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Objective: The aim of this study was to investigate the role of vitamin D replacement therapy on advanced glycation end-products in prediabetes and type 2 diabetes mellitus patients with vitamin D deficiency. Methods: One hundred twenty subjects with serum 25-hydroxyl vitamin D levels less than 20 ng/mL were included in the study. Forty type 2 diabetes mellitus patients (type 2 diabetes mellitus group), 40 prediabetes patients (prediabetes group), and 40 non-diabetes controls (non-diabetes group) were given oral vitamin D3 50 000 units/week for 8 weeks as loading and followed by 1500 U/day as a maintenance dose. We measured serum 25-hydroxyl vitamin D, glycated hemoglobin, carboxymethyl lysine levels, and skin autofluorescence before and on the fourth month of the therapy. Results: Basal serum carboxymethyl lysine and skin autofluorescence measurement in type 2 diabetes mellitus and prediabetes groups were significantly higher than the non-diabetes group. While no difference was found between glycated hemoglobin and skin autofluorescence, serum carboxymethyl lysine levels were significantly elevated for each group following vitamin D replacement. Conclusions: Vitamin D loading did not affect skin advanced glycation end-product levels and glycated hemoglobin but was associated with increased serum carboxymethyl lysine levels in all groups. [ABSTRACT FROM AUTHOR]

Purpose: There is an increased fracture risk in type 2 diabetes mellitus [DM] patients independent of bone mineral density [BMD], both in men and women. Estrogen receptor [ER]-alpha and vitamin D receptor [VDR] gene polymorphisms may predispose patients to increased osteoporosis and fracture risk. This study aims to analyze the relationship of the ER-alpha gene and VDR gene polymorphisms with indicators of bone turnover and BMD in male type 2 diabetic patients. Methods: Type 2 diabetic men diagnosed with diabetes for at least one year and healthy controls were included in this cross-sectional study. BMD was measured by dual X ray absorptiometry. Gene polymorphisms were evaluated with polymerase chain reaction-restriction length polymorphism. Serum iPTH, calcium, beta-CrossLaps (cTx), osteocalcin, and free testosterone levels were also evaluated. Results: Participants were 141 type 2 diabetic men [55 ± 8 years] and 100 healthy controls [53 ± 7 years]. BMD measurements were not statistically different between the groups. While iPTH [p < 0.05] and serum calcium levels [p = 0.03] were higher in men with type 2 DM; beta-CrossLaps [p = 0.0001], osteocalcin [p = 0.005], and free testosterone [p = 0.04] were lower than controls. The differences in terms of the frequencies of VDR Apa, Taq, Bsm, Fok and ER-alpha polymorphisms were not statistically significant between the groups. No relationship was observed between polymorphisms and BMD in both groups. Conclusions: VDR and ER-alpha gene polymorphisms seem to have no effect on BMD and bone turnover in men with DM. [ABSTRACT FROM AUTHOR]

Although the risk of bone fracture is increased in type 2 diabetes (T2DM), bone mineral density (BMD) is increased rather than decreased. Accumulation of advanced glycation end products (AGEs) adversely influences the fracture resistance of bone in T2DM. We hypothesized that SAF is also associated with BMD levels in type 2 diabetic patients and aimed to evaluate the association of SAF with BMD and the presence of osteoporosis. This cross-sectional case-control study included 237 patients with T2DM (F/M: 133/104, 56.2±11.9 yrs) and 100 age- and sex-matched controls (F/M: 70/30, 54.8±8.8 yrs). Skin autofluorescence, a validated non-invasive measure of tissue AGEs, is used to detect the accumulation of AGEs in skin collagen using AGE Reader (DiagnOptics B.V., Groningen, The Netherlands). In addition, BMD was measured with DEXA (Lunar DPX-L). Patients with T2DM had higher SAF values compared to control group (2.21±0.53 AU vs. 1.79±0.33 AU, p < 0.001). Male subjects had higher SAF compared to women (2.34±0.53 AU vs. 2.11±0.50 AU, p < 0.001). Subjects with below -2.5 femoral neck or lumbar T scores had higher SAF measurements compared to subjects with normal T scores (2.46±0.53 AU vs. 2.18±0.52 AU, p = 0.006). Femoral neck BMD was lower in subjects with T2DM (0.946±0.345 g/cm2 vs. 1.005±0.298 g/cm2, p = 0.002). There was a negative correlation between SAF and femoral neck BMD (r=−0.24, p < 0.001), femoral neck T scores (r=-0.24, p < 0.001), L1-4 BMD (r=−0.10, p = 0.005), L1-4 T score (r=−0.16, p=0.001) and a positive correlation between SAF and age (r=0.44, p < 0.001), body mass index (r:0.16, p = 0.002) and HbA1c (r=0.37, p < 0.001). Accumulation of skin AGEs was increased, and BMD levels were decreased in diabetic patients. A negative association between SAF and BMD was detected, indicating a relationship between higher AGE accumulation and low BMD and osteoporosis in diabetic patients. Long-term prospective studies are needed to identify the practical use of SAF measurement in diabetic bone disease. [ABSTRACT FROM AUTHOR]

Insulin degludec/insulin aspart (IDegAsp) is a fixed-ratio co-formulation of insulin degludec, which provides long-lasting basal insulin coverage, and insulin aspart, which targets postprandial glycaemia. This review provides expert opinion on the practical clinical use of IDegAsp, including: dose timings relative to meals, when and how to intensify treatment from once-daily (OD) to twice-daily (BID) dose adjustments, and use in special populations (including hospitalized patients). IDegAsp could be considered as one among the choices for initiating insulin treatment, preferential to starting on basal insulin alone, particularly for people with severe hyperglycaemia and/or when postprandial hyperglycaemia is a major concern. The recommended starting dose of IDegAsp is 10 units with the most carbohydrate-rich meal(s), followed by individualized dose adjustments. Insulin doses should be titrated once weekly in two-unit steps, guided by individualized fasting plasma glucose targets and based on patient goals, preferences and hypoglycaemia risk. Options for intensification from IDegAsp OD are discussed, which should be guided by HbA1c, prandial glucose levels, meal patterns and patient preferences. Recommendations for switching to IDegAsp from basal insulin, premixed insulins OD/BID, and basal-plus/ basal--bolus regimens are discussed. IDegAsp can be co-administered with other antihyperglycaemic drugs; however, sulphonylureas frequently need to be discontinued or the dose reduced, and the IDegAsp dose may need to be decreased when sodiumglucose co-transporter-2 inhibitors or glucagon-like peptide-1 receptor agonists are added. Considerations around the initiation or continuation of IDegAsp in hospitalized individuals are discussed, as well as in those undergoing medical procedures. [ABSTRACT FROM AUTHOR]

Introduction: Seckel syndrome is a disease with nine distinct phenotypes that is inherited autosomally recessively and is caused by DNA damage on chromosomes 3, 13, and 18. It is also known as 'bird-headed dwarfism' due to the disease's characteristic phenotypic features, microcephaly and dwarfism. In addition to mental retardation, other possible complications include bilateral optic atrophy, strabismus, hearing difficulties, micrognathia, microdontia, hypodontia, malocclusion of the mandible, scoliosis, bone anomalies, hematological, endocrinological, genitourinary, neurological anomalies (epilepsy, etc.), and cancers. Presented here is a patient with metabolic dysfunction who has been diagnosed with Seckel's syndrome. Clinical Case: A male patient, age 22, was admitted to the endocrinology outpatient clinic for regulation of hyperglycemia. The patient's medical history included diabetes of type 2 since 2021, hypothyroidism, mental retardation, and hepatosteatosis. His parents were related as first cousins. One of the patient's two brothers has been diagnosed with Seckel syndrome. On his physical examination, his temperature was 36.1°C, his blood pressure was 92/61 mmHg, his heart rate was 76 beats per minute, his height was 125 cm, his weight was 19 kg, and his BMI was 12 kg/m2. Microcephaly, hypodontia, and micrognotia were observed. The patient was using insulin glargin 32 units, insulin aspart 2×18 units, metformin 500mg once day, and levothyroxine sodium 50mcg. In blood glucose follow-ups, the highest was 304 mg/dl and the lowest was 127 mg/dl, whereas Hba1c was 7.5% and c-peptide was 2.44 ng/ml. Anti-GAD, anti-islet cell, anti-TPO, and antithyroglobulin antibodies were negative. Insulin glargine was changed to 34 units, and insulin aspart was changed to 2×20 units. Due to mental retardation and hypodontia, it was discovered that the patient could not pay attention to his diet, could hardly eat solid foods, and was provided primarily liquids, particularly sugar-sweetened, flavored, and carbonated soft drinks. The patient was referred to the dental polyclinic and dietitian, while the family was monitored at the genetics polyclinic. Conclusion: Follow-up care for patients with Seckel syndrome should include routine metabolic screening. Due to the patient's mental cooperation and dietary habits resulting from dental anomalies, metabolic control may be challenging. To ensure metabolic homeostasis in these patients, a multidisciplinary approach is necessary, involving the patient, his or her family, in multidisciplinary setting. [ABSTRACT FROM AUTHOR]

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Objective: The objective of this study is to evaluate the impact of sequential telephonic interviews on treatment persistence and daily adherence to insulin injections among insulin-naïve type 2 diabetes patients initiated on different insulin regimens in a 3-month period. Methods: A total of 1,456 insulin-naïve patients with type 2 diabetes (mean [standard deviation, SD] age: 56.0 [12.0] years, 49.1% were females) initiated on insulin therapy and consecutively randomized to sequential (n=733) and single (n=723) telephonic interview groups were included. Data on insulin treatment and self-reported blood glucose values were obtained via telephone interview. Logistic regression analysis was performed for factors predicting increased likelihood of persistence and skipping an injection. Results: Overall, 76.8% patients (83.2% in sequential vs 70.3% in single interview group, (P<0.001) remained on insulin treatment at the third month. Significantly higher rate for skipping doses was noted in basal bolus than in other regimens (27.0% vs 15.0% for premixed and 15.8% basal insulin, respectively, P<0.0001). Logistic regression analysis revealed sequential telephonic interview (odds ratio [OR], 1.531; 95% confidence interval [CI], 1.093-2.143; P=0.013), higher hemoglobin A1c levels (OR, 1.090; 95% CI, 0.999-1.189; P=0.049), and less negative appraisal of insulin therapy as significant predictors of higher persistence. Basal bolus regimen (OR, 1.583; 95% CI, 1.011-2.479; P=0.045) and higher hemoglobin A1c levels (OR, 1.114; 95% CI, 1.028-1.207; P=0.008) were the significant predictors of increased likelihood of skipping an injection. Conclusion: Our findings revealed positive influence of sequential telephonic interview, although including no intervention in treatment, on achieving better treatment persistence in type 2 diabetes patients initiating insulin. [ABSTRACT FROM AUTHOR]

Objective: We aimed to evaluate adherence to insulin treatment in terms of treatment persistence and daily adherence to insulin injections among insulin-naïve type 2 diabetic patients initiating insulin therapy with basal (long acting), basal-bolus, and premixed insulin regimens in a tertiary endocrinology outpatient clinic. Methods: A total of 433 (mean age of 55.5±13.0 years; 52.4% females) insulin-naïve type 2 diabetic patients initiated on insulin therapy were included in this questionnaire-based phone interview survey at the sixth month of therapy. Via the telephone interview questions, patients were required to provide information about persistence to insulin treatment, self-reported blood glucose values, and side effects; data on demographics and diabetes characteristics were obtained from medical records. Results: Self-reported treatment withdrawal occurred in 20.1% patients, while 20.3% patients were nonadherent to daily insulin. Negative beliefs about insulin therapy (24.1%) and forgetting injections (40.9%) were the most common reasons for treatment withdrawal and dose skipping, respectively. Younger age (49.5±15.0 vs 56.4±12.0 years) (P=0.001) and shorter duration of diabetes (4.8±4.3 vs 8.8±6.3 years) (P=0.0008) and treatment duration (5.2±2.4 vs 10.7±2.4 months) (P=0.0001) were noted, respectively, in discontinuers vs continuers. Basal bolus was the most commonly prescribed insulin regimen (51.0%), while associated with higher likelihood of skipping a dose than regular use (61.3% vs. 46.0%, P=0.04). Conclusions: Persistence to insulin therapy was poorer than anticipated but appeared to be higher in patients with the basal bolus regimen. Negative perceptions about insulin therapy seemed to be the main cause for poor adherence in our cohort. [ABSTRACT FROM AUTHOR]

Objective: C-reactive protein (CRP) is considered to be a cardiovascular risk marker and changes in its level have been attributed to genetic factors. The aim of the study was to determine CRP 1059G/C gene polymorphism frequency and its relationship with CRP levels and carotid artery intima-media thickness (CIMT) in type 2 diabetic patients (DM). Materials and Methods: One hundred and sixty-four type 2 diabetic patients (mean age: 57±7 years; F/M: 80/84) and 151 controls (mean age: 53±7 years; F/M: 81/70) were recruited. CIMT was assessed by carotid ultrasonography. CRP 1059G/C polymorphism was determined by polymerase chain reaction and restriction fragment length polymorphism analyses. Results: The CRP 1059G/C polymorphism distribution in diabetic group and controls were similar (1059GG in 92% vs. 88%, 1059GC in 2% vs. 5%; 1059CC in 6% vs. 7%). CRP levels (4.3±6.6 mg/L vs. 2.5±2.3 mg/L; p=0.02) and CIMT (0.67±0.18mm vs. 0.56±0.19mm; p<0.0001) were increased in diabetics compared to controls. No association of CRP and CIMT with CRP 1059G/C polymorphism was found. Conclusions: Increased CRP levels and CIMT seem to be independent of CRP 1059G/C gene polymorphism in our group of type 2 diabetic patients. [ABSTRACT FROM AUTHOR]