Impact Of Glucose Fluctuations Research Articles

Impact of glucose fluctuations on white matter hyperintensity in type 2 diabetic patients.

The mean amplitude of glycemic excursion (MAGE) is widely recognized for representing glucose fluctuation extent, its implications in cerebral small vessel disease remain unclear. This study aims to investigate the correlation between MAGE and white matter hyperintensity (WMH). This cross-sectional study, spanning from March 2021 to October 2022, included 212 type 2 diabetic patients aged between 50 and 80. Participants underwent MRI scans and continuous glucose monitoring. Clinical and laboratory data were compiled for analysis. WMH volumes were evaluated using both the Fazekas visual rating scale and a quantitative approach. Based on Fazekas scores, patients were categorized into low level of WMH (L-WMH, n = 88) and high level of WMH (H-WMH, n = 124) groups. MAGE levels were significantly higher in the H-WMH group compared to the L-WMH group. Time below range [TBR< 3.9] emerged as an independent risk factor for elevated MAGE. Both MAGE and TBR< 3.9 independently correlated with an increased WMH burden. Additionally, MAGE was identified as a partial mediator in the relationship between TBR< 3.9 and WMH volumes. MAGE and hypoglycemia exhibit independent associations with WMH in diabetic patients. Moreover, hypoglycemia may indirectly influence WMH progression through the augmentation of glucose fluctuations.

Cognitive vulnerability to glucose fluctuations: A digital phenotype of neurodegeneration.

Cognition is reduced at low and high glucose, reflecting cognitive vulnerability to glucose (CVG) fluctuations. The impact of glucose fluctuations on the aging brain remains unclear. We examined whether CVG is associated with plasma biomarkers of Alzheimer's disease (AD) pathology and neurodegeneration. Participants included N=114 adults with type 1 diabetes assessed for processing speed and sustained attention using ecological momentary assessment (EMA) combined with continuous glucose monitoring (CGM). We characterized associations between CVG and amyloid beta (Aβ) 42/40, phosphorylated tau (p-tau) 181 and 217, neurofilament light chain, and glial fibrillary acidic protein. CVG was associated with all plasma biomarkers, except Aβ 42/40. CVG for sustained attention exhibited strong associations with p-tau biomarkers that persisted across covariate specifications. CVG may be a useful digital phenotype of AD. It remains unclear whether CVG contributes to versus arises from neurodegeneration. We consider possible mechanisms linking cognitive vulnerability and long-term glucose variability to the development of neuropathology. Cognitive vulnerability to glucose (CVG) may be a useful digital phenotype of neurodegeneration. We used cognitive ecological momentary assessment and continuous glucose monitoring to investigate CVG's associations with plasma biomarkers. Associations of CVG for sustained attention and phosphorylated tau 181 remained significant across covariates. We discuss possible mechanisms relating glucose variability, cognition, and neurodegeneration.

Impact of glucose fluctuation on the paracrine secretome profile of human epicardial adipocyte

Abstract Background Glucose fluctuations (GF) is known to be the significant factor related to poor cardiovascular outcome in the diabetic patients. We investigated the potential impact of GF on paracrine effect of human epicardial adipocyte on cardiomyocyte. Methods Human EAT biopsies obtained during surgery and isolated preadipocyte/adipocytes were used to evaluate the direct impact of GF on the adipocytes. Matured adipocytes were exposed to the media containing normal glucose (100 mg/dl, NG), high glucose (300 mg/dl, HG), or high-low glucose (75-300 mg/dl, GF) for 1 week. Transcriptomic profiling of the cultured matured adipocyte was performed using microarray analysis. The impact of GF on the paracrine effect of adipocyte was evaluated using a co-culture with human iPS-derived atrial cardiomyocytes and the adipocytes. Clinical association study verified the validity of the findings. Results GF for 1 week altered the expression of 595 differentially expressed genes (up-regulated or down-regulated) with an effect size of &amp;gt;50% or `−50% and a significant statistical difference (P &amp;lt; 0.05) in human epicardial adipocytes, while the continuous HG for 1 week altered the expression of only 182 differentially expressed genes. Of the genes affected by GF, top 3 most affected genes included IL1β, IL33, IL8. Regarding the other major pro-inflammatory cytokines, IL1α, CCL2 and IL6 were also significantly increased in the adipocyte treated with GF, however these were not increased in the adipocyte treated with HG. Co-culture of human iPS cell-derived atrial cardiomyocytes and adipocytes treated with NG, HG and GF revealed that GF-treated adipocyte strikingly increased oxidative stress in the cardiomyocyte through the paracrine effect. In the real-world clinical association study, IL1β mRNA expression in human epicardial adipose tissue showed significant positive correlation with the severity of GF during hospitalization and oxidative stress in the left atrial myocardium. Conclusions GF adversely affect the paracrine secretome profile of human epicardial adipocyte. IL1β may be a critical epicardial adipocyte-derived adipokine that is enhanced by GF.

Insulin-related lipohypertrophy: ultrasound characteristics, risk factors, and impact of glucose fluctuations.

Lipohypertrophy (LHT) has been suggested as an outcome of the adipogenic effects of insulin injection-related tissue trauma. It commonly occurs in the clinical setting, but the current understanding of LHT by the medical staff and diabetes patients remains insufficient; moreover, it has not garnered attention as a research topic. To investigate the ultrasound characterization of LHT, to identify the factors associated with LHT development by assessing the prevalence of LHT and compare the accuracy of clinical palpation with that of ultrasonography in LHT detection, and to further evaluate the possible impact of LHT on patients' blood glucose fluctuations. A cross-sectional study was conducted in 120 patients with type 2 diabetes. Patients' general information were obtained using a questionnaire, and the patients were evaluated for LHT by ultrasonography and clinical palpation of the abdomen. The patients were instructed to inject equal amounts of insulin in tissues with LHT and in normal adipose tissues (NATs) in two non-consecutive d in a selected week; the possible effect of LHT on patients' blood glucose fluctuations was assessed using a continuous glucose monitoring system. LHT has characteristic ultrasonic signs. We found a high rate of missed LHT detection on clinical palpation compared with that on ultrasonography (P < 0.05). The duration of insulin treatment, rotation of injection sites, frequency of needle reuse, and number of insulin injections per day were the primary factors influencing the development of LHT (P < 0.05). Compared with NATs, LHT tissues showed extremely elevated amplitude of glycemic excursion, mean blood glucose levels, standard deviation of blood glucose levels and postprandial glucose excursion, and large fluctuations in blood glucose levels (P < 0.05). Ultrasonography can more accurately detect LHT than can clinical palpation. LHT development is associated with several factors and can lead to significant fluctuations in blood glucose levels; thus, sufficient attention should be paid to investigating the underlying mechanism of LHT.

Glucose Fluctuation and Severe Internal Carotid Artery Siphon Stenosis in Type 2 Diabetes Patients.

The impact of glucose fluctuation on intracranial artery stenosis remains to be elucidated. This study aimed to investigate the association between glucose fluctuation and intracranial artery stenosis. This was a cross-sectional study of type 2 diabetes mellitus (T2DM) patients equipped with the FreeStyle Libre Pro continuous glucose monitoring system (Abbott Laboratories) between February 2019 and June 2020. Glucose fluctuation was evaluated according to the standard deviation (SD) of blood glucose, coefficient of variation (%CV), and mean amplitude of glycemic excursions (MAGE). Magnetic resonance angiography was used to evaluate the degree of intracranial artery stenosis. Of the 103 patients, 8 patients developed severe internal carotid artery (ICA) siphon stenosis (≥70%). SD, %CV, and MAGE were significantly higher in the severe stenosis group than in the non-severe stenosis group (<70%), whereas there was no significant intergroup difference in the mean blood glucose and HbA1c. Multivariable logistic regression analysis adjusted for sex showed that SD, %CV, and MAGE were independent factors associated with severe ICA siphon stenosis. In conclusion, glucose fluctuation is significantly associated with severe ICA siphon stenosis in T2DM patients. Thus, glucose fluctuation can be a target of preventive therapies for intracranial artery stenosis and ischemic stroke.

Effects of glucose fluctuations on cellular and mitochondrial functions in HL-1 cardiac cell line

Effects of glucose fluctuations on cellular and mitochondrial functions in HL-1 cardiac cell line

Impact of Glucose Fluctuation on Acute Cerebral Infarction in Type 2 Diabetes

This study aimed to describe the frequency and temporal profile of acute cerebral infarction (ACI) using a continuous glucose monitoring system (CGMS) in patients with and without type 2 diabetes mellitus (T2DM) and explore the impact of blood glucose fluctuations on the short-term prognosis of ACI. The subjects were divided into four groups: T2DM with acute cerebral infarction (DMCI, Group A, n=56); T2DM without acute cerebral infarction (DM-NCI, Group B, n=36); Acute cerebral infarction patients without T2DM (NDM-CI, Group C, n=54); Healthy control group (NG, Group D, n=36). The National Institutes of Health Stoke Scale (NIHSS) and modified Rankin scale (mRs) were collected in Group A and C. All subjects were monitored for 72 hours using the CGMS. Indices such as fasting blood glucose (FBG) and mean amplitude of glycemic excursions (MAGE) were calculated. Glycemic excursions were compared between Group A, B, C and Group D, respectively. Multiple linear regression analysis and logistic analysis was applied. MAGE is related to NIHSS, homocysteine (HCY), HOMA-IR, FBG, CRP and IMT, while NIHSS is related to CRP, HCY, HOMA-IR, IMT. The factors impacting the short-term prognosis of ACI were NIHSS, HBA1C and MAGE. Larger glucose fluctuations are associated with more stroke risk factors and are associated with a poorer short-term prognosis. More attention should be paid to glucose fluctuations in patients with ACI and a history of T2DM.

Impact of glucose fluctuation and monocyte subsets on coronary plaque rupture

Background: It remains unclear whether glycemic fluctuation can affect plaque rupture in acute myocardial infarction (AMI). Here we investigate the impact of glucose fluctuation on plaque rupture, as observed by optical coherence tomography (OCT), and monocyte subsets in patients with AMI. Methods: We studied 26 consecutive patients with AMI. All patients underwent OCT examination, which revealed 16 patients with plaque rupture and 10 patients without plaque rupture at the culprit site. Peripheral blood sampling was performed on admission. Three monocyte subsets (CD14+CD16-, CD14brightCD16+, and CD14dimCD16+) were assessed by flow cytometry. Glycemic variability, expressed as the mean amplitude of glycemic excursion (MAGE), was determined by a continuous glucose monitoring system 7 days after the onset of AMI. Results: MAGE was significantly higher in the rupture patients than in the non-rupture patients (P=0.01). Levels of CD14brightCD16+ monocytes from the rupture patients were significantly higher than those from the non-rupture patients (P=0.03). Of interest, levels of CD14brightCD16+ monocytes correlated positively and significantly with MAGE (r=0.45, P=0.02). Conclusions: Dynamic glucose fluctuation may be associated with coronary plaque rupture, possibly through the preferential increase in CD14brightCD16+ monocyte levels.