks of daily training at either 15% (n=7) or 75% (n=7) of their maximal inspiratory pressure. Each subject underwent a pre-IMST glucose tolerance test in which their blood glucose level, blood pressure, and heart rate were measured at baseline, 15, 30, 45, 60, and 90 minutes following glucose ingestion. A post-IMST glucose tolerance test was completed after 6 weeks of training. The results indicate no training effect on baseline glucose, peak glucose, 90-minutes post-glucose, or glucose area under the curve responses, for both training intensities (P&gt;0.05). There was no significant effect of IMST on heart rate, nor was heart rate altered during the OGTT (P&gt;0.5). While mean arterial pressure was not affected during the OGTT (P&gt;0.05), baseline mean arterial pressure decreased in the 75% intensity group only (P=0.012). In summary, 6 weeks of high-intensity IMST decreases baseline blood pressure, and glucose tolerance was unaffected in both training groups. Future studies should investigate the effects of chronic IMST on other metabolic measures (e.g. lipids, triglycerides, and/or cholesterol levels) and the impact that this training has on glucose homeostasis in clinical populations. This work was supported by the Alma College CORE Summer Research Program. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Hyperglycemia and Central Obesity Disrupt Conditioned Pain Modulation: A Single-Blind Crossover Randomized Controlled Trial

Hyperglycemia and high adiposity are risk factors for pain in diabetes. To clarify these links with pain, the effects of a glucose load on sensory detection, pain sensitivity, conditioned pain modulation (primary aims), and autonomic and endothelial functions (secondary aims) were examined in 64 pain-free participants: 22 with normal adiposity (determined by dual-energy X-ray absorptiometry), 29 with high adiposity, and 13 with combined high adiposity and elevated glycated hemoglobin (HbA1c; including prediabetes and type 2 diabetes). Participants ingested either 37.5 g glucose or 200 mg sucralose (taste-matched) in the first session and crossed over to the other substance in the second session 1 month later. At baseline, painful temple cooling (the conditioning stimulus) inhibited pressure- and heat-pain in the ipsilateral arm (the test stimuli) immediately after cooling ceased (partial η2’s > .32). Glucose ingestion weakened pressure-pain inhibition irrespective of HbA1c levels (partial η2 = .11). However, a larger reduction in pressure-pain inhibition after ingesting glucose was associated with a higher waist/hip ratio (r = .31), suggesting a role of central obesity. Heat-pain inhibition was absent at baseline in unmedicated participants with elevated HbA1c, and these participants reported more occlusion-induced pain after ingesting glucose (partial η2’s > .17). Glucose ingestion interfered with parasympathetic activity in all participants (partial η2 = .11) but did not affect endothelial function (measured by reactive hyperemia) or alter other sensations (eg, feet vibration detection). The disruptive effect of hyperglycemia on conditioned pain modulation increases in line with central obesity, which might facilitate pain in diabetes. PerspectiveIngesting 37.5 g glucose (approximately 350 mL soft drink) interfered with pain modulation in pain-free adults with normal adiposity or with combined high adiposity and HbA1c levels. The interference was stronger alongside increasing central obesity, suggesting that controlling blood glucose and body fat mass might help preserve pain modulation.

Dapagliflozin Stimulates Renal Ammonia Excretion in Rats

Sodium-glucose cotransporter 2 (SGLT2) inhibitors are drugs that induce glycosuria and are used to treat type 2 diabetes mellitus, moreover it has also been used in other conditions such as heart failure and atherosclerosis. However, little is known about the effects of these drugs on renal function. Considering that the maintenance of acid-base balance is closely related to renal physiology, in this study we evaluated the influence of chronic use of dapagliflozin on global renal function and urinary excretion of ammonia and titratable acids. Objective: To evaluate global renal function and urinary acid excretion (ammonia and titratable acid) in male Wistar rats chronically treated with dapagliflozin. Methods: 3-month-old male Wistar rats were randomized to control (C) and dapagliflozin (D) groups. Animals in group D received dapagliflozin (3 mg/kg, gavage) for 4 weeks. All animals were given food and water ad libitum throughout the experimental protocol. At 4 months of age, animals were placed in metabolic cages for 24-hour urine collection followed by blood sampling. Plasma concentrations of creatinine, sodium, potassium, urea, pH, pCO2, and bicarbonate were evaluated. The following were also evaluated: body weight, water intake, urine flow, and excretion of ammonia, titratable acids, glucose, and protein. Protocol approved by CEUA-UNIFESP number: 5985180423. Values expressed as mean ± standard error; number of animals per group: 6. Results: No significant changes were observed in blood gas parameters: pH (C: 7.33±0.043; D: 7.36±0.027), pCO2 (C: 53.30±2.40; D: 52.67±3.63 mmHg) and HCO3− (C: 27.07±1.31; D: 29.75±1.72 mEq/L) and no significant changes in plasma creatinine concentration (C: 0.41±0.04; D: 0.40±0.04mg/dl), Na+ (C: 144±0.47; D: 137±2.04 mmol/l) and K+ (C: 4.30±0.21; D: 4.16±0.20 mmol/l). We observed a significant increase in urine flow (C: 0.027±0.006; D: 0.068±0.005 mL/min/kg), possibly associated with intense glycosuria (C: 0.017±0.005; D: 8.97±0.51 g/24h). The significant increase in plasma urea concentration (C: 39.17±2.57; D: 48.83±1.27 mg/dL) and proteinuria (C: 11.04±0.30; D: 15.79±0.56 mg/24h) may indicate some renal impairment. Considering the marked increase in urinary excretion of ammonia (C: 0.65±0.05; D: 3.49±2.31 mEq/24h) and titratable acids (C: 0.180±0.036; D: 0.628±0.078 mEq/24h), we can conclude that the drug-induced glycosuria may lead to biochemical adaptations to maintain blood glucose levels within the normal range, at the expense of increased metabolic acid production. However, further experiments are needed to confirm this hypothesis. CAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superior. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Targeted Metabolic Profiling of Plasma in Lean and Obese Individuals during Oral Glucose Ingestion

Obesity has long been associated with metabolic inflexibility and insulin resistance. The purpose of this study was to determine 1) if the plasma metabolite/lipid profile was altered during an oral glucose tolerance test (OGTT) with obesity and 2) whether changes in plasma metabolites/lipids were related to insulin sensitivity or metabolic flexibility. Fourteen (7M/7F), young, lean (BMI: 21.9 ± 1.8 kg/m2) and fourteen (7M/7F) young, obese (BMI: 40.6 ± 5.4 kg/m2) individuals underwent a 2-hour OGTT with plasma samples obtained at baseline, 45 min and 120 min. Plasma was immediately stored at -80°C for subsequent targeted metabolomics (Biocrates MxP® Quant 500, Biocrates Life Sciences AG, Innsbruck, Austria). A 2 (body composition group) x 3 (time point) ANOVA was performed for each sex, with the false discovery rate (FDR q-value &lt;0.10) used to account for multiple testing. Of the 73 small molecule metabolites tested, 2 (Glucose and Glutamate) differed between lean and obese females, and 34 metabolites (including 10 amino acids, 9 amino acid related, 5 bile acids, 2 biogenic amines and 2 carboxylic acids) changed with time in females. Of the 427 plasma lipid species tested, 79 (primarily triglycerides, TG) differed between lean and obese females, and 134 (primarily fatty acids and TG) changed with time. In males, 45 metabolites (similar to females) and 5 lipid species (Fatty acids only) changed with time. When examining the change in all plasma metabolites/lipid species from baseline to 120 min, the change in 9 TGs, 1 dihexosylceramide, as well as glycolithocholic acid sulfate (bile acid) were related to insulin sensitivity (Matsuda Index). Metabolic flexibility (change in respiratory exchange ratio from baseline to 120 min) was related to the change in 4 lysophosphatidylcholines, 3 TG, 2 acylcarnitines, 2 diglycerides, 3-Indoleacetic acid and glutamate. American Heart Association Grant: 18AIREA33960404. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Immunopeptidome mining reveals a novel ERS-induced target in T1D.

Autoreactive CD8+ T cells play a key role in type 1 diabetes (T1D), but the antigen spectrum that activates autoreactive CD8+ T cells remains unclear. Endoplasmic reticulum stress (ERS) has been implicated in β-cell autoantigen generation. Here, we analyzed the major histocompatibility complex class I (MHC-I)-associated immunopeptidome (MIP) of islet β-cells under steady and ERS conditions and found that ERS reshaped the MIP of β-cells and promoted the MHC-I presentation of a panel of conventional self-peptides. Among them, OTUB258-66 showed immunodominance, and the corresponding autoreactive CD8+ T cells were diabetogenic in nonobese diabetic (NOD) mice. High glucose intake upregulated pancreatic OTUB2 expression and amplified the OTUB258-66-specific CD8+ T-cell response in NOD mice. Repeated OTUB258-66 administration significantly reduced the incidence of T1D in NOD mice. Interestingly, peripheral blood mononuclear cells (PBMCs) from patients with T1D, but not from healthy controls, showed a positive IFN-γ response to human OTUB2 peptides. This study provides not only a new explanation for the role of ERS in promoting β-cell-targeted autoimmunity but also a potential target for the prevention and treatment of T1D. The data are available via ProteomeXchange with the identifier PXD041227.

Dipeptidyl-peptidase 4 (DPP4) mediates fatty acid uptake inhibition by glucose via TAS1R3 and GLUT-2 in Caco-2 enterocytes

Both high glucose intake with a high-fat meal and inhibition of dipeptidyl peptidase-4 (DPP4) have been associated with plasma lipid-lowering effects, but mechanistic understanding linking glucose and fat absorption is lacking. We here hypothesized that glucose ameliorates intestinal fatty acid uptake via a pathway involving DPP4. A concentration of 50 mM glucose reduced mean DPP4 activity in differentiated Caco-2 enterocytes by 42.5 % and fatty acid uptake by 66.0 % via nutrient sensing by the sweet taste receptor subunit TAS1R3 and glucose transporter GLUT-2. No effect of the DPP4 substrates GLP-1 and GIP or of the cellular energy status on the reduced uptake of fatty acids was seen, but a direct interaction between DPP4 and fatty acid transporters is suggested. Conclusively we identified DPP4 as a regulator of fatty acid absorption in Caco-2 enterocytes that mediates the inhibition of intestinal fatty acid uptake by glucose via an interplay of GLUT-2 and TAS1R3.

Glucose breath test for the detection of small intestine bacterial overgrowth: Impact of diet prior to the test.

Glucose breath test (GBT) is used for the diagnosis of small intestine bacterial overgrowth. A restrictive diet without fibers and/or fermentable food is recommended on the day before the test. The aim of our retrospective study was to evaluate the impact of two different restrictive diets on the results of GBT. A change of the pretest restrictive diet was applied in our lab on September 1, 2020. The recommended diet was a fiber-free diet before this date, and a fiber-free diet plus restriction of all fermentable food afterward. We thus compared the results of GBT performed before (group A) and after (group B) this pretest diet modification. Demographics, reasons to perform GBT, digestive symptoms, and hydrogen and methane baseline values and variations after glucose ingestion were compared between the two groups. 269 patients underwent GBT in group A, and 316 patients in group B. The two groups were comparable in terms of demographics. Methane and hydrogen baseline values were significantly higher in group A (respectively 14 [18] vs. 8 [14] ppm, p < 0.01 and 11 [14] vs. 6 [8] ppm, p < 0.01). The percentage of positive tests was higher in group A for methane (43% vs. 28%, p < 0.05), and for hydrogen (18% vs. 12%, p = 0.03). This retrospective study suggests the importance of the restrictive diet prior to GBT. A strict limitation of fibers and fermentable food decreased hydrogen and methane baseline values, and the prevalence of positive GBT. Thus a strict restrictive diet should be recommended on the day before the test, in order to limit the impact of food on hydrogen and methane breath levels, and possibly improve the diagnosis quality of GBT.

A bout of aerobic exercise in the heat increases carbohydrate use but does not enhance the disposal of an oral glucose load, in healthy active individuals.

We investigated if a bout of exercise in a hot environment (HEAT) would reduce the postprandial hyperglycemia induced by glucose ingestion. The hypothesis was that HEAT stimulating carbohydrate oxidation and glycogen use would increase the disposal of an ingested glucose load [i.e., oral glucose tolerance test (OGTT); 75 g of glucose]. Separated by at least 1 wk, nine young healthy individuals underwent three trials after an overnight fast in a randomized order. Two trials included 50 min of pedaling at 58 ± 5% V̇o2max either in a thermoneutral (21 ± 1°C; NEUTRAL) or in a hot environment (33 ± 1°C; HEAT) eliciting similar energy expenditure (503 ± 101 kcal). These two trials were compared with a no-exercise trial (NO EXER). Twenty minutes after exercise (or rest), subjects underwent an OGTT, while carbohydrate oxidation (CHOxid, using indirect calorimetry) plasma blood glucose, insulin concentrations (i.e., [glucose], [insulin]), and double tracer glucose kinetics ([U-13C] glucose ingestion and [6,6-2H2] glucose infusion) were monitored for 120 min. At rest, [glucose], [insulin], and rates of appearance/disappearance of glucose in plasma (glucose Ra/Rd) were similar among trials. During exercise, heart rate, tympanic temperature, [glucose], glycogen oxidation, and total CHOxid were higher during HEAT than NEUTRAL (i.e., 149 ± 35 vs. 124 ± 31 µmol·kg-1·min-1, P = 0.010). However, during the following OGTT, glucose Rd was similar in HEAT and NEUTRAL trials (i.e., 25.1 ± 3.6 vs. 25.2 ± 5.3 µmol·kg-1·min-1, P = 0.981). Insulin sensitivity (i.e., ISIndexMATSUDA) only improved in NEUTRAL compared with NO EXER (10.1 ± 4.6 vs. 8.8 ± 3.7 au; P = 0.044). In summary, stimulating carbohydrate use with exercise in a hot environment does not improve postprandial plasma glucose disposal or insulin sensitivity in a subsequent OGTT.NEW & NOTEWORTHY Exercise in the heat increases estimated muscle glycogen use. Reduced muscle glycogen after exercise in the heat could increase insulin-mediated glucose uptake during a subsequent oral glucose tolerance test (OGTT). However, plasma glucose kinetics are not improved during the OGTT in response to a bout of exercise in the heat, and insulin sensitivity worsens. Heat stress activates glucose counterregulatory hormones whose actions may linger during the OGTT, preventing increased glucose uptake.

Combined intake of caffeine and low-dose glucose to reduce exercise-related hypoglycaemia in individuals with type 1 diabetes on ultra-long-acting insulin degludec: A randomized, controlled, double-blind, cross-over trial.

To evaluate whether caffeine combined with a moderate amount of glucose reduces the risk for exercise-related hypoglycaemia compared with glucose alone or control in adult people with type 1 diabetes using ultra-long-acting insulin degludec. Sixteen participants conducted three aerobic exercise sessions (maximum 75 min) in a randomized, double-blind, cross-over design. Thirty minutes before exercise, participants ingested a drink containing either 250 mg of caffeine + 10 g of glucose + aspartame (CAF), 10 g of glucose + aspartame (GLU), or aspartame alone (ASP). The primary outcome was time to hypoglycaemia. There was a significant effect of the condition on time to hypoglycaemia (χ2 = 7.674, p = .0216). Pairwise comparisons revealed an 85.7% risk reduction of hypoglycaemia for CAF compared with ASP (p = .044). No difference was observed between GLU and ASP (p = .104) or between CAF and GLU (p = .77). While CAF increased glucose levels during exercise compared with GLU and ASP (8.3 ± 1.9 mmol/L vs. 7.7 ± 2.2 mmol/L vs. 5.8 ± 1.4 mmol/L; p < .001), peak plasma glucose levels during exercise did not differ between CAF and GLU (9.3 ± 1.4 mmol/L and 9.1 ± 1.6 mmol/L, p = .80), but were higher than in ASP (6.6 ± 1.1 mmol/L; p < .001). The difference in glucose levels between CAF and GLU was largest during the last 15 min of exercise (p = .002). Compared with GLU, CAF lowered perceived exertion (p = .023). Pre-exercise caffeine ingestion combined with a low dose of glucose reduced exercise-related hypoglycaemia compared with control while avoiding hyperglycaemia.

Effect of 0.5% Oral Intake of Glucose on Tear Production

Objective: To determine, how 0.5% oral glucose consumption affects the formation of tears Methodology: After ethical approval, this cross-sectional study involved 176 non-glycemic individuals (103 males and 73 females) with an average age of 23.7±2.70 years. Participants with normal body mass index (BMI) were included in the study, with an average BMI of 22.42kg/m2. After informed consent, tear production was measured at fasting and thirty, ninety and two hours minutes after intake of 0.5% glucose. Data was entered and analyzed in SPSS. RESULTS: The mean tear production at fasting was found to be 13.88±5.18mm. After 30 minutes of oral intake of 0.5% glucose, the mean tear production remained at 13.88±5.18mm. However, after 60 minutes of oral intake of 0.5%glucose, the mean tear production decreased to 12.96±5.196mm. After 90 minutes of glucose intake, the mean tear production increased to 13.58±5.03mm, and after 120 minutes, it further increased to 15.54±5.09mm. Statistical analysis revealed significant differences in tear production after 30, 60, and 90 minutes of oral intake of 0.5%glucose. However, after 90 minutes, the difference in tear production became insignificant.

Engineered E. coli for D-pantothenic acid production with an acetolactate isomeroreductase mutant.

D-Pantothenic acid, as a momentous vitamin, is extensively applied to feed, medicine, cosmetics and other fields. However, there are still limitations to produce D-pantothenic acid by microbial fermentation at present. In this paper, we constructed a recombinant strain for D-pantothenic acid production by blocking the organic acid pathway, boosting pyruvate biosynthesis, relieving feedback inhibition of acetolactate synthase, improving glucose intake capacity, and modifying essential genes in the metabolic pathway. In addition, a new acetolactate isomeroreductase mutant V412A origin from Escherichia coli (EcAHAIR) encoded by ilvC was obtained to explore its substrate promiscuity. Compared with the wild type, the variant EcAHAIR-V412A has reduced steric hindrance and enhanced intermolecular forces, resulting in a high affinity for 2-acetolactate. Eventually, the fermentation production of the final strain DPAN19/trc-ilvCV412A reached 4.65g/L, increased by 192.5% compared with strain DPA8 in shake flask cultivation and produced 62.82g/L D-pantothenic acid in a 5L bioreactor. The metabolic engineering strategies and enzyme modification approaches described in this paper provide a particular perspective for the bio-manufacturing of D-pantothenic acid, branched-chain amino acids and its derivates.

Isomers-oriented separation of forty-five plasma bile acids with liquid chromatography-tandem mass spectrometry

Some bile acids (BAs) were considered as biomarkers or have therapeutical effect on metabolic diseases. However, due to the existence of isomers and limitations in sensitivity, simultaneous quantification of multiple BAs remains a challenge. The aim of this study is to establish an accurate and sensitive method for the determination of multiple BAs with similar polarity. A LC-MS/MS analytical method capable of quantifying forty-five BAs simultaneously using nine stable isotope internal standards was developed and fully validated based on key isomers-oriented separation strategy. The method was further applied to analyze plasma samples to describe the dynamic profile of BAs after high glucose intake. The chromatography and mass spectrum conditions were optimized to enable the accurate quantification of forty-five BAs, while ensuring the lower limit of quantification between 0.05–10 ng/mL. The results of system suitability, linearity, dilution integrity, accuracy and precision demonstrated the good quantitative capacity and robustness of the method. A total of thirty-five BAs were quantified in plasma samples from twelve healthy Chinese individuals. The established method featured superior sensitivity and better separation efficiency compared to previous studies. Meanwhile, BAs exhibited correlations with glucose and insulin, suggesting their potential as biomarkers for metabolic disorders.

Glucose ingestion before and after resistance training sessions does not augment ribosome biogenesis in healthy moderately trained young adults

PurposeResistance training-induced skeletal muscle hypertrophy seems to depend on ribosome biogenesis and content. High glucose treatment may augment ribosome biogenesis through potentiating resistance training-induced adaptations. This was investigated with total RNA and ribosomal RNA abundances as main outcomes, with relevant transcriptional/translational regulators (c-Myc/UBF/rpS6) as a secondary outcome.MethodsSixteen healthy, moderately trained individuals [male/female, n = 9/7; age, 24.1 (3.3)] participated in a within-participant crossover trial with unilateral resistance training (leg press and knee extension, 3 sets of 10 repetitions maximum) and pre- and post-exercise ingestion of either glucose (3 × 30 g, 90 g total) or placebo supplements (Stevia rebaudiana, 3 × 0.3 g, 0.9 g total), together with protein (2 × 25 g, 50 g total), on alternating days for 12 days. Six morning resistance exercise sessions were conducted per condition, and the sessions were performed in an otherwise fasted state. Micro-biopsies were sampled from m. vastus lateralis before and after the intervention.ResultsGlucose ingestion did not have beneficial effects on resistance training-induced increases of ribosomal content (mean difference 7.6% [− 7.2, 24.9], p = 0.34; ribosomal RNA, 47S/18S/28S/5.8S/5S, range 7.6–37.9%, p = 0.40–0.98) or levels of relevant transcriptional or translational regulators (c-MYK/UBF/rpS6, p = 0.094–0.292). Of note, both baseline and trained state data of total RNA showed a linear relationship with UBF; a ∼14% increase in total RNA corresponded to 1 SD unit increase in UBF (p = 0.003).ConclusionGlucose ingestion before and after resistance training sessions did not augment ribosomal RNA accumulation during twelve days of heavy-load resistance training in moderately trained young adults.

Supplementing Glucose Intake Reverses the Inflammation Induced by a High-Fat Diet by Increasing the Expression of Siglec-E Ligands on Erythrocytes.

Siglec-9/E is a cell surface receptor expressed on immune cells and can be activated by sialoglycan ligands to play an immunosuppressive role. Our previous study showed that increasing the expression of Siglec-9 (the human paralog of mouse Siglec-E) ligands maintains functionally quiescent immune cells in the bloodstream, but the biological effects of Siglec-9 ligand alteration on atherogenesis were not further explored. In the present study, we demonstrated that the atherosclerosis risk factor ox-LDL or a high-fat diet could decrease the expression of Siglec-9/E ligands on erythrocytes. Increased expression of Siglec-E ligands on erythrocytes caused by dietary supplementation with glucose (20% glucose) had anti-inflammatory effects, and the mechanism was associated with glucose intake. In high-fat diet-fed apoE-/- mice, glucose supplementation decreased the area of atherosclerotic lesions and peripheral inflammation. These data suggested that increased systemic inflammation is attenuated by increasing the expression of Siglec-9/E ligands on erythrocytes. Therefore, Siglec-9/E ligands might be valuable targets for atherosclerosis therapy.

Chronic intermittent hypoxia aggravated diabetic cardiomyopathy through LKB1/AMPK/Nrf2 signaling pathway.

Chronic intermittent hypoxia (CIH) may play an important role in the development of diabetic cardiomyopathy (DCM). However, the exact mechanism of CIH-induced myocardial injury in DCM remains unclear. In vivo, the db/db mice exposed to CIH were established, and in vitro, the H9C2 cells were exposed to high glucose (HG) combined with intermittent hypoxia (IH). The body weight (BW), fasting blood glucose (FBG) and food intake were measured every two weeks. The glycolipid metabolism was assessed with the oral glucose tolerance test (OGTT) and insulin resistance (IR). Cardiac function was detected by echocardiography. Cardiac pathology was detected by HE staining, Masson staining, and transmission electron microscopy. The level of reactive oxygen species (ROS) in myocardial tissue was detected by dihydroethidium (DHE). The apoptosis was detected by TUNEL staining. The cell viability, ROS, and the mitochondrial membrane potential were detected by the cell counting kit-8 (CCK-8) assay and related kits. Western blotting was used to analyze the liver kinase B1/AMP-activated protein kinase/ nuclear factor-erythroid 2-related factor 2 (LKB1/AMPK/Nrf2) signaling pathway. CIH exposure accelerated glycolipid metabolism disorders and cardiac injury, and increased the level of cardiac oxidative stress and the number of positive apoptotic cells in db/db mice. IH and HG decreased the cell viability and the level of mitochondrial membrane potential, and increased ROS expression in H9C2 cells. These findings indicate that CIH exposure promotes glycolipid metabolism disorders and myocardial apoptosis, aggravating myocardial injury via the LKB1/AMPK/Nrf2 pathway in vitro and in vivo.