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A numerical detection of the τ -driven transition of galaxy spins is presented, where τ is the degree of misalignment between the initial tidal field and protogalaxy inertia tensors. Analyzing the data from the IllustrisTNG300-1 simulations, we first measure the values of τ at the protogalactic sites found by tracing the constituents of the galactic halos in the mass range of $10.5\leqslant \mathrm{log}\left[{M}_{h}/({h}^{-1}{M}_{\odot })\right]\leqslant 13$ back to the initial stage, z _i = 127. The probability density functions of τ are shown to be well modeled by the Γ-distributions, whose shape and scale parameters turn out to have universal values on a certain critical scale. Then, we investigate how the strength and tendency of the galaxy spin alignments with the principal axes of the local tidal fields depend on the initial condition, τ . It is found that on a scale lower than the critical one, the galaxy spin transition occurs at two different thresholds from the major to intermediate and from the intermediate to minor principal axes of the local tidal fields, respectively. Noting that the τ -dependent spin transition supersedes the strength of the previously found mass-dependent, morphology-dependent, and radius-dependent counterparts, we suggest that τ should be the key driver of all types of galaxy spin transitions and that the present galaxy spins are indeed excellent fossil records of their origin.

Enhanced star formation (SF) with star-forming neighboring galaxies bolsters the hydrodynamical contributions during paired interactions. Although the relative spin orientation between interacting galaxies can influence this effect, it has not been comprehensively explored. In this study, utilizing a meticulously curated sample of nearby (0.02 < z < 0.06) spiral+spiral pairs and an isolated control sample from Sloan Digital Sky Survey Data Release 7, coupled with Galaxy Zoo 2, and an approach to estimate spin–spin alignment (SSA), we systematically compare the impact of relative orientation, $\cos \,\xi $ , on interaction-induced SF. We reveal that SSA plays a pivotal role along with the conventionally recognized parameters of projected separation and SF of neighboring galaxies. Our results show an increase in SF augmentation as configurations transition from perpendicular ( $\cos \,\xi \sim 0$ ) to well aligned ( $\cos \,\xi \gt 0.7$ ). This enhancement is especially pronounced when neighboring galaxies have higher SF, suggesting that hydrodynamical processes drive the effects of relative orientation. The heightened hydrodynamical friction, attributed to increased ram pressure and the propensity for prograde orbits in well-aligned pairs, is consistent with our findings.

In linear theory, the galaxy angular momentum vectors that originate from initial tidal interactions with surrounding matter distribution intrinsically develop perpendicular alignments with the directions of maximum matter compression, regardless of galaxy mass. In simulations, however, galaxy spins exhibit parallel alignments in the mass range lower than a certain threshold, which depends on redshift, web type, and background cosmology. We show that the observed three-dimensional spins of the spiral galaxies located on the void surfaces from the Sloan Digital Sky Survey indeed transit from perpendicular to parallel alignments with the directions toward the nearest void centers at the threshold zone, $9.51\leqslant \mathrm{log}[{M}_{\mathrm{th},\star }/(\,{h}^{-1}\,{M}_{\odot })]\leqslant 10.03$ . This study presents the first direct observational evidence for the occurrence of mass-dependent spin transition of real galaxies with respect to non-filamentary structures of the cosmic web, opening a way to constrain the initial conditions of the early universe by measuring the spin transition threshold.

Galaxy spins are believed to retain the initially acquired tendency of being aligned with the intermediate principal axis of the linear tidal field, which disseminates the prospect of using them as a probe of early universe physics. This roseate prospect, however, is contingent upon the key assumption that the observable stellar spins of present galaxies measured at inner radii have the same alignment tendency toward the initial tidal field as their dark matter counterparts measured at virial limits. We test this assumption directly against a high-resolution hydrodynamical simulation by tracing the galaxy component particles back to the protogalactic stage. It is discovered that the galaxy stellar spins at z = 0 have strong but reoriented memory for the early universe, exhibiting a significant signal of cross-correlation with the major principal axis of the initial tidal field at z = 127. An analytic single-parameter model for this reorientation of the present galaxy stellar spins relative to the initial tidal field is devised and shown to be in good accord with the numerical results.

We develop a new model within which the radius-dependent transition of the subhalo inner spins with respect to the cosmic web and the variation of the transition threshold radius ( r _th ) with subhalo mass ( M _vir ), smoothing scale ( r _f ), and redshift ( z ) can be coherently explained. The key tenet of this model is that the competition between the pressure effect of the inner mass and the compression effect of the local tidal field determines which principal direction of the tidal field the inner spins are aligned with. If the former predominates, then only the tidal torques turn on, resulting in the alignments of the inner spins with the intermediate principal axes of the tidal field. Otherwise, the subhalo spins acquire a tendency to be aligned with the shortest axes of the subhalo shapes, which is in the major principal directions of the tidal field. Quantifying the two effects in terms of the densities, we make a purely analytical prediction for r _th ( M _vir , z , r _f ). Testing this model against the numerical results from a high-resolution dark-matter-only N -body simulation in the redshift range of 0 ≤ z ≤ 3 on the galactic mass scale of $11.8\leqslant \mathrm{log}{M}_{\mathrm{vir}}/(\,{h}^{-1}\,{M}_{\odot })\leqslant 12.6$ for two different cases of r _f /(h ^-1 Mpc) = 0.5 and 1, we find excellent agreements of the model predictions with the numerical results. It is also shown that this model naturally predicts the alignments between the inner spins of the present subhalos with the principal axes of the high- z tidal field at the progenitors’ locations.

We aim to unravel the interplay between bars, star formation (SF), and active galactic nuclei (AGNs) in barred galaxies. To this end, we utilize the SDSS DR12 to select a sample of nearby (0.02 < z < 0.06) disk galaxies that are suitable for bar examination ( M _r < −20.12 and inclination ≲53°). We identify 3662 barred galaxies and measure the length and axis ratio of each bar. We invent new bar parameters that mitigate the stellar and bulge mass biases and show, for the first time, that the evolution of non-AGN and AGN-hosting barred galaxies should be tracked using different bar parameters: the bar length for non-AGN galaxies and the bar axis ratio for AGN-hosting galaxies. Our analysis confirms that barred galaxies have a higher specific SF rate than unbarred control galaxies. Moreover, we find a positive correlation of bar length with both the SF enhancement and the centrally star-forming galaxy fraction, indicating the interconnectivity of bars and SF through the bar-driven gas inflow. We also find that, while the AGN fraction of barred galaxies is the same as that of the unbarred control sample, galaxies hosting more massive black holes (BHs) have rounder (i.e., higher axis ratio) bars, implying that the bar is not a cause of AGN activity; rather, AGNs appear to regulate bars. Our findings corroborate theoretical predictions that bars in non-AGN galaxies grow in length, and bars in AGN-hosting galaxies become rounder as BHs grow and eventually get destroyed.

A numerical detection of the radius-dependent spin transition of dark matter halos is reported. Analyzing the data from the IllustrisTNG simulations, we measure the halo spin vectors at several inner radii within the virial boundaries and investigate their orientations in the principal frames of the tidal and velocity shear fields, called the Tweb and Vweb, respectively. The halo spin vectors in the high-mass section exhibit a transition from the Tweb intermediate to major principal axes as they are measured at more inner radii, which holds for both the dark matter and baryonic components. The radius threshold at which the transition occurs depends on the smoothing scale, R _f , becoming larger as R _f decreases. For the case of the Vweb, the occurrence of the radius-dependent spin transition is witnessed only when R _f ≥ 1 h ^−1 Mpc. Repeating the same analysis but with the vorticity vectors, we reveal a critical difference from the spins. The vorticity vectors are always perpendicular to the Tweb (Vweb) major principal axes, regardless of R _f , which indicates that the halo inner spins are not strongly affected by the generation of vorticity. It is also shown that the halo spins, as well as the Tweb (Vweb) principal axes, have more directional coherence over a wide range of radial distances in the regions where the vorticity vectors have higher magnitudes. The physical interpretations and implications of our results are discussed.

Metabolic stress impairs pancreatic β-cell survival and function in diabetes. Although the pathophysiology of metabolic stress is complex, aberrant tissue damage and β-cell death are brought on by an imbalance in redox equilibrium due to insufficient levels of endogenous antioxidant expression in β-cells. The vulnerability of β-cells to oxidative damage caused by iron accumulation has been linked to contributory β-cell ferroptotic-like malfunction under diabetogenic settings. Here, we take into account recent findings on how iron metabolism contributes to the deregulation of the redox response in diabetic conditions as well as the ferroptotic-like malfunction in the pancreatic β-cells, which may offer insights for deciphering the pathomechanisms and formulating plans for the treatment or prevention of metabolic stress brought on by β-cell failure.

The cluster of differentiation 36 (CD36) is a scavenger receptor present on various types of cells and has multiple biological functions that may be important in inflammation and in the pathogenesis of metabolic diseases, including diabetes. Here, we consider recent insights into how the CD36 response becomes deregulated under metabolic conditions, as well as the therapeutic benefits of CD36 inhibition, which may provide clues for developing strategies aimed at the treatment or prevention of diabetes associated with metabolic diseases. To facilitate this process further, it is important to pinpoint regulatory mechanisms that are relevant under physiological and pathological conditions. In particular, understanding the mechanisms involved in dictating specific CD36 downstream cellular outcomes will aid in the discovery of potent compounds that target specific CD36 downstream signaling cascades.

In type 2 diabetes, metabolic stress has a negative impact on pancreatic β-cell function and survival (T2D). Although the pathogenesis of metabolic stress is complex, an imbalance in redox homeostasis causes abnormal tissue damage and β-cell death due to low endogenous antioxidant expression levels in β-cells. Under diabetogenic conditions, the susceptibility of β-cells to oxidative damage by NADPH oxidase has been related to contributing to β-cell dysfunction. Here, we consider recent insights into how the redox response becomes deregulated under diabetic conditions by NADPH oxidase, as well as the therapeutic benefits of NOX inhibitors, which may provide clues for understanding the pathomechanisms and developing strategies aimed at the treatment or prevention of metabolic stress associated with β-cell failure.

Abstract Background The endocrine disruption of perfluorinated compounds is an emerging issue. We aimed to examine the association of serum perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS) levels with incident diabetes and fasting serum glucose concentration. Methods This prospective cohort study was based on an urban-based cohort subpopulation from the Korean Genome and Epidemiology Study. Serum samples (600 µL) were received from 100 participants in the normoglycemic baseline survey (2004–2013), and concentrations of PFOA and PFOS were measured using mass spectrometry. The incidence of diabetes was tracked in the follow-up survey (2012–2016). Results The mean age was 56.4 years (men, 59%). The median serum PFOA and PFOS concentrations were 4.29 ng/mL and 9.44 ng/mL, respectively. PFOA and PFOS concentrations differed according to age, sex, and residential area. After 60 months, 23 patients had diabetes. Log-transformed PFOA (lnPFOA) and log-transformed PFOS (lnPFOS) were significantly higher in those who transitioned to diabetes than in those who did not (both p

Background: We examined the impact of gout on the end-stage renal disease (ESRD) risk in patients with type 2 diabetes mellitus (T2DM) and determined whether this association differs according to chronic kidney disease (CKD) status. Methods: Using the Korean National Health Insurance Service, this nationwide cohort study enrolled 847,884 patients with T2DM who underwent health checkups in 2009. Based on the presence of CKD (estimated glomerular filtration rate <60 mL/min/1.73 m²) and gout (two outpatient visits or one hospitalization within 5 years), patients were classified into four groups: CKD−Gout−, CKD− Gout+, CKD+Gout−, and CKD+Gout+. Patients with incident ESRD were followed up until December 2018. Results: Among 847,884 patients, 11,825 (1.4%) experienced progression to ESRD. ESRD incidence increased in the following order: 0.77 per 1,000 person-years (PY) in the CKD−Gout− group, 1.34/1,000 PY in the CKD−Gout+ group, 8.20/1,000 PY in the CKD+Gout− group, and 23.06/1,000 PY in the CKD+Gout+ group. The presence of gout modified the ESRD risk in a status-dependent manner. Hazard ratios (HR) were 1.49 (95% confidence interval [CI], 1.32 to 1.69) and 2.24 (95% CI, 2.09 to 2.40) in patients without and with CKD, respectively, indicating a significant interaction (P<0.0001). The CKD+Gout+ group had a markedly higher risk of developing ESRD (HR, 18.9; 95% CI, 17.58 to 20.32) than the reference group (CKD−Gout−). Conclusion: Gout substantially enhances the risk of ESRD, even in the absence of CKD. Concurrent CKD and gout synergistically increase the risk of ESRD. Therefore, physicians should carefully screen for hyperuricemia to prevent progression to ESRD. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular autonomic neuropathy (CAN) is known to affect patients with diabetes mellitus (DM) and cause adverse renal outcomes. We aimed to analyze the association between CAN and diabetic kidney disease (DKD). Method: We enrolled 254 DM patients (mean age, 56.7 ± 15.2 years; male: female ratio, 1.17:1) with 19 (7.5%) type 1 DM patients and 235 (92.5%) type 2 DM patients. All patients had undergone cardiovascular autonomic function tests between January 2019 and December 2021 in a tertiary hospital in Korea. Cardiovascular autonomic neuropathy was categorized as normal, early, or definite after measuring three heart rate variability parameters. Diabetic kidney disease refers to a persistently elevated urinary albumin-creatinine ratio (uACR =30 mg/g) or reduced estimated glomerular filtration rate (eGFR <60 mL/min/1.73 m2). Logistic and Cox regression analyses were performed. Results: Patients with elevated uACR (n=107) and reduced eGFR (n=32) had a higher rate of definite CAN. After adjusting for covariates, definite CAN was associated with elevated uACR (OR=2.4, 95% CI 1.07-5.36) but not with reduced eGFR (OR=3.43, 95% CI 0.62-18.90). A total of 94 patients repeated uACR measurements within 2 years (mean follow-up, 586.3 ± 116.8 days). Both definite and early CAN were independent risk factors for elevated uACR (HR=8.61 and 8.35, respectively; both p<0.05). In addition, high-density lipoprotein cholesterol, ACE inhibitors/angiotensin receptor blockers and glucagon-like peptide-1 receptor agonists were independent protective factors for elevated uACR (HR=0.96, 0.25, and 0.07, respectively; all p<0.05). Conclusion: Cardiovascular autonomic neuropathy is a potential indicator of DKD. Comprehensive management of DKD in the early stages of CAN may prevent microalbuminuria. [ABSTRACT FROM AUTHOR]

Background Based on recent evidence on the importance of the presence of diabetes mellitus (DM) and fibrosis-4 (FIB-4) index in coronavirus disease 2019 (COVID-19) mortality, we analyzed whether these factors could additively predict such mortality. Methods This multicenter observational study included 1,019 adult inpatients admitted to university hospitals in Daegu. The demographic and laboratory findings, mortality, prevalence of severe disease, and duration of quarantine were compared between patients with and without DM and/or a high FIB-4 index. The mortality risk and corresponding hazard ratio (HR) were analyzed using the Kaplan-Meier method and Cox proportional hazard models. Results The patients with DM (n=217) exhibited significantly higher FIB-4 index and mortality compared to those without DM. Although DM (HR, 2.66; 95% confidence interval [CI], 1.63 to 4.33) and a high FIB-4 index (HR, 4.20; 95% CI, 2.21 to 7.99) were separately identified as risk factors for COVID-19 mortality, the patients with both DM and high FIB-4 index had a significantly higher mortality (HR, 9.54; 95% CI, 4.11 to 22.15). Higher FIB-4 indices were associated with higher mortality regardless of DM. A high FIB-4 index with DM was more significantly associated with a severe clinical course with mortality (odds ratio, 11.24; 95% CI, 5.90 to 21.41) than a low FIB-4 index without DM, followed by a high FIB-4 index alone and DM alone. The duration of quarantine and hospital stay also tended to be longer in those with both DM and high FIB-4 index. Conclusion Both DM and high FIB-4 index are independent and additive risk factors for COVID-19 mortality.

Since the first outbreak of coronavirus disease 2019 (COVID-19), ongoing efforts have been made to discover an efficacious vaccine against COVID-19 to combat the pandemic. In most countries, both mRNA and DNA vaccines have been administered, and their side effects have also been reported. The clinical course of COVID-19 and the effects of vaccination against COVID-19 are both influenced by patients’ health status and involve a systemic physiological response. In view of the systemic function of endocrine hormones, endocrine disorders themselves and the therapeutics used to treat them can influence the outcomes of vaccination for COVID-19. However, there are very limited data to support the development of clinical guidelines for patients with specific medical backgrounds based on large clinical trials. In the current severe circumstances of the COVID-19 pandemic, position statements made by clinical specialists are essential to provide appropriate recommendations based on both medical evidence and clinical experiences. As endocrinologists, we would like to present the medical background of COVID-19 vaccination, as well as precautions to prevent the side effects of COVID-19 vaccination in patients with specific endocrine disorders, including adrenal insufficiency, diabetes mellitus, osteoporosis, autoimmune thyroid disease, hypogonadism, and pituitary disorders.

The 2023 Clinical Practice Guidelines for Diabetes Management in Korea, recommended by the Korean Diabetes Association, provide evidence-based recommendations for the diagnosis, screening, prevention, and treatment of diabetes and its complications. The guidelines emphasize individualized care and continuous education for individuals with diabetes, and cover various topics such as diagnosis, screening, prevention, nutrition therapy, exercise, and pharmacologic therapy. The document also discusses management strategies for type 1 and type 2 diabetes, as well as specific considerations for diabetes in older adults and children and adolescents. The guidelines are based on clinical studies and expert opinions, and highlight the benefits and risks of different interventions and medications. The text acknowledges the need for further research, particularly in the Korean population, and provides a list of references to studies and trials related to continuous glucose monitoring in patients with type 2 diabetes and pregnant women with diabetes. The findings suggest that continuous glucose monitoring can improve glycemic control and reduce hypoglycemia, but more research is needed to fully understand its benefits and limitations. [Extracted from the article]

Background A diabetic foot is the most common cause of non-traumatic lower extremity amputations (LEA). The study seeks to assess the risk factors of amputation in patients with diabetic foot ulcers (DFU). Methods The study was conducted on 351 patients with DFUs from January 2010 to December 2018. Their demographic characteristics, disease history, laboratory data, ankle-brachial index, Wagner classification, osteomyelitis, sarcopenia index, and ulcer sizes were considered as variables to predict outcome. A chi-square test and multivariate logistic regression analysis were performed to test the relationship of the data gathered. Additionally, the subjects were divided into two groups based on their amputation surgery. Results Out of the 351 subjects, 170 required LEA. The mean age of the subjects was 61 years and the mean duration of diabetes was 15 years; there was no significant difference between the two groups in terms of these averages. Osteomyelitis (hazard ratio [HR], 6.164; 95% confidence interval [CI], 3.561−10.671), lesion on percutaneous transluminal angioplasty (HR, 2.494; 95% CI, 1.087−5.721), estimated glomerular filtration rate (eGFR; HR, 0.99; 95% CI, 0.981−0.999), ulcer size (HR, 1.247; 95% CI, 1.107−1.405), and forefoot ulcer location (HR, 2.475; 95% CI, 0.224−0.73) were associated with risk of amputation. Conclusion Osteomyelitis, peripheral artery disease, chronic kidney disease, ulcer size, and forefoot ulcer location were risk factors for amputation in diabetic foot patients. Further investigation would contribute to the establishment of a diabetic foot risk stratification system for Koreans, allowing for optimal individualized treatment.

Background Coronavirus disease 2019 (COVID-19) has become a global pandemic, which prompts a consensus for the necessity to seek risk factors for this critical disease. Risk factors affecting mortality of the disease remain elusive. Diabetes and hyperglycemia are known to negatively affect a host’s antiviral immunity. We evaluated the relationship between a history of diabetes, fasting plasma glucose (FPG) levels and mortality among severely ill patients with COVID-19. Methods This was a retrospective cohort study that assessed 106 adult inpatients (aged ≥18 years) from two tertiary hospitals in Daegu, South Korea. The participants were transferred to tertiary hospitals because their medical condition required immediate intensive care. The demographic and laboratory data were compared between COVID-19 patients who survived and those who did not. Results Compared with the survivor group, age, and the proportions of diabetes, chronic lung disease and FPG were significantly higher in the deceased group. In the Cox proportional hazards regression model for survival analysis, FPG level and age were identified as significant predictors of mortality (P68 years and FPG of 168 mg/dL, respectively. Among those without diabetes, high FPG remained a significant predictor of mortality (P

BackgroundCoronavirus disease 2019 (COVID-19) is a global pandemic that had affected more than eight million people worldwide by June 2020. Given the importance of the presence of diabetes mellitus (DM) for host immunity, we retrospectively evaluated the clinical characteristics and outcomes of moderate-to-severe COVID-19 in patients with diabetes.MethodsWe conducted a multi-center observational study of 1,082 adult inpatients (aged ≥18 years) who were admitted to one of five university hospitals in Daegu because of the severity of their COVID-19-related disease. The demographic, laboratory, and radiologic findings, and the mortality, prevalence of severe disease, and duration of quarantine were compared between patients with and without DM. In addition, 1:1 propensity score (PS)-matching was conducted with the DM group.ResultsCompared with the non-DM group (n=847), patients with DM (n=235) were older, exhibited higher mortality, and required more intensive care. Even after PS-matching, patients with DM exhibited more severe disease, and DM remained a prognostic factor for higher mortality (hazard ratio, 2.40; 95% confidence interval, 1.38 to 4.15). Subgroup analysis revealed that the presence of DM was associated with higher mortality, especially in older people (≥70 years old). Prior use of a dipeptidyl peptidase-4 inhibitor or a renin-angiotensin system inhibitor did not affect mortality or the clinical severity of the disease.ConclusionDM is a significant risk factor for COVID-19 severity and mortality. Our findings imply that COVID-19 patients with DM, especially if elderly, require special attention and prompt intensive care.

This study compared short-term walking outcomes in diabetic amputees after prosthesis fitting compared to that in non-diabetic amputees. We retrospectively investigated walking outcomes at 3 months after starting gait training with a prosthesis. Forty-four unilateral transtibial amputees with (n=18) and without diabetes (n=26) were included. At 3 months after gait training with a prosthesis, only 2/18 (11.1%) and 3/18 (16.7%) diabetic amputees were capable of independent outdoor and indoor walking without cane, respectively. However, 21/26 (80.8%) and 24/26 (92.3%) non-diabetic amputees were capable of independent outdoor and indoor walking without cane, respectively. With assistance of cane, most of non-diabetic amputees (n=24, 92.3%) were capable of walking in both outdoor and indoor but only seven (38.9%) and nine (50.0%) diabetic amputees were capable, respectively. Thus, short-term walking outcome were poor in transtibial amputee with diabetes compare to those without diabetes, and these results suggest intensive rehabilitation would be needed to them.

BackgroundTo determine the role of diabetes mellitus (DM) in the coronavirus disease 2019 (COVID-19), we explored the clinical characteristics of patients with DM and compared risk factors such as age, glycemic control, and medications to those without DM.MethodsThis was a retrospective cohort study of 117 confirmed patients with COVID-19 which conducted at a tertiary hospital in Daegu, South Korea. The primary outcome was defined as the severe and critical outcome (SCO), of which the composite outcomes of acute respiratory distress syndrome, septic shock, intensive care unit care, and 28-day mortality. We analyzed what clinical features and glycemic control-related factors affect the prognosis of COVID-19 in the DM group.ResultsAfter exclusion, 110 participants were finally included. DM patients (n=29) was older, and showed higher blood pressure compared to non-DM patients. DM group showed higher levels of inflammation-related biomarkers and severity score, and highly progressed to SCO. After adjustment with other risk factors, DM increased the risk of SCO (odds ratio [OR], 10.771; P

Impaired β-cell function is the key pathophysiology of type 2 diabetes mellitus, and chronic exposure of nutrient excess could lead to this tragedy. For preserving β-cell function, it is essential to understand the cause and mechanisms about the progression of β-cells failure. Glucotoxicity, lipotoxicity, and glucolipotoxicity have been suggested to be a major cause of β-cell dysfunction for decades, but not yet fully understood. Fatty acid translocase cluster determinant 36 (CD36), which is part of the free fatty acid (FFA) transporter system, has been identified in several tissues such as muscle, liver, and insulin-producing cells. Several studies have reported that induction of CD36 increases uptake of FFA in several cells, suggesting the functional interplay between glucose and FFA in terms of insulin secretion and oxidative metabolism. However, we do not currently know the regulating mechanism and physiological role of CD36 on glucolipotoxicity in pancreatic β-cells. Also, the downstream and upstream targets of CD36 related signaling have not been defined. In the present review, we will focus on the expression and function of CD36 related signaling in the pancreatic β-cells in response to hyperglycemia and hyperlipidemia (ceramide) along with the clinical studies on the association between CD36 and metabolic disorders.

Since the first case was contracted by coronavirus disease-19 (COVID-19) in Daegu, Korea in February 2020, about 6,800 cases and 130 deaths have been reported on April 9, 2020. Recent studies have reported that patients with diabetes showed higher mortality and they had a worse prognosis than the group without diabetes. In poorly controlled patients with diabetes, acute hyperglycemic crises such as diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS) also might be precipitated by COVID-19. Thus, intensive monitoring and aggressive supportive care should be needed to inadequately controlled patients with diabetes and COVID-19 infection. Here, we report two cases of severe COVID-19 patients with acute hyperglycemic crises in Korea.

BackgroundChronic hyperglycemia has deleterious effects on pancreatic β-cell function and turnover. Recent studies support the view that cyclin-dependent kinase 5 (CDK5) plays a role in β-cell failure under hyperglycemic conditions. However, little is known about how CDK5 impair β-cell function. Myricetin, a natural flavonoid, has therapeutic potential for the treatment of type 2 diabetes mellitus. In this study, we examined the effect of myricetin on high glucose (HG)-induced β-cell apoptosis and explored the relationship between myricetin and CDK5.MethodsTo address this question, we subjected INS-1 cells and isolated rat islets to HG conditions (30 mM) in the presence or absence of myricetin. Docking studies were conducted to validate the interaction between myricetin and CDK5. Gene expression and protein levels of endoplasmic reticulum (ER) stress markers were measured by real-time reverse transcription polymerase chain reaction and Western blot analysis.ResultsActivation of CDK5 in response to HG coupled with the induction of ER stress via the down regulation of sarcoendoplasmic reticulum calcium ATPase 2b (SERCA2b) gene expression and reduced the nuclear accumulation of pancreatic duodenal homeobox 1 (PDX1) leads to β-cell apoptosis. Docking study predicts that myricetin inhibit CDK5 activation by direct binding in the ATP-binding pocket. Myricetin counteracted the decrease in the levels of PDX1 and SERCA2b by HG. Moreover, myricetin attenuated HG-induced apoptosis in INS-1 cells and rat islets and reduce the mitochondrial dysfunction by decreasing reactive oxygen species production and mitochondrial membrane potential (Δψm) loss.ConclusionMyricetin protects the β-cells against HG-induced apoptosis by inhibiting ER stress, possibly through inactivation of CDK5 and consequent upregulation of PDX1 and SERCA2b.

Aims: Our aim was to investigate the effects of peripheral arterial stiffness on the risk of progression of renal disease in patients with type 2 diabetes (T2D).Methods: This was a single center, retrospective cohort study. Brachial-ankle pulse wave velocity (baPWV) tests were performed on T2D patients in 2015. Increased arterial stiffness was defined as baPWV of ≥ 1800 cm/s. We applied criteria for progression of renal disease according to EMPA-REG OUTCOME trial.Results: In total, 186 patients were enrolled in the final study. The mean age was 59.1 years and male:female ratio was 1.73:1. Thirteen (7%) patients progressed to renal disease during the average follow-up time of 35.3 months. In particular, the risk of progression to macroalbuminuria was significantly higher in the baPWV ≥ 1800 cm/s group (HR 6.216, p = 0.020). Individuals with a baPWV of ≥ 1800 cm/s (when comparisons were adjusted for age, sex, blood pressure, diabetes duration, eGFR, and use of renin-angiotensin system inhibitors) had a significantly higher risk of the progression of renal disease (HR = 8.480, p = 0.014).Conclusion: These results suggest that peripheral arterial stiffness (baPWV ≥ 1800 cm/s) may be a risk factor for the progression of renal disease in T2D patients.

BackgroundThis study aims to describe the trends in the severity and treatment modality of patients with diabetic foot ulcer (DFU) at a single tertiary referral center in Korea over the last 10 years and compare the outcomes before and after the introduction of a multidisciplinary diabetic foot team.MethodsIn this retrospective observational study, electronic medical records of patients from years 2002 to 2015 at single tertiary referral center were reviewed. Based on the year of first admission, patients were assigned to a group either before or after the year 2012, the year the diabetes team launched.ResultsOf the 338 patients with DFU, 229 were first admitted until the year 2011 (group A), while 109 were first admitted since the year 2012 (group B). Mean age was higher in group B, and ulcer size was larger than those of group A. Whereas duration of diabetes was longer in group B, glycemic control was improved (mean glycosylated hemoglobin, 9.48% vs. 8.50%). The proportion of minor lower extremity amputation (LEA) was increased, but length of hospital stay was decreased (73.7±79.6 days vs. 39.8±36.9 days). As critical ischemic limb increased, the proportion of major LEA was not decreased.ConclusionImproved glycemic control, multidisciplinary strategies with prompt surgical treatment resulted in reduced length of hospital stay, but these measures did not reduce major LEAs. The increase in critical ischemic limb may have played a role in the unexpected outcome, and may suggest the need for increased vascular intervention strategies in DFU treatment.

BackgroundHemorheologic indices are known to be related to vascular complications in variable clinical settings. However, little is known about the associations between hemorheologic parameters and acute myocardial infarction (AMI) in type 2 diabetes mellitus (T2DM). The purpose of this study was to demonstrate the changes of hemorheologic environment inside of blood using hemorheologic parameters, especially the elongation index (EI) and critical shear stress (CSS) in diabetics with versus without AMI.MethodsA total of 195 patients with T2DM were enrolled. Patients were divided into the study group with AMI (AMI+, n=77) and control group (AMI−, n=118) who had no history of coronary artery disease. Hemorheologic parameters such as EI and CSS were measured and compared between the two groups.ResultsThe EI was lower (30.44%±1.77% in AMI+ and 31.47%±1.48% in AMI−, P

BackgroundHypoglycemia is an important complication in the treatment of patients with diabetes. We surveyed the insight by patients with diabetes into hypoglycemia, their hypoglycemia avoidance behavior, and their level of worry regarding hypoglycemia.MethodsA survey of patients with diabetes, who had visited seven tertiary referral centers in Daegu or Gyeongsangbuk-do, Korea, between June 2014 and June 2015, was conducted. The survey contained questions about personal history, symptoms, educational experience, self-management, and attitudes about hypoglycemia.ResultsOf 758 participants, 471 (62.1%) had experienced hypoglycemia, and 250 (32.9%) had experienced hypoglycemia at least once in the month immediately preceding the study. Two hundred and forty-two (31.8%) of the participants had received hypoglycemia education at least once, but only 148 (19.4%) knew the exact definition of hypoglycemia. Hypoglycemic symptoms identified by the participants were dizziness (55.0%), sweating (53.8%), and tremor (40.8%). They mostly chose candy (62.1%), chocolate (37.7%), or juice (36.8%) as food for recovering hypoglycemia. Participants who had experienced hypoglycemia had longer duration of diabetes and a higher proportion of insulin usage. The mean scores for hypoglycemia avoidance behavior and worry about hypoglycemia were 21.2±10.71 and 23.38±13.19, respectively. These scores tended to be higher for participants with higher than 8% of glycosylated hemoglobin, insulin use, and experience of emergency room visits.ConclusionMany patients had experienced hypoglycemia and worried about it. We recommend identifying patients that are anxious about hypoglycemia and educating them about what to do when they develop hypoglycemic symptoms, especially those who have a high risk of hypoglycemia.

BackgroundPlasma soluble cluster determinant 36 (sCD36) level is closely related with insulin resistance and atherosclerosis, but little is known whether it could be a surrogate for estimating risk of developing diabetes or not. To address this, we evaluated association between sCD36 index, the product of sCD36 and fasting plasma glucose (FPG), and the prevalence of type 2 diabetes mellitus (T2DM), and then compared with triglyceride-glucose (TyG) index which has been suggested simple index for insulin resistance.MethodsThis was cross-sectional study, and participants were classified as normal glucose tolerance (NGT), prediabetes, and T2DM according to glucose tolerance. The formula of TyG index was ‘ln [FPG (mg/dL)×triglyceride (mg/dL)/2],’ and the sCD36 index was ‘ln [sCD36 (pg/mL)×FPG (mg/dL)/2].’ResultsOne hundred and fifty-five subjects (mean age, 55.2 years) were enrolled, and patients with T2DM were 75. Both indexes were significantly increased in prediabetes and T2DM rather than NGT, and sCD36 index was positively correlated with both glycosylated hemoglobin and homeostasis model assessment of insulin resistance (r=0.767 and r=0.453, respectively; P

We recently reported that cluster determinant 36 (CD36), a fatty acid transporter, plays a pivotal role in glucotoxicity-induced β-cell dysfunction. However, little is known about how glucotoxicity influences CD36 expression. Emerging evidence suggests that the small GTPase Rac1 is involved in the pathogenesis of beta cell dysfunction in type 2 diabetes (T2D). The primary objective of the current study was to determine the role of Rac1 in CD36 activation and its impact on β-cell dysfunction in diabetes mellitus. To address this question, we subjected INS-1 cells and human beta cells (1.1B4) to high glucose conditions (30 mM) in the presence or absence of Rac1 inhibition either by NSC23766 (Rac1 GTPase inhibitor) or small interfering RNA. High glucose exposure in INS-1 and human beta cells (1.1b4) resulted in the activation of Rac1 and induced cell apoptosis. Rac1 activation mediates NADPH oxidase (NOX) activation leading to elevated ROS production in both cells. Activation of the Rac1-NOX complex by high glucose levels enhanced CD36 expression in INS-1 and human 1.1b4 beta cell membrane fractions. The inhibition of Rac1 by NSC23766 inhibited NADPH oxidase activity and ROS generation induced by high glucose concentrations in INS-1 & human 1.1b4 beta cells. Inhibition of Rac1-NOX complex activation by NSC23766 significantly reduced CD36 expression in INS-1 and human 1.1b4 beta cell membrane fractions. In addition, Rac1 inhibition by NSC23766 significantly reduced high glucose-induced mitochondrial dysfunction. Furthermore, NADPH oxidase inhibition by VAS2870 also attenuated high glucose-induced ROS generation and cell apoptosis. These results suggest that Rac1-NADPH oxidase dependent CD36 expression contributes to high glucose-induced beta cell dysfunction and cell death. Keywords: Rac1, NADPH oxidase, Beta-cell dysfunction, CD36, Oxidative stress

Many studies have demonstrated that an alteration in hemorheological properties is closely correlated with diabetic microcirculatory diseases. However, most of these studies have been limited to animal studies or used a small number of clinical samples, due to a lack of effective point-of-care (POC) devices to measure such properties within clinical environments. Owing to recent developments in microfluidic technology, several hemorheological POC devices have been designed that allow for the possibility of conducting extensive clinical studies using hemorheological measurements. Here, we reviewed recent clinical studies of diabetic kidney disease (DKD) associated with hemorheological parameters. We found that RBC deformability alone did not show a significant difference according to the degree of DKD, whereas critical shear stress (CSS) was found to be closely related to the ratio of albumin to creatinine and glomerular filtration rate. We also reviewed studies that alteration of hemorheological properties are associated with the development of DKD, which showed that CSS could be considered as a potential index to diagnose other diabetic complications as well as DKD.

This article discusses the potential benefits of combining the medications rosuvastatin and ezetimibe for patients with type 2 diabetes mellitus (T2DM). While statins are commonly used to lower cholesterol and prevent cardiovascular diseases, they have been associated with an increased risk of new-onset diabetes. The combination therapy of rosuvastatin and ezetimibe has been shown to effectively reduce LDL cholesterol levels while potentially mitigating the risk of inadequate glucose control associated with high-dose statin therapy. Two studies comparing the effects of this combination therapy to rosuvastatin monotherapy in patients with T2DM and dyslipidemia found that the combination therapy was more effective in reducing LDL cholesterol levels and showed additional benefits in terms of metabolic parameters. However, there were some differences in the effects on glycemic homeostasis parameters between the studies, which could be attributed to variations in treatment regimens, treatment duration, and demographic features of the study populations. Further research is needed to confirm the impact of ezetimibe on glucose homeostasis. [Extracted from the article]

Background: This study investigates the long-term efficacy and safety of evogliptin add-on therapy in patients with inadequately controlled type 2 diabetes mellitus (T2DM) previously received dapagliflozin and metformin (DAPA/MET) combination. Methods: In this multicenter randomized placebo-controlled phase 3 trial, patients with glycosylated hemoglobin (HbA1c) levels 7.0% to 10.5% (n=283) previously used DAPA 10 mg plus MET (=1,000 mg) were randomly assigned to the evogliptin 5 mg once daily or placebo group (1:1). The primary endpoint was the difference in the HbA1c level from baseline at week 24, and exploratory endpoints included the efficacy and safety of evogliptin over 52 weeks (trial registration: ClinicalTrials.gov NCT04170998). Results: Evogliptin add-on to DAPA/MET therapy was superior in HbA1c reduction compared to placebo at weeks 24 and 52 (least square [LS] mean difference, -0.65% and -0.55%; 95% confidence interval [CI], -0.79 to -0.51 and -0.71 to -0.39; P<0.0001). The proportion of patients achieving HbA1c <7% was higher in the triple combination group at week 52 (32.14% vs. 8.51% in placebo; odds ratio, 5.62; P<0.0001). Evogliptin significantly reduced the fasting glucose levels and mean daily glucose levels with improvement in homeostatic model assessment of ß-cell function (LS mean difference, 9.04; 95% CI, 1.86 to 16.21; P=0.0138). Adverse events were similar between the groups, and no serious adverse drug reactions were reported in the evogliptin group. Conclusion: Long-term triple combination with evogliptin added to DAPA/MET showed superior HbA1c reduction and glycemic control compared to placebo at 52 weeks and was well tolerated. [ABSTRACT FROM AUTHOR]

Background: To investigate the efficacy and safety of moderate-intensity rosuvastatin/ezetimibe combination compared to highintensity rosuvastatin in high atherosclerotic cardiovascular disease (ASCVD) risk patients with type 2 diabetes mellitus (T2DM). Methods: This study was a randomized, multicenter, open, parallel phase 4 study, and enrolled T2DM subjects with an estimated 10-year ASCVD risk =7.5%. The primary endpoint was the low-density lipoprotein cholesterol (LDL-C) change rate after 24-week rosuvastatin 10 mg/ezetimibe 10 mg treatment was non-inferior to that of rosuvastatin 20 mg. The achievement proportion of 10-year ASCVD risk <7.5% or comprehensive lipid target (LDL-C <70 mg/dL, non-high-density lipoprotein cholesterol <100 mg/dL, and apolipoprotein B <80 mg/dL) without discontinuation, and several metabolic parameters were explored as secondary endpoints. Results: A hundred and six participants were assigned to each group. Both groups showed significant reduction in % change of LDL-C from baseline at week 24 (-63.90±6.89 vs. -55.44±6.85, combination vs. monotherapy, P=0.0378; respectively), but the combination treatment was superior to high-intensity monotherapy in LDL-C change (%) from baseline (least square [LS] mean difference, -8.47; 95% confidence interval, -16.44 to -0.49; P=0.0378). The combination treatment showed a higher proportion of achieved comprehensive lipid targets rather than monotherapy (85.36% vs. 62.22% in monotherapy, P=0.015). The ezetimibe combination significantly improved homeostasis model assessment of ß-cell function even without A1c changes (LS mean difference, 17.13; P=0.0185). Conclusion: In high ASCVD risk patients with T2DM, the combination of moderate-intensity rosuvastatin and ezetimibe was not only non-inferior but also superior to improving dyslipidemia with additional benefits compared to high-intensity rosuvastatin monotherapy. [ABSTRACT FROM AUTHOR]

INTRODUCTION:Low urine pH (UpH) and high serum uric acid are considered evidence of metabolic disorders. The effect of low UpH on the development of metabolic syndrome (MetS) is less clear than that of high serum uric acid. We investigated the association between low UpH on the development of MetS and its components: central obesity, dyslipidemia, hypertension, and dysglycemia. METHODS:Two studies were conducted based on 2 datasets. The cross-sectional study included 14,511 subjects aged 19-80 years, based on the Korea National Health and Nutrition Examination Survey in 2013-2015. The retrospective cohort study included 3,453 subjects aged 19-80 years without MetS at the first checkup, who underwent at least 3 health checkups at a single tertiary hospital between 2011 and 2017. UpH was measured using an automatic urine analyzer in the range of 5.0-9.0 at first visit. RESULTS:In the cross-sectional study, low UpH (= 5.0) was associated with the prevalence of MetS (odds ratio [OR] = 1.480, 95% confidence interval [CI] 1.334-1.643, p