Glucose 50% in glycerol nasal drops

ObjectiveCerebral microdialysis (CMD) enables bedside monitoring of cerebral metabolism after traumatic brain injury (TBI). This systematic review evaluates associations between CMD-derived analytes and mortality and functional outcome in adults with moderate-to-severe TBI.MethodsA systematic review was conducted of adult patients with moderate-to-severe TBI (Glasgow Coma Scale ≤12) undergoing CMD monitoring of glucose, lactate, pyruvate, lactate/pyruvate ratio (LPR), glutamate, and/or glycerol. Prespecified outcomes were mortality and functional outcome (Glasgow Outcome Scale, Glasgow Outcome Scale-Extended or modified Rankin Scale). Due to substantial between-study heterogeneity, findings were synthesized qualitatively.ResultsThe database search identified 1342 records; 33 studies met inclusion criteria. CMD-glucose and CMD-lactate were the most commonly measure analytes (26 studies each), and the least was CMD-glycerol (12 studies). 9 studies have analyzed as a combined biochemical pattern or multimodal modality in relation to outcome. Higher CMD-glucose levels were mostly associated with better outcomes, whereas lower CMD-glucose and elevated CMD- LPR, CMD-glutamate and CMD-glycerol levels were associated with mortality or unfavorable functional outcome. However, analyte thresholds, probe locations, monitoring windows and outcome definitions varied widely and adjusted prognostic estimates were rarely reported. Certainty of evidence was predominantly low to very low.ConclusionCMD biomarkers show directional associations with outcome after moderate-to-severe TBI, but the evidence is heterogeneous and of low certainty, insufficient to support routine use of CMD analytes for prognostic stratification. Standardization of analyte thresholds, probe location, monitoring windows is needed before their prognostic value can be established.

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The purpose of this study is to determine in humans whether lactate inhibits exercise-stimulated lipolysis, fat oxidation, and plasma glucose turnover. Eight healthy active individuals (3 women) completed 4 trials in a semi-randomized order. In two trials, subjects exercised for 60 min at 65±11% (mean±SD) of VO2 MAX while receiving isovolumetric infusions of either sodium lactate (MOD+LACT trial) or saline (MOD trial). In another trial, exercise intensity was increased to 82±11% of VO2 MAX (INT trial) to match lactate concentrations to those in the MOD+LACT trial. A trial without exercise was included. Stable isotopes of glycerol and glucose were infused to assess whole-body lipolysis (Ra Glycerol) and glucose turnover rates (Ra Glucose). Fat and carbohydrate oxidation were measured using indirect calorimetry. Basal metabolic rate and plasma concentrations of lactate, glucose, insulin, FFA, and glycerol were similar across trials. Plasma lactate was clamped at 4.31±1.68 mM during the MOD+LACT trial, which tripled MOD concentrations (1.42±0.93 mM; p=0.001) and matched INT concentrations (4.39±1.25 mM; p=0.819). MOD+LACT blunted the exercise-induced elevation in Ra Glycerol of MOD (average during exercise, 7.9±2.0 vs 10.5±2.2 µmol·kg-1·min-1; p=0.014). However, fat oxidation rates were similar in MOD+LACT and MOD (7.70 ±2.02 vs 7.38±1.47 µmol·kg-1·min-1; p=0.612) but reduced during INT (5.30±2.93 µmol·kg-1·min-1; p=0.045). Ra Glucose, plasma glucose, and insulin were elevated during INT but not affected by lactate infusion. Raising circulating lactate concentrations to levels observed during high-intensity exercise blunts exercise-stimulated whole-body lipolysis. However, in these metabolically healthy individuals, that reduction was not sufficient to compromise fat oxidation during moderate intensity exercise.

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BackgroundRobust randomized controlled trials (RCTs) are unavailable to delineate the effects of nutrition in gestational diabetes (GDM) on placental-fetal fuel exposures from glucose, triglycerides (TG), and free fatty acids (FFA). TG/FFA may increase maternal insulin resistance and be used as a substrate for fetal fat accretion.ObjectiveIn an RCT, we tested the hypothesis that 7-8 wks of a higher complex carbohydrate (60%)/lower fat (25%) diet (CHOICE) would result in lower postprandial FFA (pre-specified secondary outcome) compared to a conventional lower-carbohydrate (40%)/higher fat (45%) diet (LC/CONV) in GDM.MethodsAfter diagnosis (∼28-30 wks'), 59 BMI-matched diet-controlled participants with GDM (mean±SEM; BMI 32±1 kg/m2) were randomized to a eucaloric LC/CONV or CHOICE diet (7.2±1 wks; all meals provided; 35% saturated fat [of total fat] and 70±5g/d simple sugars, both diets). At 30-31 and 36-37 wks' after fasting, a breakfast test meal was administered (30% of total calories) and hourly blood sampled x5. Five-hour glucose, TG, FFA, and glycerol areas-under-the curve (AUC) were calculated.ResultsOf 59, 13 met exclusions. By ANCOVA (n=23/group), weight gain, birthweight, and newborn adiposity were similar. At 36-37 wks', the FFA AUC was 20% higher on LC/CONV compared to CHOICE (p=0.016) without differences in TG or glycerol. Participants on LC/CONV had 12% lower glucose AUC (pConclusion/interpretationCHOICE resulted in 20% less postprandial FFA exposure and blunting of the expected rise in TG/glycerol, which may mitigate maternal IR and fetal fat accretion. Glycemic control was clinically acceptable despite a 12% greater post-breakfast glucose exposure. Thus, lower dietary fat and higher quality carbohydrates produced a synergistic attenuation of TG/FFA with effective glycemic control in GDM.ClinicaltrialsGov registryNCT02244814, https://clinicaltrials.gov/study/NCT02244814.

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