The objective of the present study is to assess the performance of fasting blood glucose (FBG), postprandial blood glucose (PBG), and glycated hemoglobin (HbA1c) as screening for coronary heart disease (CHD) in an inpatient population undergoing coronary angiography. 1852 consecutive patients scheduled for coronary angiography were classified into Normal Glucose Tolerance (NGT), Impaired Glucose Regulation (IGR), and diabetes, based on FBG, PBG, and HbA1c. Correlations of Gensini score with glucose metabolism and insulin resistance were analyzed. The associations between glycemic variables and Gensini score or the presence of CHD were analyzed by multiple linear regression and logistic regression, respectively. CHD was diagnosed in 488, 622, and 414 patients with NGT, IGR, and diabetes, respectively. Gensini score was positively correlated with FBG (r = 0.09, p < 0.01), PBG (r = 0.20, p < 0.01), and HbA1c (r = 0.19, p < 0.01). Gensini score was not correlated with fasting insulin (r = -0.081, p = 0.36), post-prandial insulin (r = -0.02, p = 0.61), or HOMAIR (r = -0.0059, p = 0.13). When FBG, PBG and HbA1c were pooled altogether, only PBG persisted in its association with Gensini score and the prevalence of CHD. The severity of CHD was associated with glucose rather than insulin resistance in this Chinese population. PBG was optimally correlated with the presence and severity of CHD.

To examine the relationship between admission random blood glucose (RBG), fasting blood glucose (FBG), and Gensini score in patients with acute myocardial infarction (AMI) to clarify the effects of RBG and FBG on the severity of coronary artery disease.

Adropin is a liver- and brain-secreted peptide hormone with striking effects on fuel metabolism regulation in a number of tissues. Previous studies demonstrated that adropin secretion is decreased in obese mice subjected to a long-term high-fat diet (HFD), and that whole-body loss of adropin expression resulted in systemic insulin resistance. Treatment of obese mice with adropin improves glucose tolerance, which has been linked to increased glucose oxidation and inhibition of fatty acid utilization in isolated skeletal muscle homogenates. In this study, we used in vivo physiological measurements to determine how treatment of obese mice with adropin affects whole-body glucose metabolism. Treatment with adropin reduced fasting blood glucose and, as shown previously, increased glucose tolerance in HFD mice during standard glucose tolerance tests. Under hyperinsulinemic-euglycemic clamp conditions, adropin treatment led to a nonsignificant increase in whole-body insulin sensitivity, and a significant reduction in whole-body glucose uptake. Finally, we show that adropin treatment suppressed hepatic glucose production and improved hepatic insulin sensitivity. This correlated with reduced expression of fatty acid import proteins and gluconeogenic regulatory enzymes in the liver, suggesting that adropin treatment may impact the pathways that drive vital aspects of hepatic glucose metabolism.

Excessive increase in blood glucose level after eating increases the risk of macroangiopathy, and a method for not increasing the postprandial blood glucose level is desired. However, a logical design method of the dietary ingestion pattern controlling the postprandial blood glucose level has not yet been established. We constructed a mathematical model of blood glucose control by oral glucose ingestion in three healthy human subjects, and predicted that intermittent ingestion 30 min apart was the optimal glucose ingestion patterns that minimized the peak value of blood glucose level. We confirmed with subjects that this intermittent pattern consistently decreased the peak value of blood glucose level. We also predicted insulin minimization pattern, and found that the intermittent ingestion 30 min apart was optimal, which is similar to that of glucose minimization pattern. Taken together, these results suggest that the glucose minimization is achieved by suppressing the peak value of insulin concentration, rather than by enhancing insulin concentration. This approach could be applied to design optimal dietary ingestion patterns.

The aim of this study was to evaluate the association between gingival crevicular blood glucose levels (GCBG) and finger capillary blood glucose levels (FCBG) according to the periodontal status of patients.

Metformin is currently the most prescribed drug for treatment of type 2 diabetes mellitus in humans. It has been well established that long-term treatment with metformin improves glucose tolerance in mice by inhibiting hepatic gluconeogenesis. Interestingly, a single dose of orally administered metformin acutely lowers blood glucose levels, however, little is known about the mechanism involved in this effect. Glucose tolerance, as assessed by the glucose tolerance test, was improved in response to prior oral metformin administration when compared to vehicle-treated mice, irrespective of whether the animals were fed either the standard or high-fat diet. Blood glucose-lowering effects of acutely administered metformin were also observed in mice lacking functional AMP-activated protein kinase, and were independent of glucagon-like-peptide-1 or N-methyl-D-aspartate receptors signaling. [18F]-FDG/PET revealed a slower intestinal transit of labeled glucose after metformin as compared to vehicle administration. Finally, metformin in a dose-dependent but indirect manner decreased glucose transport from the intestinal lumen into the blood, which was observed ex vivo as well as in vivo. Our results support the view that the inhibition of transepithelial glucose transport in the intestine is responsible for lowering blood glucose levels during an early response to oral administration of metformin.

Past studies on how blood glucose levels vary across the menstrual cycle have largely shown inconsistent results based on limited blood draws. In this study, 49 individuals wore a Dexcom G6 continuous glucose monitor and a Fitbit Sense smartwatch while measuring their menstrual hormones and self-reporting characteristics of their menstrual cycles daily. The average duration of participation was 79.3 ± 21.2 days, leading to a total of 149 cycles and 554 phases in our dataset. We use periodic restricted cubic splines to evaluate the relationship between blood glucose and the menstrual cycle, after which we assess phase-based changes in daily median glucose level and associated physiological parameters using mixed-effects models. Results indicate that daily median glucose levels increase and decrease in a biphasic pattern, with maximum levels occurring during the luteal phase and minimum levels occurring during the late-follicular phase. These trends are robust to adjustments for participant characteristics (e.g., age, BMI, weight) and self-reported menstrual experiences (e.g., food cravings, bloating, fatigue). We identify negative associations between each of daily estrogen level, step count, and low degrees of fatigue with higher median glucose levels. Conversely, we find positive associations between higher food cravings and higher median glucose levels. This study suggests that blood glucose could be an important parameter for understanding menstrual health, prompting further investigation into how the menstrual cycle influences glucose fluctuation.

The traditional treatment for diabetes usually requires frequent insulin injections to maintain normoglycemia, which is painful and difficult to achieve blood glucose control.

Some previous studies have shown that an increase in blood glucose level makes people more future oriented, however, results are inconsistent, other studies failing to replicate this effect. Here, we tested whether psychological factors (in this instance, perception of food pleasantness after consumption of more palatable or less palatable meal) can play a moderating role. We hypothesized that consuming more palatable food (perceived as rewarding) should cause blood glucose levels to affect future discounting, but that this should not occur for the consumption of less palatable food. A high-powered, independent groups experiment (N = 149, power β = .90) showed that, subsequent to performing an initial discounting task, the two groups consuming a meal (a control group consumed no meal) displayed a significant increase in blood glucose levels 10 minutes after meal consumption and just before repeating the discounting task. However, the increased blood glucose levels did not cause changes in delay discounting in either experimental group.

The aim of this study was to investigate the associations between blood-glucose levels in one-day-old-piglets (ODOP), intrauterine growth restriction (IUGR) and pre-weaning mortality in a commercial piglet-producing herd in Norway.

The glucose-6-phosphatase catalytic subunit 2 (G6PC2) gene encodes an islet-specific glucose-6-phosphatase catalytic subunit. G6PC2 forms a substrate cycle with glucokinase that determines the glucose sensitivity of insulin secretion. Consequently, deletion of G6pc2 lowers fasting blood glucose (FBG) without affecting fasting plasma insulin. Although chronic elevation of FBG is detrimental to health, glucocorticoids induce G6PC2 expression, suggesting that G6PC2 evolved to transiently modulate FBG under conditions of glucocorticoid-related stress. We show, using competition and mutagenesis experiments, that the synthetic glucocorticoid dexamethasone (Dex) induces G6PC2 promoter activity through a mechanism involving displacement of the islet-enriched transcription factor MafA by the glucocorticoid receptor. The induction of G6PC2 promoter activity by Dex is modulated by a single nucleotide polymorphism, previously linked to altered FBG in humans, that affects FOXA2 binding. A 5-day repeated injection paradigm was used to examine the chronic effect of Dex on FBG and glucose tolerance in wild-type (WT) and G6pc2 knockout mice. Acute Dex treatment only induces G6pc2 expression in 129SvEv but not C57BL/6J mice, but this chronic treatment induced G6pc2 expression in both. In 6-hour fasted C57BL/6J WT mice, Dex treatment lowered FBG and improved glucose tolerance, with G6pc2 deletion exacerbating the decrease in FBG and enhancing the improvement in glucose tolerance. In contrast, in 24-hour fasted C57BL/6J WT mice, Dex treatment raised FBG but still improved glucose tolerance, with G6pc2 deletion limiting the increase in FBG and enhancing the improvement in glucose tolerance. These observations demonstrate that G6pc2 modulates the complex effects of Dex on both FBG and glucose tolerance.

An evaluation of the use of a glucose reflectance meter for the cotside measurement of plasma rather than whole blood glucose was undertaken. Three hundred and twelve samples were obtained for examination. There is a closer correlation between plasma glucose than whole blood glucose to laboratory values. Confidence and prediction intervals show that even separating plasma from whole blood at the cotside does not improve the reliability of glucose reflectance meters when predicting blood glucose values in the context of managing high risk newborn infants. The cotside measurement of blood glucose using glucose reflectance meters should be abandoned and improved methods for quickly obtaining accurate laboratory data should be instituted.

Blood glucose measurement is one of the most commonly performed clinical diagnostic tests used to monitor glycaemia in several animal diseases. Usually, these laboratory analyses are performed on blood venous samples in remote laboratories, and the results are delayed, at best. The use of portable glucometers could evidently solve many constraints but veterinary-use glucometers are not usually available. The present study aimed to compare blood glucose levels obtained by Bionime glucometer to the reference method using glucose oxidase. Venous blood was collected from a total number of 140 healthy dogs (72 males and 68 females), of different breeds (28 German Shepherd, 27 Pitt bull, 21 Boxer, 24 Rottweiler and 40 cross-bred dogs) and different ages (range: 3 months-14 years) for glucose measurement using the reference laboratory method. Capillary blood samples were used to conduct a glucose measurement with a human-use glucometer. Our results revealed that there was no significant difference between the mean capillary blood glucose (CBG) measured with the human-use glucometer (5.06 ± 0.84 mmol/L) and the mean venous blood glucose (VBG) measured with the laboratory reference method (4.90 ± 0.73 mmol/L) (p = 0.42). Similarly, there was no significant difference of the mean CBG and VBG in male dogs (5.11 ± 0.88 and 4.97 ± 0.75 mmol/L, respectively) and female dogs (5.01 ± 0.81 and 5.07 ± 0.72 mmol/L, respectively) (p = 0.73 and 0.21, respectively), and no correlation to neither age (5.43 ± 0.90 and 5.20 ± 0.70 mmol/L in 3 to 6 month-old dogs, 5.03 ± 0.82 and 4.94 ± 0.79 mmol/L in 6 months to 1 year-old, 4.94 ± 0.67 and 5.13 ± 0.66 mmol/L in 1 to 4 year-old dogs; 4.88 ± 0.94 and 4.80 ± 0.75 mmol/L in dogs older than 4 years, respectively, p < 0.05), nor to breed (4.94 ± 1.01 and 4.99 ± 0.79 mmol/L in German Shepherd, 5.13 ± 0.84 and 4.99 ± 0.79 mmol/L in Pitt Bull, 5.07 ± 0.94 and 5.07 ± 0.77 mmol/L in Boxer, 5.40 ± 0.59 and 5.48 ± 0.55 mmol/L in Rottweiler and 4.89 ± 0.75 and 4.77 ± 0.59 mmol/L in cross-bred dogs, respectively, p < 0.05). The present study confirms that human glucometer can be used to measure glucose in dogs with a good accuracy.

Continuous Glucose Monitoring (CGM) data play an increasing role in clinical practice as they provide detailed quantification of blood glucose levels during the entire 24-hour period. The R package iglu implements a wide range of CGM-derived metrics for measuring glucose control and glucose variability. The package also allows one to visualize CGM data using time-series and lasagna plots. A distinct advantage of iglu is that it comes with a point-and-click graphical user interface (GUI) which makes the package widely accessible to users regardless of their programming experience. Thus, the open-source and easy to use iglu package will help advance CGM research and CGM data analyses. R package iglu is publicly available on CRAN and at https://github.com/irinagain/iglu.

Hydroxyethyl starch (HES), a commonly used resuscitation fluid, has the property to induce hyperglycemia as it contains large ethyl starch, which can be metabolized to produce glucose. We evaluated the effect of 6% HES-130 on the blood glucose levels in non-diabetic patients undergoing surgery under spinal anesthesia.

A flash glucose monitoring (FGM) system has become available. To clarify the relationship between FGM and self-monitoring blood glucose (SMBG) values, we compared the two values after simultaneous measurement in Japanese patients with type 1 diabetes, under daily life settings.

Our previous studies have raised the possibility that altered blood glucose levels may influence and/or be predictive of methamphetamine (METH) neurotoxicity. This study evaluated the effects of exogenous glucose and corticosterone (CORT) pretreatment alone or in combination with METH on blood glucose levels and the neural and vascular toxicity produced. METH exposure consisted of four sequential injections of 5, 7.5, 10, and 10 mg/kg (2 h between injections) D-METH. The three groups given METH in combination with saline, glucose (METH+Glucose), or CORT (METH+CORT) had significantly higher glucose levels compared to the corresponding treatment groups without METH except at 3 h after the last injection. At this last time point, the METH and METH+Glucose groups had lower levels than the non-METH groups, while the METH+CORT group did not. CORT alone or glucose alone did not significantly increase blood glucose. Mortality rates for the METH+CORT (40%) and METH+Glucose (44%) groups were substantially higher than the METH (< 10%) group. Additionally, METH+CORT significantly increased neurodegeneration above the other three METH treatment groups (≈ 2.5-fold in the parietal cortex). Thus, maintaining elevated levels of glucose during METH exposure increases lethality and may exacerbate neurodegeneration. Neuroinflammation, specifically microglial activation, was associated with degenerating neurons in the parietal cortex and thalamus after METH exposure. The activated microglia in the parietal cortex were surrounding vasculature in most cases and the extent of microglial activation was exacerbated by CORT pretreatment. Our findings show that acute CORT exposure and elevated blood glucose levels can exacerbate METH-induced vascular damage, neuroinflammation, neurodegeneration and lethality. Cover Image for this issue: doi. 10.1111/jnc.13819.

Numerous recent studies suggest that abnormal intracellular calcium concentration ([Ca2+]i) is a common defect in diabetic animal models and patients. Abnormal calcium handling is an important mechanism in the defective pancreatic β-cell function in type 2 diabetes. T-type Ca2+ channel antagonists lower blood glucose in type 2 diabetes, but the mechanism remains unknown.

The gut microbiota affects tissue physiology, metabolism, and function of both the immune and nervous systems. We found that intrinsic enteric-associated neurons (iEANs) in mice are functionally adapted to the intestinal segment they occupy; ileal and colonic neurons are more responsive to microbial colonization than duodenal neurons. Specifically, a microbially responsive subset of viscerofugal CART+ neurons, enriched in the ileum and colon, modulated feeding and glucose metabolism. These CART+ neurons send axons to the prevertebral ganglia and are polysynaptically connected to the liver and pancreas. Microbiota depletion led to NLRP6- and caspase 11-dependent loss of CART+ neurons and impaired glucose regulation. Hence, iEAN subsets appear to be capable of regulating blood glucose levels independently from the central nervous system.

The A1C-Derived Average Glucose study recommended reporting A1C in estimated average glucose (eAG) equivalents. We compared eAG with self-monitored mean blood glucose (MBG) to determine whether eAG is systematically biased due to biological variation in the relationship between MBG and A1C.