Abstract:BACKGROUND: Polycystic ovary syndrome is a complex endocrine-metabolic disorder associated with various dermatological manifestations. However, the histomorphological alterations underlying these skin findings remain poorly characterized. This study aimed to investigate skin alterations associated with polycystic ovary syndrome in an experimental mouse model using histochemical staining, morphometric evaluation, and immunofluorescence analysis. Abstract:METHODS: An experimental study was performed using 16 Swiss albino female mice. The polycystic ovary syndrome model was induced by dehydroepiandrosterone (6 mg/100 g body weight; subcutaneous). Model validation was performed using ovarian histology, estrous cycle monitoring, body weight, fasting blood glucose, and the intraperitoneal glucose tolerance test. Skin tissues were evaluated using haematoxylin and eosin staining for epidermal and dermal thicknesses, Masson's trichrome staining for collagen content (quantified with ImageJ), and immunofluorescence staining for Ki-67 and vascular endothelial growth factor immunoreactivity. Abstract:RESULTS: The polycystic ovary syndrome model was successfully validated using histological, reproductive, and metabolic parameters. The epidermal thickness was significantly reduced in the polycystic ovary syndrome group compared with the control group, and the dermal collagen content was also decreased. Ki-67 immunoreactivity appeared reduced in the polycystic ovary syndrome group, suggesting decreased cellular proliferative activity. Vascular endothelial growth factor immunoreactivity showed a similar staining pattern in both groups. Abstract:CONCLUSIONS: Dehydroepiandrosterone-induced polycystic ovary syndrome resulted in significant histological alterations in the skin, including epidermal thinning, reduced proliferative activity, and decreased dermal collagen content. These findings suggest that PCOS-associated skin alterations may be linked to impaired epidermal renewal and disrupted extracellular matrix organization, supporting the concept that polycystic ovary syndrome exerts systemic effects beyond the reproductive organs.
Abstract:BACKGROUND: : The significance of muscle-bone interactions in bone metabolism and the pathophysiology of osteoporosis has been recognized. However, the effects of thyroid hormones on muscle-bone interactions remain unclear. Abstract:METHODS:: We herein investigated the effects of hyperthyroidism on muscle and bone by administering L-thyroxin to male mice for 4 weeks. Abstract:RESULTS:: A micro-computed tomography analysis showed that the administration of L-thyroxin significantly decreased trabecular bone mineral density, bone volume/tissue volume, trabecular number, trabecular thickness, and connectivity density at the femurs of mice and slightly reduced cortical thickness. However, the administration of L-thyroxin did not affect muscle mass in the lower limbs, tissue weights of the soleus and gastrocnemius muscles, or grip strength. Among the myokines examined, the administration of L-thyroxin significantly decreased the messenger RNA level of follistatin in the soleus muscle and simple regression analyses showed a positive correlation between follistatin levels and bone volume/tissue volume; however, it did not affect serum follistatin levels. Abstract:CONCLUSIONS:: The present results suggest that hyperthyroidism induced by the administration of L-thyroxin caused trabecular-dominant osteopenia without reducing muscle mass or grip strength in mice. The direct effects of thyroid hormones on bone, but not muscle-bone interactions, may be crucial for hyperthyroidism-induced osteoporosis.
INTRODUCTION:Skeletal muscle is an essential tissue for insulin-stimulated glucose uptake. Myokines are proteins, peptides, and other metabolites that are released by muscles and exhibit metabolic functions. Decorin, apelin and TRIM72 are myokines with connection to insulin action. The aim of this paper was to study the expression of these selected myokines in skeletal muscle in relation to insulin sensitivity in individuals without overt metabolic disturbances. METHODS:Thirty healthy young male volunteers with normal glucose tolerance, 14 normal-weight, 8 with overweight and 8 with obesity, were included in the study population. The vastus lateralis muscle biopsies were performed. Insulin sensitivity (IS) was tested with hyperinsulinemic-euglycemic clamp. Muscle tissue mRNA expresion was assessed via quantitative PCR. RESULTS:Group consisting of individuals with obesity had lower insulin sensitivity compared to those with normal weight and overweight. Apelin expression was significantly higher in the obese group compared to the normal-weight and overweight groups. All myokines' expressions correlated with insulin sensitivity, decorin - positively, apelin and TRIM72 - negatively. Only apelin was correlated positively with BMI. Apelin was correlated with insulin sensitivity independently of BMI, decorin was also correlated with insulin sensitivity independently of BMI. CONCLUSION:Apelin, decorin and TRIM72 are correlated with insulin sensitivity and decorin and apelin have BMI-independent associations. This suggests that these molecules can be linked to metabolic health.
Introduction:Treatment guidelines recommend nutrition therapy and nutrition counselling as essential components in diabetes management. Little is known about how nutrition therapy/nutrition counselling is implemented in diabetes care. Therefore, the aim of this survey was to collect data on nutrition therapy/nutrition counselling in persons with diabetes in Germany. Research design and methods:An online survey using a standardized questionnaire was conducted from August 2021 to April 2022. People with diabetes were invited to answer questions on their diabetes management with a focus on nutrition counselling. The dataset was descriptively analyzed. Results:In total, 1,208 adults were included in the analysis. Approximately half of all participants (49.2%, n=594) suffered from type 1 diabetes and the other half (50.8%, n=614) from type 2 diabetes. Among the participants with type 1 diabetes, 66.8% reported to have had any dietary counselling as compared to 62.9% of those with type 2 diabetes. In addition, repeated dietary counselling was reported by 44.9% of participants with type 1 diabetes and 36.3% of those with type 2 diabetes. In these, dietary counselling was provided in 42.1% (type 1 diabetes) and 40.6% (type 2 diabetes), respectively, by nutritionists/dietitians. Provision of nutrition counselling was not related to body mass index or the mode of medication in both types of diabetes. The majority of survey participants expressed interest in receiving more and regular dietary counselling and identified a need for improvements regarding nutrition counselling. Conclusions:This survey showed that nutrition counselling in patients with diabetes in Germany is not in accordance with current treatment guidelines and widely underutilized. With respect to the potential of an adequate diet for metabolic control and prevention of cardiovascular diseases, there is an urgent need for a better and more structured implementation of nutrition counselling in diabetes care.
Abstract:OBJECTIVES: Fibroblast growth factor 21 is a metabolic regulator involved in glucose and lipid homeostasis. However, its relationship with excessive intrapancreatic fat deposition in type 2 diabetes mellitus remains unclear. We aimed to evaluate the association between serum fibroblast growth factor 21 levels and excessive intrapancreatic fat deposition in patients with type 2 diabetes mellitus. Abstract:METHODS: This prospective cross-sectional study included 101 participants who had previously undergone abdominal computed tomography. Group 1 consisted of patients with type 2 diabetes mellitus and excessive intrapancreatic fat deposition (n=31), Group 2 consisted of patients with type 2 diabetes mellitus without excessive intrapancreatic fat deposition (n=40), and Group 3 consisted of individuals without type 2 diabetes mellitus or excessive intrapancreatic fat deposition (n=30). Excessive intrapancreatic fat deposition was assessed on computed tomography by a blinded radiologist. Correlation, multivariable logistic regression, and receiver operating characteristic analyses were performed. Abstract:RESULTS: Fibroblast growth factor 21 levels were higher in Group 1 than in Groups 2 and 3 (82.32 pg/mL vs. 48.36 pg/mL vs 48.36 pg/mL, respectively; p<0.001). Serum fibroblast growth factor 21 levels were inversely correlated with the pancreas-to-spleen ratio in the overall cohort (ρ=- 0.527, p<0.001) and in the type 2 diabetes mellitus subgroup (ρ=- 0.510, p<0.001). In multivariate analysis, higher serum fibroblast growth factor 21 levels were independently associated with excessive intrapancreatic fat deposition both in the subgroup with diabetes (odds ratio: 1.03, 95% confidence interval: 1.01-1.05; p=0.004) and in the overall study population (odds ratio: 1.03, 95% confidence interval: 1.01-1.05; p=0.003). Receiver operating characteristic analysis showed an area under the curve (AUC) of 0.796 for fibroblast growth factor 21 in predicting excessive intrapancreatic fat deposition. A fibroblast growth factor 21 cutoff value of>62.15 pg/mL yielded a sensitivity of 83.87% and a specificity of 67.14%. Abstract:CONCLUSIONS: Serum fibroblast growth factor 21 levels were increased in patients with type 2 diabetes mellitus and excessive intrapancreatic fat deposition and were independently associated with excessive intrapancreatic fat deposition. Circulating fibroblast growth factor 21 may reflect pancreatic fat accumulation in the setting of metabolic dysfunction.
Background:Mild cognitive impairment may occur early in type 2 diabetes mellitus, but data on its prevalence and longitudinal dynamics in newly diagnosed patients without overt vascular complications remain limited. Methods:We prospectively followed 937 adults with newly diagnosed type 2 diabetes mellitus without baseline microvascular or macrovascular complications for a mean of 62.7±21.5 months. Cognitive status was assessed using the Montreal Cognitive Assessment, and mild cognitive impairment was defined as Montreal Cognitive Assessment-defined cognitive impairment. We evaluated the prevalence of mild cognitive impairment at diagnosis, the rate of mild cognitive impairment remission among patients with baseline mild cognitive impairment, and the incidence of mild cognitive impairment among cognitively normal patients. Multivariable models were used to identify clinical correlates of these outcomes. Results:At baseline, 286 patients (30.5%) had mild cognitive impairment. During the follow-up, 43/286 patients (15.0%) experienced remission, whereas 96/651 cognitively normal patients (14.7%) developed incident mild cognitive impairment. Higher C-peptide was strongly associated with prevalent mild cognitive impairment, and continuous C-peptide remained significantly associated with Montreal Cognitive Assessment performance in multivariable analyses. Smoking was associated with a less favorable cognitive profile, uric acid showed an inverse association with prevalent mild cognitive impairment, and participation in therapeutic patient education was independently associated with a lower risk of incident mild cognitive impairment. Incident retinopathy was also associated with incident mild cognitive impairment. Conclusions:In newly diagnosed, complication-free type 2 diabetes mellitus, mild cognitive impairment defined by Montreal Cognitive Assessment is common and clinically dynamic. Our findings suggest that metabolic, behavioral, educational, and microvascular factors are associated with cognitive outcomes, but they should be interpreted as observational and hypothesis-generating rather than as evidence for immediate clinical risk stratification.
Background: Neuropathic pain is a frequent and disabling complication of type 2 diabetes mellitus. Although poor glycemic control is known to contribute to diabetic neuropathy, its specific relationship with painful manifestations remains incompletely characterized. Objective: To evaluate the association between hemoglobin A1c levels and the presence of neuropathic pain in patients with type 2 diabetes mellitus. Methods: A cross-sectional analytical study was conducted in 172 adults with type 2 diabetes mellitus attending outpatient clinics at a tertiary hospital in northern Peru. Neuropathic pain was assessed using the validated Spanish version of the Self-Administered Leeds Assessment of Neuropathic Symptoms and Signs questionnaire. Glycemic control was evaluated using hemoglobin A1c, analyzed both as a continuous variable and dichotomized at seven percent. Clinical, metabolic, and demographic variables were compared between patients with and without neuropathic pain. Associations were examined using Poisson regression with robust variance and logistic regression, estimating crude and adjusted effect measures with ninety-five percent confidence intervals. Results: Neuropathic pain was identified in fifty percent of participants. Patients with neuropathic pain showed higher hemoglobin A1c values and a greater proportion of values equal to or above seven percent. In adjusted models, elevated hemoglobin A1c remained independently associated with neuropathic pain, both when analyzed as a dichotomous and as a continuous variable. Dyslipidemia and hypertension also showed independent associations. Conclusion: Higher hemoglobin A1c levels are independently associated with neuropathic pain in patients with type 2 diabetes mellitus, underscoring the importance of sustained glycemic control.
Abstract:BACKGROUND: Cardiovascular disease remains the leading cause of mortality worldwide, largely driven by modifiable cardiometabolic risk factors. Adults with metabolic syndrome represent a particularly high cardiometabolic risk group in whom preventive strategies are crucial; however, their level of knowledge regarding cardiovascular disease, its risk factors, and related lifestyle behaviours remains insufficiently characterized. This study aimed to assess the knowledge of cardiovascular disease and its risk factors among adults with metabolic syndrome and examine their associations with lifestyle behaviors and metabolic control. Abstract:METHODS: In this single-center cross-sectional study, 350 adults with metabolic syndrome diagnosed according to Adult Treatment Panel III criteria were evaluated. Cardiovascular knowledge was assessed using the validated Cardiovascular Disease Risk Factor Knowledge Level scale. Lifestyle behaviors, anthropometric measurements, laboratory parameters, and medication use were recorded. Associations between Cardiovascular Disease Risk Factor Knowledge Level scores and patient characteristics, lifestyle behaviours, and metabolic control were examined. Abstract:RESULTS: The mean age of the study population was 45.7±11.5 years, and 72% were women. The mean total Cardiovascular Disease Risk Factors Knowledge Level score was 21±3, with 42% of participants demonstrating high knowledge levels (≥80% correct responses). Despite this, adherence to lifestyle recommendations was suboptimal, with only 6% reporting regular physical activity and 26% adhering to dietary recommendations. Notably, only 9% of participants were aware of their metabolic syndrome diagnosis. Higher knowledge scores were associated with higher educational level, better dietary adherence, and lipid-lowering therapy use (p<0.05), as well as lower rates of smoking and alcohol consumption. However, no significant associations were observed with physical activity or weight-related measures. Abstract:CONCLUSIONS: Although adults with metabolic syndrome demonstrated the moderate to high awareness of cardiovascular disease and its risk factors, this knowledge did not consistently translate into healthier lifestyle behaviors. Prevention strategies targeting high cardiometabolic-risk populations should extend beyond information dissemination and incorporate behavioral and motivational components to improve cardiovascular outcomes.
Background:Metabolic dysfunction-associated steatotic liver disease is highly prevalent among patients with type 2 diabetes mellitus, exacerbating the risk of severe hepatic and cardiovascular complications. While metformin remains the first-line therapy, the optimal second-line oral antidiabetic drug for mitigating liver disease progression remains unclear. Patients and methods:This retrospective observational study (2019-2023) evaluated 250 patients with type 2 diabetes mellitus and metabolic dysfunction-associated steatotic liver disease (defined by a fatty liver index score of>60) treated at the Outpatient Clinics of the 2nd University Department of Internal Medicine of University General Hospital of Alexandroupolis (Greece). Patients were on baseline metformin and initiated one of four oral antidiabetic drug classes: sodium-glucose cotransporter-2 inhibitors (n = 72), thiazolidinediones (n=36), dipeptidyl peptidase-4 inhibitors (n=77), and sulfonylureas (n=65). The primary end point was metabolic dysfunction-associated steatotic liver disease regression (a fatty liver index score of<30). The secondary end point encompassed severe liver-related outcomes and mortality. Results:Sodium-glucose cotransporter-2 inhibitors demonstrated the highest probability of metabolic dysfunction-associated steatotic liver disease regression compared to sulfonylureas (adjusted sub-distribution hazard ratio: 1.99 and 95% confidence interval: 1.75-2.27), dipeptidyl peptidase-4 inhibitors (adjusted sub-distribution hazard ratio: 1.45 and 95% confidence interval: 1.30-1.62), and thiazolidinediones (adjusted sub-distribution hazard ratio: 1.40 and 95% confidence interval: 1.12-1.75). Furthermore, sodium-glucose cotransporter-2 inhibitors significantly reduced the risk of severe liver-related outcomes compared to sulfonylureas (adjusted sub-distribution hazard ratio: 0.37 and 95% confidence interval: 0.17-0.82). Conclusions:In patients with type 2 diabetes mellitus and metabolic dysfunction-associated steatotic liver disease, the addition of sodium-glucose cotransporter-2 inhibitors to metformin significantly promotes fatty liver regression and protects against severe liver-related outcomes compared to other standard oral antidiabetic drug classes.
Background:Diabetic neuropathy is a common microvascular complication of type 2 diabetes mellitus associated with chronic inflammation and metabolic dysregulation. The hemoglobin-albumin-lymphocyte-platelet score is a composite index reflecting nutritional and inflammatory status, but its association with diabetic neuropathy remains insufficiently characterized. Methods:In this retrospective cross-sectional study, 212 patients with type 2 diabetes mellitus were evaluated. Diabetic neuropathy was defined using electrophysiological criteria. Multivariable logistic regression analysis was performed to assess the association between the hemoglobin-albumin-lymphocyte-platelet score and diabetic neuropathy after adjustment for age, sex, diabetes duration, body mass index, and glycated hemoglobin. The hemoglobin-albumin-lymphocyte-platelet score was analyzed as a continuous variable (per 0.1-unit increase) and in quartiles. Receiver operating characteristic curve analysis was used to evaluate model discrimination. Results:Diabetic neuropathy was present in 45.2% of patients. The hemoglobin-albumin-lymphocyte-platelet levels were significantly lower in patients with diabetic neuropathy compared to those without diabetic neuropathy (0.36±0.18 vs. 0.72±0.39, p<0.001). In multivariable analysis, the hemoglobin-albumin-lymphocyte-platelet score remained independently associated with diabetic neuropathy (odds ratio per 0.1-unit increase: 0.46, 95% confidence interval: 0.35-0.58, p<0.001). Quartile analysis showed a graded inverse association (p for trend<0.001). The addition of the hemoglobin-albumin-lymphocyte-platelet score improved model discrimination compared to the base model (area under the curve: 0.868 vs. 0.567). Conclusions:The hemoglobin-albumin-lymphocyte-platelet score is inversely associated with diabetic neuropathy in patients with type 2 diabetes mellitus and may represent an integrated marker of metabolic and inflammatory burden.
Aims Symptoms related to gastrointestinal autonomic neuropathy, which can involve gallbladder, are prevalent in patients with diabetes. We hypothesize that diabetes duration may impact gallbladder volume and motility. This study aims to explore relationships between gallbladder volume parameters and diabetes duration in individuals with type 2 diabetes compared with non-diabetic controls. Autonomic neuropathy will also be explored. Methods In this cross-sectional observational case-control study, matched individuals with longstanding type 2 diabetes, early type 2 diabetes, and non-diabetic controls were included. Gallbladder motility was investigated by gallbladder volume changes measured by three-dimensional ultrasound. Gallbladder volumes were collected at predefined time intervals before and after an intake of a standardized high-fat meal. Autonomic neuropathy was evaluated by cardiovascular (Vagus) and sudomotor (Sudoscan) testing. Results Sixty-one adults were included in the final analysis, of which 18 adults had longstanding type 2 diabetes, 15 adults had early type 2 diabetes, and 28 adults were non-diabetic controls. Subjects with longstanding type 2 diabetes had significantly higher fasting gallbladder volume and ejection volume compared to the controls ( p =0.020 and p =0.019, respectively). No other significant differences in gallbladder motility were observed. Only five participants had autonomic neuropathy. Conclusions Specific gallbladder volumes and motility parameters were associated with diabetes duration. Associations between gallbladder motility and autonomic neuropathy could not be analyzed.
Background:This study evaluates the diagnostic value of serum carcinoembryonic antigen, carbohydrate antigen, neuron-specific enolase, and lipid metabolism markers (total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol) in pancreatic neuroendocrine tumors. Methods:A total of 175 pancreatic neuroendocrine tumor patients (experimental group) and 88 healthy individuals (control group) were enrolled. Serum levels of carcinoembryonic antigen, carbohydrate antigen, neuron-specific enolase, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and body mass index were analyzed. A logistic regression analysis model was constructed, and the receiver operating characteristic curve was utilized to evaluate the efficacy of individual indicators with statistically significant differences, as well as the combined detection model, in predicting the occurrence, pathological grading, and metastasis of pancreatic neuroendocrine tumors. Results:Pancreatic neuroendocrine tumor patients showed higher levels of carcinoembryonic antigen, neuron-specific enolase, low-density lipoprotein cholesterol and lower levels of high-density lipoprotein cholesterol than the control group. High-grade pancreatic neuroendocrine tumor patients showed higher carcinoembryonic antigen, carbohydrate antigen, neuron-specific enolase, total cholesterol, and low-density lipoprotein cholesterol levels than low-grade cases, with increased metastasis risk. Elevated carcinoembryonic antigen, carbohydrate antigen, and neuron-specific enolase levels were linked to metastasis. The results are statistically significant. High neuron-specific enolase and low high-density lipoprotein cholesterol were pancreatic neuroendocrine tumor risk factors, with area under the curves of 0.899 and 0.666, respectively, improving to 0.911 when combined. Elevated carbohydrate antigen and neuron-specific enolase levels predicted high-grade (area under the curves: 0.728, 0.645; combined area under the curve: 0.765) and metastatic pancreatic neuroendocrine tumors (area under the curves: 0.693, 0.651; combined area under the curves: 0.689). Conclusions:Increased neuron-specific enolase is a strong predictor of pancreatic neuroendocrine tumor occurrence, grading, and metastasis. Lower high-density lipoprotein cholesterol predicts pancreatic neuroendocrine tumor occurrence but not grading or metastasis. Combined markers enhance diagnostic accuracy for pancreatic neuroendocrine tumor detection and grading.
Background:Fibrocalculous pancreatic diabetes is a unique form of diabetes prevalent in tropical regions, characterized by chronic calcific pancreatitis and a high burden of diabetic complications. Sudomotor dysfunction remains underexplored in this population. Aim:To determine the prevalence and clinical determinants of sudomotor dysfunction in individuals with fibrocalculous pancreatic diabetes. Methods:In this cross-sectional study, 90 patients with fibrocalculous pancreatic diabetes were evaluated at a tertiary care endocrinology centre. Sudomotor function was assessed using electrochemical skin conductance. Large fiber neuropathy was evaluated using vibration perception threshold testing and nerve conduction studies. Agreement between modalities was assessed using Cohen's kappa, and logistic regression was used to identify the predictors of sudomotor dysfunction. Results:Sudomotor dysfunction was present in 43.3% of patients, compared with abnormalities in vibration perception threshold (17.8%) and nerve conduction studies (21.1%). Agreement between electrochemical skin conductance and large fiber measures was fair to moderate (κ=0.39-0.47), while the vibration perception threshold and nerve conduction studies showed substantial concordance (κ=0.61). In multivariable analysis, increasing age (odds ratio: 1.08; 95% confidence interval: 1.00-1.16) and longer duration of diabetes (odds ratio: 1.26; 95% confidence interval: 1.07-1.49) were independently associated with sudomotor dysfunction. Conclusions:Sudomotor dysfunction assessed by electrochemical skin conductance was common in fibrocalculous pancreatic diabetes and detected more frequently than abnormalities on vibration perception threshold or nerve conduction studies. Electrochemical skin conductance may serve as a practical adjunctive tool for evaluating sudomotor dysfunction in this population, although longitudinal studies are needed to clarify its clinical significance.
First-degree relatives of patients with type 2 diabetes mellitus may exhibit metabolic abnormalities and subclinical myocardial dysfunction before the onset of overt disease. Left Ventricular Speckle-tracking echocardiography (LV-STE) enables early detection of left ventricular impairment, while osteogenic biomarkers such as osteoprotegerin, osteocalcin, and osteopontin have been linked to cardiometabolic risk. This study aimed to evaluate myocardial strain parameters and serum osteogenic biomarkers in normoglycemic first-degree relatives of patients with type 2 diabetes mellitus.We enrolled 160 normoglycemic participants, comprising 80 individuals with at least one first-degree relative diagnosed with type 2 diabetes mellitus and 80 controls without such a family history. Serum osteocalcin, osteopontin, and osteoprotegerin levels were measured by ELISA. LV-STE was used to assess global longitudinal and circumferential strain from apical four-chamber (A4C), two-chamber (A2C), three-chamber (A3C), and short-axis basal/mid/apical views.Compared with the control group, the study group presented significantly lower mean short-axis basal/mid/apical and A4C/A2C/A3C strain values. The serum osteocalcin level was significantly lower and weakly negatively correlated with the fasting plasma glucose level. osteoprotegerin was positively correlated with LDL-C. No significant associations were found between strain parameters and biomarkers.Normoglycemic first-degree relatives of type 2 diabetes mellitus patients exhibit early myocardial impairment detectable by LV-STE and reduced osteocalcin levels. LV-STE may enhance early risk stratification in this population. Longitudinal studies are needed to determine the prognostic value of osteogenic biomarkers in the progression to type 2 diabetes mellitus and cardiovascular disease.
Aims:To develop and evaluate the German versions of the Diabetes Stigma Assessment Scales for type 1 (DSAS-1) and type 2 diabetes (DSAS-2). Methods:The questionnaires were translated using a standardized translation and back-translation procedure. Adults with type 1 (N=636) and type 2 diabetes (N=177) completed the DSAS-1 and DSAS-2 via an online panel. Factor analyses, internal consistency (Cronbach's α), and correlations with convergent measures and discriminant constructs were conducted to assess reliability and validity. Results:For the DSAS-1, the expected three-factor structure was confirmed; for the DSAS-2, a two-factor solution emerged, although a forced three-factor analysis supported the original structure with minor cross-loadings. Scale consistencies were excellent (DSAS-1: 0.94, DSAS-2: 0.95, and subscales: 0.86-0.93). Both scales showed good concurrent, convergent and discriminant validity. The DSAS-2 showed stronger associations with weight self-stigma and self-esteem than the DSAS-1, consistent with its focus on internalized stigma. Three in four persons (type 1 diabetes: 74% and type 2 diabetes: 72%) endorsed at least one stigma item, mostly related to "blame and judgement." Conclusions:Diabetes stigma constitutes an important psychosocial problem. The German DSAS-1and DSAS-2 are reliable, valid instruments for assessing diabetes stigma. Blame and judgement appeared as the most common form of stigma experienced in this sample.
