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Introduction—Aim: Adopting a lifestyle that incorporates regular physical activity confers substantial benefits to both physical and mental health and is recommended for prediabetic individuals. The aim of this study is to investigate the impact of activity tracking apps on increasing physical activity and its effect on glycemic control in people with prediabetes. Materials and Methods: This pilot study included 37 participants, 18 in the prediabetic group and 19 in the normoglycemic group matched for age and gender (mean age 53 years, 40% males). Participants used the Google Fit app for 3 months. The number of daily steps was recorded via the app, and blood and urine tests as well as body fat measurements were conducted before and following 3 months of app use. The co-primary outcome was the change in steps, and the change in HbA1c in both groups. Secondary outcomes were the change in fasting plasma glucose (FPG) (main secondary outcome), as well as lipid parameters, body mass index, visceral fat, and kidney function indices among the two groups. Results: Both groups increased the daily step count following the app intervention, without any statistically significant difference when we compared the steps change between the two groups. We found a statistically significant difference between HbA1c levels in favor of the prediabetic compared to the normoglycemic group [mean difference (MD) 0.16, 95%CI 0.04, 0.28, p-value 0.01)], following the 3-month intervention. Additionally, there was a statistically significant difference between FPG levels in favor of the prediabetic compared to the normoglycemic group (MD 9.06, 95%CI 4.16, 13.96, p-value 0.001). Conclusions: The present study suggests that the use of activity tracking apps, combined with tailored activity goals and monthly supportive phone calls, may contribute to improved glycemic control among individuals with prediabetes. [ABSTRACT FROM AUTHOR]

People with HIV (PWH) have an elevated risk of cardiovascular disease compared to those without HIV. This study aimed to investigate the relative serum expression of microRNAs (miRNAs) associated with arterial stiffness, a significant marker of cardiovascular disease. A total of 36 male PWH and 36 people without HIV, matched for age, body mass index, pack years, and dyslipidemia, were included in the study. Participants with a history of hypertension, diabetes mellitus, cardiovascular disease, cancer, or intravenous drug use were excluded. Markers of arterial stiffness, including carotid–femoral pulse wave velocity (cfPWV) and augmentation index adjusted to 75 beats per minute (AIx@75), were measured via applanation tonometry. We analyzed the relative expression of 11 circulating miRNAs using real-time PCR: let-7b-5p, miR-19b-3p, miR-21-5p, miR-29a-3p, miR-126-3p, miR-130a-3p, miR-145-5p, miR-181b-5p, miR-221-3p, miR-222-3p, and miR-223-3p. cfPWV was significantly higher in PWH compared to people without HIV (9.3 vs. 8.6 m/s, p = 0.019), while AIx@75, peripheral, and aortic blood pressures did not differ among groups. The relative expression of circulating miRNAs was significantly higher in PWH compared to controls for let-7b-5p (fold change: 5.24, p = 0.027), miR-21-5p (fold change: 3.41, p < 0.001), miR-126-3p (fold change: 1.23, p = 0.019), and miR-222-3p (fold change: 3.31, p = 0.002). Conversely, the relative expression of circulating miR-19b-3p was significantly lower in PWH (fold change: 0.61, p = 0.049). Among HIV-related factors, the nadir CD4+T-cell count of <200 cells/mm3 was independently associated with the relative expression of circulating let-7b-5p (β = 0.344, p = 0.049), while current non-nucleoside reverse transcriptase inhibitor (NNRTI) treatment was independently associated with the relative expression of circulating miR-126-3p (β = 0.389, p = 0.010). No associations were found between the duration of HIV infection or the duration of ART and the serum miRNA expression. This study highlights a distinct circulating miRNA profile in PWH with higher cfPWV compared to those without HIV, which may contribute to increased arterial stiffness. [ABSTRACT FROM AUTHOR]

As the incidence of type 2 diabetes mellitus (T2DM) continues to increase globally, researchers are keen to investigate various interventions to mitigate its impact. Among these, vitamin D supplementation has attracted significant attention due to its influence on insulin secretion from the pancreas and insulin receptors in body cells. A substantial body of evidence indicates that vitamin D supplementation can reduce low-grade inflammation, a critical factor in developing insulin resistance. In addition, vitamin D aids in sustaining low resting concentrations of reactive oxygen species and free radicals, normalizes Ca2+ signaling, diminishes the expression of cytokines that are pro-inflammatory, and enhances the production of cytokines that are anti-inflammatory. This review discusses the effects of vitamin D on the glycemic control of individuals with T2DM and evaluates the impact of vitamin D supplementation on glycemic markers in this population. The investigation employs a comprehensive analysis of the existing literature with a special focus on recent studies published in the past decade. Based on the findings in the literature, it can be concluded that vitamin D supplementation alongside anti-diabetic medications may enhance glycemic control and potentially reduce the risk of diabetic complications. The evidence supports the notion that vitamin D supplementation can be a valuable addition to pharmacological agents for the management of T2DM, potentially enhancing glycemic control and overall health outcomes in affected individuals. [ABSTRACT FROM AUTHOR]

Systemic inflammation has been recognized as the cause and consequence of metabolic dysregulation in diabetes mellitus (DM). Presepsin has recently emerged as a promising biomarker for the detection of bacterial infections and sepsis. There is evidence that gut dysbiosis results in the increased circulating concentrations of Gram-negative bacteria lipopolysaccharide, the linkage of presepsin, which in turn promotes insulin resistance and correlates with the risk of diabetic complications. Thus, we hypothesized that presepsin could reflect the magnitude of systemic inflammation and metabolic decompensation in patients with DM even in the absence of infection. In this cross-sectional pilot study, we included 75 infection-free individuals with well-controlled (n = 19) and uncontrolled (n = 23) type 2 diabetes (T2D), well-controlled (n = 10) and uncontrolled (n = 10) type 1 diabetes (T1D), and normoglycemic controls (n = 13). Presepsin levels were compared between the groups and potential associations with demographic, clinical, and laboratory parameters were explored. We observed that the duration of DM was associated with presepsin values (p = 0.008). When the participants were classified into the type of DM groups, the presepsin levels were found to be lower in the patients with T2D compared to those with T1D (p = 0.008). However, significance in that case was driven by the difference between the well-controlled groups. After adjusting for the effects of DM duration, presepsin was significantly lower in the well-controlled T2D group compared to the well-controlled T1D group [1.34 (2.02) vs. 2.22 (4.20) ng/mL, p = 0.01]. Furthermore, we adjusted our findings for various confounders, including age, body mass index, and waist circumference, and found that the difference in the presepsin values between the adequately controlled groups remained significant (p = 0.048). In conclusion, our findings suggest that presepsin could potentially serve as a surrogate marker of inflammation and metabolic control in people with DM. [ABSTRACT FROM AUTHOR]

Metabolic dysfunction-associated steatotic liver disease (MASLD) and polycystic ovary syndrome (PCOS) are prevalent conditions that have been correlated with infertility through overlapped pathophysiological mechanisms. MASLD is associated with metabolic syndrome and is considered among the major causes of chronic liver disease, while PCOS, which is characterized by ovulatory dysfunction and hyperandrogenism, is one of the leading causes of female infertility. The pathophysiological links between PCOS and MASLD have not yet been fully elucidated, with insulin resistance, hyperandrogenemia, obesity, and dyslipidemia being among the key pathways that contribute to liver lipid accumulation, inflammation, and fibrosis, aggravating liver dysfunction. On the other hand, MASLD exacerbates insulin resistance and metabolic dysregulation in women with PCOS, creating a vicious cycle of disease progression. Understanding the intricate relationship between MASLD and PCOS is crucial to improving clinical management, while collaborative efforts between different medical specialties are essential to optimize fertility and liver health outcomes in individuals with MASLD and PCOS. In this review, we summarize the complex interplay between MASLD and PCOS, highlighting the importance of increasing clinical attention to the prevention, diagnosis, and treatment of both entities. [ABSTRACT FROM AUTHOR]

Over the last few years, given the increase in the incidence and prevalence of both type 2 diabetes mellitus (T2DM) and heart failure (HF), it became crucial to develop guidelines for the optimal preventive and treatment strategies for individuals facing these coexisting conditions. In patients aged over 65, HF hospitalization stands out as the predominant reason for hospital admissions, with their prognosis being associated with the presence or absence of T2DM. Historically, certain classes of glucose-lowering drugs, such as thiazolidinediones (rosiglitazone), raised concerns due to an observed increased risk of myocardial infarction (MI) and cardiovascular (CV)-related mortality. In response to these concerns, regulatory agencies started requiring CV outcome trials for all novel antidiabetic agents [i.e., dipeptidyl peptidase-4 inhibitors (DPP-4 inhibitors), glucagon-like peptide-1 receptor agonists (GLP-1 RAs), and sodium-glucose cotransporter-2 inhibitors (SGLT2is)] with the aim to assess the CV safety of these drugs beyond glycemic control. This narrative review aims to address the current knowledge about the impact of glucose-lowering agents used in T2DM on HF prevention, prognosis, and outcome. [ABSTRACT FROM AUTHOR]

Author(s): Theocharis Koufakis [sup.1] , Spyridon N Karras [sup.1] , Pantelis Zebekakis [sup.1] , Kalliopi Kotsa [sup.1] Author Affiliations: (1) Division of Endocrinology and Metabolism--Diabetes Center, First Department of Internal [...], Previous studies have reported inconclusive results regarding the effects of Orthodox religious fasting (OF) on common cardiovascular risk factors, including arterial hypertension and diabetes. Contrariwise, an optimal effect on dyslipidemia has been demonstrated and significant reductions in total cholesterol (TC) and low-density lipoprotein-cholesterol (LDL-C) concentrations, in Orthodox populations without comorbidities, have been consistently reported. This favorable effect on lipid homeostasis is probably facilitated by a broad lifestyle modification related to OF, extended beyond dietary habits. However, several clinical issues require further clarification by future trials including the efficacy and safety of OF in specific groups of patients with dyslipidemia, mainly those with cardiovascular disease and diabetes, the effects of OF on high-density lipoprotein-cholesterol (HDL-C), the dietary limitations of specific vitamins and minerals during fasting, as well as the optimal duration of this dietary intervention. The present article aims to discuss, whether there is a strong enough theoretical background, to currently support the implementation of OF as a medical nutrition therapy for dyslipidemia in the daily clinical setting, with a discourse on available evidence and future research agenda.

Background Myasthenia gravis (MG) is a rare autoimmune disorder affecting the neuromuscular junction (NMJ). Here, we investigate the genetic architecture of MG via a genome-wide association study (GWAS) of the largest MG data set analysed to date. Methods We performed GWAS meta-analysis integrating three different data sets (total of 1401 cases and 3508 controls). We carried out human leucocyte antigen (HLA) fine-mapping, gene-based and tissue enrichment analyses and investigated genetic correlation with 13 other autoimmune disorders as well as pleiotropy across MG and correlated disorders. Results We confirmed the previously reported MG association with TNFRSF11A (rs4369774; p=1.09×10-13, OR=1.4). Furthermore, gene-based analysis revealed AGRN as a novel MG susceptibility gene. HLA fine-mapping pointed to two independent MG loci: HLA-DRB1 and HLA-B. MG onset-specific analysis reveals differences in the genetic architecture of early-onset MG (EOMG) versus late-onset MG (LOMG). Furthermore, we find MG to be genetically correlated with type 1 diabetes (T1D), rheumatoid arthritis (RA), late-onset vitiligo and autoimmune thyroid disease (ATD). Cross-disorder meta-analysis reveals multiple risk loci that appear pleiotropic across MG and correlated disorders. Discussion Our gene-based analysis identifies AGRN as a novel MG susceptibility gene, implicating for the first time a locus encoding a protein (agrin) that is directly relevant to NMJ activation. Mutations in AGRN have been found to underlie congenital myasthenic syndrome. Our results are also consistent with previous studies highlighting the role of HLA and TNFRSF11A in MG aetiology and the different risk genes in EOMG versus LOMG. Finally, we uncover the genetic correlation of MG with T1D, RA, ATD and late-onset vitiligo, pointing to shared underlying genetic mechanisms. [ABSTRACT FROM AUTHOR]