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Prophylactic Dextrose Gel Does Not Prevent Neonatal Hypoglycemia: A Quasi-Experimental Pilot Study.
Coors, SM, Cousin, JJ, Hagan, JL, Kaiser, JR
The Journal of pediatrics. 2018;:156-161
Abstract
OBJECTIVE To test the hypothesis that prophylactic dextrose gel administered to newborn infants at risk for hypoglycemia will increase the initial blood glucose concentration after the first feeding and decrease neonatal intensive care unit (NICU) admissions for treatment of asymptomatic neonatal hypoglycemia compared with feedings alone. STUDY DESIGN This quasi-experimental study allocated asymptomatic at-risk newborn infants (late preterm, birth weight <2500 or >4000 g, and infants of mothers with diabetes) to receive prophylactic dextrose gel (Insta-Glucose; Valeant Pharmaceuticals North America LLC, Bridgewater, New Jersey); other at-risk infants formed the control group. After the initial feeding, the prophylactic group received dextrose gel (0.5 mL/kg) rubbed into the buccal mucosa. The blood glucose concentration was checked 30 minutes later. Initial glucose concentrations and rate of NICU admissions were compared between the prophylactic group and controls using bivariate analyses. A multivariable linear regression compared first glucose concentrations between groups, adjusting for at-risk categories and age at first glucose concentration. RESULTS There were 236 subjects (72 prophylactic, 164 controls). The first glucose concentration was not different between the prophylactic and control groups in bivariate analysis (52.1 ± 17.1 vs 50.5 ± 15.3 mg/dL, P = .69) and after adjusting for covariates (P = .18). Rates of NICU admission for treatment of transient neonatal hypoglycemia were 9.7% and 14.6%, respectively (P = .40). CONCLUSIONS Prophylactic dextrose gel did not reduce transient neonatal hypoglycemia or NICU admissions for hypoglycemia. The carbohydrate concentration of Insta-Glucose (77%) may have caused a hyperinsulinemic response, or alternatively, exogenous enteral dextrose influences glucose homeostasis minimally during the first few hours when counter-regulatory mechanisms are especially active. TRIAL REGISTRATION ClinicalTrials.gov: NCT02523222.
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Sucralose enhances GLP-1 release and lowers blood glucose in the presence of carbohydrate in healthy subjects but not in patients with type 2 diabetes.
Temizkan, S, Deyneli, O, Yasar, M, Arpa, M, Gunes, M, Yazici, D, Sirikci, O, Haklar, G, Imeryuz, N, Yavuz, DG
European journal of clinical nutrition. 2015;(2):162-6
Abstract
BACKGROUND/OBJECTIVE Artificial sweeteners were thought to be metabolically inactive, but after demonstrating that the gustatory mechanism was also localized in the small intestine, suspicions about the metabolic effects of artificial sweeteners have emerged. The objective of this study was to determine the effect of artificial sweeteners (aspartame and sucralose) on blood glucose, insulin, c-peptide and glucagon-like peptide-1 (GLP-1) levels. SUBJECTS/METHODS Eight newly diagnosed drug-naive type 2 diabetic patients (mean age 51.5±9.2 years; F/M: 4/4) and eight healthy subjects (mean age 45.0±4.1 years; F/M: 4/4) underwent 75 g oral glucose tolerance test (OGTT). During OGTT, glucose, insulin, c-peptide and GLP-1 were measured at 15- min intervals for 120 min. The OGTTs were performed at three settings on different days, where subjects were given 72 mg of aspartame and 24 mg of sucralose in 200 ml of water or 200 ml of water alone 15 min before OGTT in a single-blinded randomized order. RESULTS In healthy subjects, the total area under the curve (AUC) of glucose was statistically significantly lower in the sucralose setting than in the water setting (P=0.002). There was no difference between the aspartame setting and the water setting (P=0.53). Total AUC of insulin and c-peptide was similar in aspartame, sucralose and water settings. Total AUC of GLP-1 was significantly higher in the sucralose setting than in the water setting (P=0.04). Total AUC values of glucose, insulin, c-peptide and GLP-1 were not statistically different in three settings in type 2 diabetic patients. CONCLUSIONS Sucralose enhances GLP-1 release and lowers blood glucose in the presence of carbohydrate in healthy subjects but not in newly diagnosed type 2 diabetic patients.
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A human volunteer study to assess the impact of confectionery sweeteners on the gut microbiota composition.
Beards, E, Tuohy, K, Gibson, G
The British journal of nutrition. 2010;(5):701-8
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Abstract
Sweeteners are being sourced to lower the energetic value of confectionery including chocolates. Some, especially non-digestible carbohydrates, may possess other benefits for human health upon their fermentation by the colonic microbiota. The present study assessed non-digestible carbohydrate sweeteners, selected for use in low-energy chocolates, for their ability to beneficially modulate faecal bacterial profiles in human volunteers. Forty volunteers consumed a test chocolate (low-energy or experimental chocolate) containing 22.8 g of maltitol (MTL), MTL and polydextrose (PDX), or MTL and resistant starch for fourteen consecutive days. The dose of the test chocolates was doubled every 2 weeks over a 6-week period. Numbers of faecal bifidobacteria significantly increased with all the three test treatments. Chocolate containing the PDX blend also significantly increased faecal lactobacilli (P = 0.00 001) after the 6 weeks. The PDX blend also showed significant increases in faecal propionate and butyrate (P = 0.002 and 0.006, respectively). All the test chocolates were well tolerated with no significant change in bowel habit or intestinal symptoms even at a daily dose of 45.6 g of non-digestible carbohydrate sweetener. This is of importance not only for giving manufacturers a sugar replacement that can reduce energetic content, but also for providing a well-tolerated means of delivering high levels of non-digestible carbohydrates into the colon, bringing about improvements in the biomarkers of gut health.
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Influence of artificial sweetener on human blood glucose concentration.
Skokan, I, Endler, PC, Wulkersdorfer, B, Magometschnigg, D, Spranger, H
TheScientificWorldJournal. 2007;:1618-21
Abstract
Artificial sweeteners, such as saccharin or cyclamic acid are synthetically manufactured sweetenings. Known for their low energetic value they serve especially diabetic and adipose patients as sugar substitutes. It has been hypothesized that the substitution of sugar with artificial sweeteners may induce a decrease of the blood glucose. The aim of this study was to determine the reliability of this hypothesis by comparing the influence of regular table sugar and artificial sweeteners on the blood glucose concentration. In this pilot-study 16 patients were included suffering from adiposity, pre-diabetes and hypertension. In the sense of a cross-over design, three test trials were performed at intervals of several weeks. Each trial was followed by a test free interval. Within one test trial each patient consumed 150 ml test solution (water) that contained either 6 g of table sugar ("Kandisin") with sweetener free serving as control group. Tests were performed within 1 hr after lunch to ensure conditions comparable to patients having a desert. Every participant had to determine their blood glucose concentration immediately before and 5, 15, 30 and 60 minutes after the intake of the test solution. For statistics an analysis of variance was performed. The data showed no significant changes in the blood glucose concentration. Neither the application of sugar (F(4;60) = 1.645; p = .175) nor the consumption of an artificial sweetener (F(2.068;31.023) = 1.551; p > .05) caused significant fluctuations in the blood sugar levels. Over a time frame of 60 minutes in the control group a significant decrease of the blood sugar concentration was found (F(2.457;36.849) = 4.005; p = .020) as a physiological reaction during lunch digestion.
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Treatment of painful advanced internal lumbar disc derangement with intradiscal injection of hypertonic dextrose.
Miller, MR, Mathews, RS, Reeves, KD
Pain physician. 2006;(2):115-21
Abstract
BACKGROUND Degenerative discs are thought to produce nerve root pain either mechanically or chemically. Particularly in the case of advanced degenerative disc disease, this clinical entity has often proven to be symptomatically resistant to peridural steroids, Intra-discal Electrothermoplasty (IDET) and direct surgical intervention. Exposure of irritated nerves to hypertonic dextrose is thought to have chemoneuromodulatory potential. Sustained pain reduction has been demonstrated in a pilot study involving injection of a combination of dextrose, glucosamine, chondroitin and dimethylsulfoxide into degenerative discs of patients with chronic low back pain of discogenic origin. OBJECTIVE To assess the effects of disc space injections of hypertonic dextrose in patients experiencing chronic advanced degenerative discogenic leg pain, with or without low back pain. STUDY DESIGN Prospective consecutive patient series. METHODS Patients with moderate to severe degenerative disc disease without herniation and with concordant pain reproduction with CT discography were included. All had failure of a physical therapy trial and substantial but temporary relief with two fluoroscopically guided epidural steroid injections. Patients underwent bi-weekly disc space injection of a solution consisting of 50% dextrose and 0.25% Bupivacaine in the disc(s) found positive on discography. The study was performed in an out-patient surgery center in the United States. Outcome measures included an 11-scale numeric pain score (0-10). RESULTS Each patient was injected an average of 3.5 times. Overall, 43.4% of patients fell into the sustained improvement group with an average improvement in numeric pain scores of 71%, comparing pretreatment and 18 month measurements. CONCLUSION The results suggest that intradiscal injection of hypertonic dextrose may have a place in the management of pain arising from advanced lumbar degenerative disc disease.
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Physiological mechanisms mediating aspartame-induced satiety.
Hall, WL, Millward, DJ, Rogers, PJ, Morgan, LM
Physiology & behavior. 2003;(4-5):557-62
Abstract
Aspartame has been previously shown to increase satiety. This study aimed to investigate a possible role for the satiety hormones cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) in this effect. The effects of the constituents of aspartame, phenylalanine and aspartic acid, were also examined. Six subjects consumed an encapsulated preload consisting of either 400 mg aspartame, 176 mg aspartic acid+224 mg phenylalanine, or 400 mg corn flour (control), with 1.5 g paracetamol dissolved in 450 ml water to measure gastric emptying. A 1983-kJ liquid meal was consumed 60 min later. Plasma CCK, GLP-1, glucose-dependent insulinotropic polypeptide (GIP), glucose, and insulin were measured over 0-120 min. Gastric emptying was measured from 0 to 60 min. Plasma GLP-1 concentrations decreased following the liquid meal (60-120 min) after both the aspartame and amino acids preloads (control, 2096.9 pmol/l min; aspartame, 536.6 pmol/l min; amino acids, 861.8 pmol/l min; incremental area under the curve [AUC] 60-120 min, P<.05). Desire to eat was reduced from 60 to 120 min following the amino acids preload (control, -337.1 mm min; aspartame, -505.4 mm min; amino acids, -1497.1 mm min; incremental AUC 60-120 min, P<.05). However, gastric emptying rates, plasma CCK, GIP, insulin, and glucose concentrations were unaffected. There was a correlation between the increase in plasma phenylalanine and decrease in desire to eat after the liquid meal following the constituent amino acids (r=-.9774, P=.004). In conclusion, it is unlikely that aspartame increases satiety via CCK- or GLP-1-mediated mechanisms, but small changes in circulating phenylalanine concentrations may influence appetite.
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The effects of sugar-free vs sugar-rich beverages on feelings of fullness and subsequent food intake.
Holt, SH, Sandona, N, Brand-Miller, JC
International journal of food sciences and nutrition. 2000;(1):59-71
Abstract
This study compared the effects of equal volumes of sugar-rich and sugar-free beverages on feelings of hunger and fullness and the ad libitum consumption of a palatable, fat-rich snack. Eleven healthy males consumed equal volumes (375 mL) of three drinks (sugar-rich cola, sugar-free cola, mineral water) in random order on separate mornings. After 20 min, the subjects were able to snack freely on potato crisps during the next 90 min. Each subject's individual bowl of potato crisps was covertly replenished at 15 min intervals while the subjects were completing appetite and mood ratings. After the 110 min experimental period, the subjects' ad libitum food intake from a buffet-style lunch was covertly recorded. On leaving the laboratory, the subjects filled in a weighed food dairy for the rest of the day. The equal-volume preloads initially decreased hunger to a similar degree and potato crisp intake during the first 15 min interval was not significantly different among the three preloads. On average, total energy intakes from the crisps and lunch were not significantly different among the preloads, and by the end of the day, total energy intakes were similar for the three test conditions. Therefore, the low-calorie/low-sugar drinks did not facilitate a reduced energy intake by the lean, non-dieting male subjects.