Hyperglycemia In People Research Articles

Cardiomodulatory Effects of Cardiometabolic and Antihyperglycemic Medications: The Roles of Oxidative and Endoplasmic Reticulum Stress.

Uncontrolled hyperglycemia in people with diabetes is an established risk of premature cardiovascular disease. Repeated hypoglycemic events are also associated with increased cardiovascular mortality. Both hyperglycemia and hypoglycemia induce cellular stress, notably endoplasmic reticulum (ER) stress, a known promoter of cardiovascular disease. Contemporary anti-hyperglycemic drugs such as glucagon-like peptide 1 (GLP-1) receptor agonists and sodium-glucose cotransporter 2 (SGLT-2) inhibitors simultaneously inhibit oxidative stress and ER stress in human coronary artery endothelial cells. Similarly, other known cardioprotective drugs, such as statins and inhibitors of the renin-angiotensin-aldosterone system (RAAS) share a common pleiotropic effect of reducing cellular stress. Antioxidants reduce oxidative stress but may aggravate ER stress. This dichotomy of antioxidant effects may underline the unfavorable outcomes of clinical trials with antioxidant vitamin use. The aim of this review is to highlight the potential role of cellular stress reduction in cardioprotective effects of contemporary diabetes drugs. Future clinical trials are needed to test the hypothesis that cellular stress is the fundamental culprit in cardiovascular disease.

The Endogenous Inhibitor of CETP, apoC1, Remains Ineffective In Vivo after Correction of Hyperglycemia in People with Type 1 Diabetes.

ApolipoproteinC1 (apoC1) is the main physiological inhibitor of the cholesterol ester transfer protein (CETP). Increased CETP activity is associated with macrovascular complications in patients with type 1 diabetes (T1D). ApoC1 has lost its ability to inhibit CETP in patients with T1D, and in vitro glycation of apoC1 increases CETP activity, suggesting that hyperglycemia could be a factor implicated in the loss of the inhibitory effect of apoC1 on CETP. Thus, we aimed to see whether improvement of glycemic control might restore apoC1 inhibitory effect on CETP. We studied 98 patients with T1D and HbA1c > 9% at baseline and 3 months after improvement of glycemic control by a medical intervention (insulin introduction or changes in multi-injection therapy or pump therapy introduction/therapeutic education for all patients). CETP activity was assessed by a radioactive method and plasma apoC1 levels were measured by ELISA. The different isoforms of apoC1 were determined by mass spectrometry. CETP activity was not significantly modified after improvement of glycemic control, despite a significant reduction in mean HbA1c (8.7 ± 1.7 vs. 10.8 ± 2, p < 0.0001). No association between plasma apoC1 and CETP activity was observed in patients with T1D at baseline, nor at 3 months, even in the subgroup of patients with optimal control (3-month HbA1c < 7%). We did not find any glycated form of apoC1 using mass spectrometry in people with T1D. Hyperglycemia in vivo does not seem to be a major factor implicated in the loss of apoC1 ability to inhibit CETP activity observed in T1D. Other factors, such as qualitative abnormalities of lipoproteins, could be involved. Our data emphasize the fact that hyperglycemia is not the only factor involved in lipid abnormalities and macrovascular complications in T1D. Clinical trial reg. no. NCT02816099 ClinicalTrials.gov.

Evaluation of the Tissue Immune Microenvironment in the Diabetic Patients with Dental Implant

Long-term hyperglycemia in people with diabetes very frequently leads to damage and/or dysfunction of many tissues and organs of the human body, causing increased clinical morbidity. There is, however, an increased correlation between glycemic control and the onset of these consequences and in particular microvascular and macrovascular complications. The results of some studies have suggested that diabetes exerts an influence on the failure rates of implants compared to non-diabetic patients. One study demonstrates that HbA1c level (higher or lower than the threshold of 8.1) also influences the survival rate of dental implants. Biopsy fragments from 8 consecutive patients who had a titanium dental implant as well as diabetes were included in our study. The control group was represented by 4 patients with dental implants and who did not have diabetes. After the histological processing of the tissues, cell counts of CD4, CD8, CD20 and CD3 lymphocytes were performed by using QuPath. The findings characterize the composition of lymphocyte populations in the oral mucosa surrounding dental implants. In diabetic patients, poor glycemic control has been associated with a decreased CD4/ CD8, contrary to our findings in tissue. The decreased number of CD20 positive lymphocytes could be associated with the dysfunction of humoral immunity generally observed in patients with diabetes. In our study, a 2.5 x higher value of TCD4+ lymphocytes was noted compared to the average of TCD8+ type lymphocytes. These results support the involvement of these types of inflammatory cells in the potimplant bone healing processes. This process starts on the 10th day post-implant. Different studies raise, in these cases, the question of innate immune response vs adaptive immune response. Suppression of processes induced by CD8+ lymphocytes is associated with stimulation of bone formation. Our results support this hypothesis.

Hyperglycaemia in people with diabetes and chronic kidney disease

Assessment and treatment of hyperglycaemia in people with diabetes and chronic kidney disease (CKD) are challenging. In advanced CKD HbA1c can be unreliable, and treatment adjustments should be supported by other glucose measurements (e.g., continuous glucose monitoring (CGM) or blood glucose measurements). Glucose-lowering treatments should be evaluated based on CKD and an individualised assessment of risk factors especially hypoglycaemia. This review aims at providing an overview of the options for glycaemic monitoring and glucose-lowering treatments in people with diabetes and CKD.

Incidence of hypercholesterolaemia and hyperglycaemia in schizophrenic patients: Atypical antipsychotic medication and clinical variables

Background: Atypical or second-generation antipsychotic drugs commonly used in the management of schizophrenia include risperidone. Risperidone is linked to the incidence of metabolic syndrome-related adverse effects. Objective: This study aims to investigate the correlation between the administration of risperidone therapy and the incidence of metabolic syndrome in outpatients diagnosed with schizophrenia. This inquiry involves an examination of relevant laboratory parameters, specifically cholesterol, blood glucose, and haemoglobin A1c (HbA1C) levels, alongside an evaluation of pertinent clinical variables that may exert an influence. Methods: This study adopted a cross-sectional approach to receiving risperidone therapy for a minimum of three months at Grhasia Mental Hospital in Yogyakarta, Indonesia. Sampling was executed using an accidental sampling technique, targeting patients who met the predefined inclusion criteria. Results: The study enrolled a total of 97 participants, comprising 58 males and 39 females. Subsequent statistical analyses failed to demonstrate any statistically significant associations between hyperglycemia and various factors, including the risperidone regimen (p = 0.574), risperidone dosage (p = 0.619), and the duration of risperidone therapy (p = 1.000). Conclusion: Risperidone has a long-term risk of causing hyperglycemia in people with schizophrenia; consequently, blood glucose and HbA1C levels must be monitored on a regular basis.

Impaired plasma glucose clearance is a key determinant of fasting hyperglycemia in people with obesity.

The objective of this study was to evaluate the relative importance of the basal rate of glucose appearance (Ra) in the circulation and the basal rate of plasma glucose clearance in determining fasting plasma glucose concentration in people with obesity and different fasting glycemic statuses. The authors evaluated basal glucose kinetics in 33 lean people with normal fasting glucose (<100 mg/dL; Lean < 100 group) and 206 people with obesity and normal fasting glucose (Ob < 100 group, n = 118), impaired fasting glucose (100-125 mg/dL; Ob 100-125 group, n = 66), or fasting glucose diagnostic of diabetes (≥126 mg/dL; Ob ≥ 126 group, n = 22). Although there was a large (up to three-fold) range in glucose Ra within each group, the ranges in glucose concentration in the Lean < 100, Ob < 100, and Ob 100-125 groups were small because of a close relationship between glucose Ra and clearance rate. However, the glucose clearance rate at any Ra value was lower in the hyperglycemic than the normoglycemic groups. In the Ob ≥ 126 group, plasma glucose concentration was primarily determined by glucose Ra, because glucose clearance was markedly attenuated. Fasting hyperglycemia in people with obesity represents a disruption of the precisely regulated integration of glucose production and clearance rates.

Abstract A009: Association between unstable diabetes mellitus and risk of pancreatic cancer

Abstract Worsening of hyperglycemia in people with pre-existing diabetes mellitus may be an indicator of undiagnosed pancreatic cancer. However, there is limited evidence from longitudinal studies regarding the association between deterioration of diabetes and pancreatic cancer in people with previously stable diabetes. The size of the association between deterioration of diabetes and pancreatic cancer, and how the association changes over time, needs further investigation. A population-based matched cohort study was conducted within Australian women with stable diabetes mellitus. Unstable diabetes, the exposure of interest, was defined as change in the type of antidiabetic medication or addition of another antidiabetic medication after at least 24 months of stable antidiabetic medication use. The date of exposure was defined as the index date. Each woman with unstable diabetes was matched to 4 women with stable diabetes by birth year (±1 year) at the index date. Flexible parametric survival models were used to estimate hazard ratios (HR) (overall and at different times) and 95% confidence intervals (CI), and absolute risk in both groups at different time points. We identified 134,954 women with unstable diabetes; these were matched to women who had not developed unstable diabetes at the index date. The mean age of the cohort was 68 years. Over a median follow-up period of 2.8 years, 1,315 pancreatic cancer cases were diagnosed. Overall, women who experienced deterioration in glycemic control had a 2.5-fold increased risk of developing pancreatic cancer (HR 2.55; 95% CI 2.29 – 2.85). The risk was very high during the initial few months [HRs at 3 months (5.76; 95% CI 4.72 – 7.04), 6 months (4.56; 95% CI 3.81 – 5.46), and 12 months (3.33; 95% CI 2.86 – 3.89)]. The risk then progressively declined with time. Worsening of glycemic control in those with previously stable diabetes may be an early clinical manifestation of pancreatic cancer. Further research is warranted to differentiate this pancreatic cancer-associated deterioration of glycemic control from other causes. The longer-term (3-7 years) weaker association between pancreatic cancer and deterioration of glycemic control suggests that poorly controlled hyperglycemia is a predisposing factor for pancreatic cancer. Citation Format: Sitwat Ali, Michael Coory, Peter Donovan, Renhua Na, Nirmala Pandeya, Sallie-Anne Pearson, Katrina Spilsbury, Louise Stewart, Bridie Thompson, Karen Tuesley, Mary Waterhouse, Penelope Webb, Susan Jordan, Rachel Neale. Association between unstable diabetes mellitus and risk of pancreatic cancer [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Pancreatic Cancer; 2023 Sep 27-30; Boston, Massachusetts. Philadelphia (PA): AACR; Cancer Res 2024;84(2 Suppl):Abstract nr A009.

GC-MS and in silico analyses revealed the potential inhibitory activity of compounds isolated from Ciplukan herb (Physalis angulata L.) targeting GLUT-4 receptors

The escalating prevalence of diabetes mellitus (DM), a major global health threat and one of the top 10 causes of mortality, is a worrying trend. Prolonged hyperglycemia in people with diabetes triggers oxidative stress, leading to accelerated tissue damage, increased levels of free radicals, and the onset of complications. Our initial exploration of Physalis angulata L, using bioassay-guided isolation and C2C12 insulin resistance monitoring, revealed the compound’s ability to increase cellular glucose uptake. Consequently, there is an urgent need for further drug discovery efforts aimed at deciphering the mechanism of action of compounds targeting GLUT4 receptors in silico. The focus of this study was to predict the mechanism of action of compounds against the AS160 protein to facilitate GLUT4 translocation to the cell surface. Using GC-MS analysis and molecular docking via Autodock Vina, a mixture of blind and targeted docking approaches, isolated compounds were identified. Notably, this study marks the first identification, to the best of our knowledge, of campesterol and stigmasterol in P. angulata L herbs by GC-MS analysis. Through in silico simulations, campesterol and stigmasterol show promising potential in the treatment of type 2 diabetes by targeting the glucose transporter GLUT4 via facilitating GLUT4 translocation. Given their favorable pharmacokinetic properties, these phytoconstituents are potential hypoglycemic agents.

Effects of the COVID-19 booster vaccine on glycemia and insulin resistance in people with type 1 diabetes: A prospective pilot study

AimsInflammation can trigger hyperglycemia in people with type 1 diabetes (T1D). Vaccines purposefully intend to cause an acute immunogenic response, and booster vaccines may cause even more potent immunologic responses. However, the effects of vaccines on glycemic control and insulin requirements in the days immediately post-vaccination remains poorly understood. The aim of this study was to examine the changes in glycemic control and insulin usage immediately preceding and following a COVID-19 booster vaccine among adults with T1D. MethodsIn this prospective cohort study of adults with T1D, participants wore blinded Dexcom G6 Pro continuous glucose monitors for 10 days. After a baseline period, participants received a COVID-19 booster vaccine, and subsequent changes in glycemic indices were evaluated. ResultsAmong the 21 enrolled participants, 38% received a Moderna and 62% Pfizer-BioNTech booster. Compared to baseline (162.9 ± 44.1 mg/dL), mean glucose was significantly increased at Day 2 (172.8 ± 47.0 mg/dL; p = 0.04) and Day 3 (173.1 ± 45.0 mg/dL; p = 0.02) post-vaccination. Insulin resistance was also increased on Day 2 (p = 0.03). There were no differences in outcome metrics between booster vaccine manufacturers. ConclusionsThese results suggest that adults with type 1 diabetes may experience transient mild glycemic elevations after receiving a COVID-19 booster vaccination. Studies examining the effects of other vaccines are warranted.

Management of hyperglycaemia in people with obesity

Diabetes and obesity are closely interlinked. Obesity is a major risk factor for the development of type 2 diabetes mellitus and appears to be an important risk factor for diabetic micro- and macrovascular complications. Management of hyperglycaemia in people with diabetes is important to reduce diabetes-related complications. Previously, there was a significant tension between management of hyperglycaemia and mitigating weight gain. Older drugs, such as sulfonylureas, glitazones, and insulin, although effective antihyperglycaemic agents, tend to induce weight gain. There is now an increasing recognition in people with obesity and diabetes that the focus should be on aiding weight loss, initially with improvements in diet and physical activity, possibly with the use of low-calorie diet programmes. Subsequent addition of metformin and newer agents, such as sodium-glucose transporter-2 inhibitors and glucagon-like peptide-1 analogues, will aid glucose control and weight reduction, and offer cardiovascular and renal protection. These drugs are now much higher in the therapeutic pathway in many national and international guidelines. Bariatric surgery may also be an effective way to manage hyperglycaemia or induce remission in individuals with both obesity and diabetes.

1646-P: The Effect of Glucagon-Like Peptide-1 Receptor Blockade and Acute Insulin Resistance on Islet Function and Glucose Metabolism in People without Diabetes

Intra-islet Glucagon-Like Peptide-1 (GLP-1) is increased by islet inflammation and diabetes. GLP-1 Receptor (GLP1R) blockade with exendin-9,39 impairs fasting islet function in people with and without type 2 diabetes (DM2). In addition, it decreases insulin secretion and glucagon suppression in response to hyperglycemia in people with DM2. We sought to examine if free fatty acid (FFA) elevation to induce acute insulin resistance in people without DM2 replicated the effects of GLP1R blockade seen in DM2. We studied 6 nondiabetic individuals (54 ± 4 years, 33 ± 1 kg/m2) on 4 occasions in random order. Glucose metabolism was measured after an overnight fast and during a hyperglycemic clamp (~9 mmol/l) using [3-3H] glucose. On two occasions Intralipid® and heparin were infused to raise FFA. Exendin-9,39 (300pmol/kg/min) was infused to block GLP1R in the presence or absence of FFA elevation, while on the other days saline was infused. In the absence of FFA elevation, exendin-9,39 infusion increased fasting glucose concentrations (5.0 ± 0.1 vs. 5.4 ± 0.1 mmol/l, saline vs. exendin-9,39 respectively, p = 0.01). This pattern was also observed when FFA were elevated (5.3 ± 0.1 vs. 5.7 ± 0.2 mmol/l, p = 0.02). Fasting insulin, C-peptide (without FFA: 0.9 ± 0.1 vs. 0.8 ± 0.1 nmol/l, p = 0.17; with FFA: 1.1 ± 0.1 vs. 1.0 ± 0.1 nmol/l, p = 0.08) and glucagon concentrations were unchanged, but inappropriate for the higher fasting glucose observed during exendin-9,39 infusion. Exendin-9,39 infusion did not alter islet hormone secretion during the clamp in the presence or absence of FFA elevation. The magnitude of changes induced by exendin-9,39 did not differ in the presence or absence of FFA elevation (p &amp;gt; 0.10). These experiments confirm the effects of GLP1R blockade on fasting α- and β-cell function in people without DM2. However, FFA elevation does not replicate the abnormalities of islet function observed in people with DM2 when exendin-9,39 is infused. Disclosure M. Zeini: None. R.A. Farahani: None. A.A. Welch: None. M.C. Laurenti: None. C. Cobelli: None. C. Dalla Man: Research Support; Sanofi-Aventis Deutschland GmbH, Becton, Dickinson and Company. A.M. Egan: None. A. Vella: Other Relationship; Novo Nordisk. Advisory Panel; Rezolute, Inc. Consultant; Crinetics Pharmaceuticals, Inc., Hanmi Pharm. Co., Ltd., Zealand Pharma A/S. Funding National Institutes of Health (DK126206)

Brief Review: Pancreatic Islet Transplantation for Type 1 Diabetes in Humans

Pancreatic islet transplantation (ITx) has moved from the experimental phase of development to a position of an accepted and appropriate procedure to apply in clinical medicine. The primary indication for use of ITx is for management of dangerous and recurrent hypoglycemia secondary to use of exogenous insulin for management of hyperglycemia in people with type 1 diabetes. ITx involves procurement of a pancreas donated by a person who has died. The organ is taken to a specialized laboratory for isolation of islets that will be infused into the liver via a cannula put into the hepatic portal vein of an awake recipient by a radiologist. Success rates of maintaining normal blood glucose after the ITx are very high and almost as effective as transplanting an entire pancreas via surgery. Often more than one procedure is required to achieve success. One major attraction to the procedure is that it avoids the more dangerous and complicated procedure of surgical transplantation of the entire pancreas. However, in both instances recipients must undergo and maintain immunosuppressive drugs to avoid rejection of the islets. ITx is also used for management of patients with chronic, painful pancreatitis who undergo pancreatectomy. In this instance the patient’s own islets are returned by infusion into the liver as is done with type 1 diabetes patients. No immunosuppression is required. Success rates of autoislet transplantations are also quite high if a sufficiently mass of islets can be recovered from the resected pancreas.

Stroke Prevention and Treatment in People With Type 2 Diabetes: Is There a Role for GLP-1 (Glucagon-Like Peptide-1) Analogues?

Stroke is a leading cause of disability and death, and people with type 2 diabetes (T2D) have a greater risk of stroke and death or disability from stroke. The underlying pathophysiology associating stroke and T2D is complicated by the association of risk factors for stroke frequently seen in people with T2D. Treatments to reduce the excess risk of new-onset stroke or to improve outcomes in people with T2D following stroke would be of major clinical interest. In practice, the focus of care in people with T2D remains treating risk factors for stroke, such as lifestyle and pharmacological interventions for hypertension, dyslipidemia, obesity, and glycemic control. More recently, cardiovascular outcome trials primarily designed to assess the cardiovascular safety of GLP-1RAs (glucagon-like peptide-1 receptor analogues) have consistently observed a reduced stroke risk in people with T2D. This is supported by several meta-analyses of cardiovascular outcome trials observing clinically important risk reductions in stroke. Moreover, phase II trials have described reductions in poststroke hyperglycemia in people with acute ischemic stroke suggestive of improved outcomes following admission to hospital with acute stroke. In this review, we discuss the increased risk of stroke in people with T2D and outline the key associated mechanisms responsible. We discuss the evidence from cardiovascular outcome trials exploring GLP-1RA use and highlight areas of potential interest for future work in this rapidly developing area of clinical research.

Using Continuous Glucose Monitoring to Prescribe a Time to Exercise for Individuals with Type 2 Diabetes.

This study examines the potential utility of using continuous glucose monitoring (CGM) to prescribe an exercise time to target peak hyperglycaemia in people with type 2 diabetes (T2D). The main aim is to test the feasibility of prescribing an individualised daily exercise time, based on the time of CGM-derived peak glucose, for people with T2D. Thirty-five individuals with T2D (HbA1c: 7.2 ± 0.8%; age: 64 ± 7 y; BMI: 29.2 ± 5.2 kg/m2) were recruited and randomised to one of two 14 d exercise interventions: i) ExPeak (daily exercise starting 30 min before peak hyperglycaemia) or placebo active control NonPeak (daily exercise starting 90 min after peak hyperglycaemia). The time of peak hyperglycaemia was determined via a two-week baseline CGM. A CGM, accelerometer, and heart rate monitor were worn during the free-living interventions to objectively measure glycaemic control outcomes, moderate-to-vigorous intensity physical activity (MVPA), and exercise adherence for future translation in a clinical trial. Participation in MVPA increased 26% when an exercise time was prescribed compared to habitual baseline (p < 0.01), with no difference between intervention groups (p > 0.26). The total MVPA increased by 10 min/day during the intervention compared to the baseline (baseline: 23 ± 14 min/d vs. intervention: 33 ± 16 min/d, main effect of time p = 0.03, no interaction). The change in peak blood glucose (mmol/L) was similar between the ExPeak (-0.44 ± 1.6 mmol/L, d = 0.21) and the NonPeak (-0.39 ± 1.5 mmol/L, d = 0.16) intervention groups (p = 0.92). Prescribing an exercise time based on CGM may increase daily participation in physical activity in people with type 2 diabetes; however, further studies are needed to test the long-term impact of this approach.

Increase in hypoglycaemia and hyperglycaemia in people with diabetes admitted to hospital during COVID-19 pandemic

BackgroundWe used detailed information on patients with diabetes admitted to hospital to determine differences in clinical outcomes before and during the COVID-19 pandemic in the UK. MethodsThe study used electronic patient record data from Imperial College Healthcare NHS Trust. Hospital admission data for patients coded for diabetes was analysed over three time periods: pre-pandemic (31st January 2019–31st January 2020), Wave 1 (1st February 2020–30th June 2020), and Wave 2 (1st September 2020–30th April 2021). We compared clinical outcomes including glycaemia and length of stay. ResultsWe analysed data obtained from 12,878, 4008 and 7189 hospital admissions during the three pre-specified time periods. The incidence of Level 1 and Level 2 hypoglycaemia was significantly higher during Waves 1 and 2 compared to the pre-pandemic period (25 % and 25.1 % vs. 22.9 % for Level 1 and 11.7 % and 11.5 % vs. 10.3 % for Level 2). The incidence of hyperglycaemia was also significantly higher during the two waves. The median hospital length of stay increased significantly (4.1[1.6, 9.8] and 4.0[1.4, 9.4] vs. 3.5[1.2, 9.2] days). ConclusionsDuring the COVID-19 pandemic in the UK, hospital in-patients with diabetes had a greater number of hypoglycaemic/hyperglycaemic episodes and an increased length of stay when compared to the pre-pandemic period. This highlights the necessity for a focus on improved diabetes care during further significant disruptions to healthcare systems and ensuring minimisation of the impact on in-patient diabetes services. SummaryDiabetes is associated with poorer outcomes from COVID-19. However the glycaemic control of inpatients before and during the COVID-19 pandemic is unknown. We found the incidence of hypoglycaemia and hyperglycaemia was significantly higher during the pandemic highlighting the necessity for a focus on improved diabetes care during further pandemics.

A Pharmacist-Led Practice to Improve Perioperative Glycemic Control in Elective Surgery.

Quality Improvement Success Stories are published by the American Diabetes Association in collaboration with the American College of Physicians and the National Diabetes Education Program. This series is intended to highlight best practices and strategies from programs and clinics that have successfully improved the quality of care for people with diabetes or related conditions. Each article in the series is reviewed and follows a standard format developed by the editors of Clinical Diabetes. The following article describes an effort to facilitate the timely identification and treatment of pre- and postoperative hyperglycemia in people with diabetes having elective surgery at a tertiary care hospital in Calgary, Alberta, Canada.

Empagliflozin reduced progression of kidney disease and cardiovascular death in patients with or without diabetes who are at high risk of disease progression

Sodium glucose co-transporter inhibitor (SGLT2i) has emerged not only as a novel therapy to manage hyperglycaemia in people with type 2 diabetes but also shown to confer benefits in reducing a host of cardio-metabolic-renal outcomes. The SGLT2i, Empagliflozin has been shown to reduce cardiovascular death and improve outcomes from heart failure, but its effect in patients with chronic kidney disease (CKD) who are at risk for disease progression are not well understood. A study published in the New England Journal Medicine by the Empa-Kidney Collaborative group was designed to assess the effects of treatment with empaglifozin in a broad range of such patients. The study recruited patients with CKD who had an estimated glomerular filtration rate (eGFR) between 20 and 45 mL/minute/1.73 m2 of body-surface area, or who had an eGFR of between 45 and 90 mL/minute/1.73 m2 with a urinary albumin-to-creatinine ratio of at least 200. Patients were randomly assigned to receive empagliflozin (10 mg once daily) or matching placebo. The primary outcome was a composite of progression of kidney disease (defined as end-stage kidney disease, a sustained decrease in eGFR to <10 mL per minute per 1.73 m2, a sustained decrease in eGFR of ≥40% from baseline, or death from renal causes) or death from cardiovascular causes. 6609 patients underwent randomization. During a median of 2.0 years of follow-up, Empagliflozin was associated with a significant 28% reduction in the progression of kidney disease or death from cardiovascular causes. Results were consistent among patients with or without diabetes and across subgroups defined according to eGFR ranges. The rate of hospitalization from any cause was also 14% lower in the empagliflozin group than in the placebo group, but there were no significant between-group differences with respect to the composite outcome of hospitalization for heart failure or death from cardiovascular causes or death from any cause. This finding support the wider use of empagliflozin for renal protection in patients irrespective of diabetes status. Reassuringly also, the rates of serious adverse events were similar between empagliflozin and placebo. To optimize clinical safety, clinical implementation of evidence derived from this study require collaborative working between renal and diabetes teams, emphasising the sick day rules for SGLT2i as well as close monitoring of renal and clinical outcomes.

Use of a simplified local guideline improves “front door” management of diabetes and hyperglycaemia in people admitted to hospital with COVID-19

Use of a simplified local guideline improves “front door” management of diabetes and hyperglycaemia in people admitted to hospital with COVID-19

Abstract #1324963: The Altered Nomenclature of “Natural Hormone”!! A Psychotherapeutic Modality to Overcome Insulin Phobia!! Experience in a Primary Care Setting From Karachi, Pakistan

The problem of uncontrolled hyperglycemia in people with diabetes remains a challenge for many health care providers across the globe despite availability of several classes of antidiabetic agents. Due to several factors, insulin remains the mainstay of treatment for people with diabetes who cannot achieve glycemic targets on oral medicines or those who have type 1 diabetes. The darker side of the picture is that the insulin is perceived in the Pakistani society as a punishment rather than a therapy.

Stress-Induced Diabetes: A Review.

It has long been established that stress has a significant impact on metabolic function. Type 2 diabetes may be initiated by psychological and physical stress. The central and peripheral nervous systems are both involved in the neuroendocrine framework that underlies the underlying processes. The release of catecholamines and a rise in serum glucocorticoid concentrations caused by psychological stress enhance the requirement for insulin and insulin resistance. Experiencing persistent hyperglycemia in people with diabetes may be influenced by stress. Blood sugar levels may rise due to hormones being released in response to stress. Although this has adaptive significance in a healthy patient, in the long run, it can cause insulin resistance and lead to diabetes. Additionally, diabetes may cause abnormalities in the regulation of these stress hormones.