Current diabetes reviews最新文献

Introduction: Impaired hypoglycemic awareness (IAH) in type 2 diabetes mellitus (T2DM) is linked to mild cognitive impairment (MCI), but the underlying mechanisms are unclear. This study aimed to explore the chain mediating role of two psychological factors, illness perception (IP) and fear of hypoglycemia (FOH), in the relationship between IAH and MCI.

Methods: A cross-sectional survey of 251 T2DM patients was conducted using convenience sampling at two tertiary hospitals. Data on IAH, IP, FOH, and MCI were collected using standardized questionnaires. Data were analyzed and compared using SPSS 27.0 and AMOS 27.0.

Results: There were significant correlations among IAH, IP, FOH, and MCI. Higher IAH was associated with increased FOH and more negative IP, which were both linked to worse cognitive function. Mediation analysis showed that IAH indirectly affects MCI through three pathways: independently via FOH, independently via IP, and via a chained effect of FOH and IP.

Discussion: The findings underscored that the link between IAH and cognitive decline is not solely physiological, but is substantially mediated by psychological responses. Negative illness perceptions and heightened fear, triggered by the unpredictability of IAH, drive maladaptive behaviors and emotional distress that contribute to worse cognitive outcomes.

Conclusion: The findings highlighted the role of psychological factors in cognitive decline among T2DM patients with IAH. We recommend that future interventions consider the associations between these variables. Diverse interventions aimed at improving IP and FOH levels could help slow cognitive decline in patients with IAH.

Type 2 diabetes mellitus is a chronic metabolic disorder associated with microvascular and macrovascular complications. Hyperglycemia and insulin resistance are core pathophysiological components of diabetes, linked to subclinical inflammation and persistent oxidative stress, which result in endothelial dysfunction and subsequent atherogenesis. Nowadays, several arrows in the diabetologist's quiver are available for the management of diabetes, providing flexibility and the ability to adopt a personalized approach tailored to each patient's needs. Two of the most commonly prescribed antidiabetic drugs are sodium-glucose cotransporter 2 inhibitors and glucagon- like peptide-1 receptor agonists. Both agents are associated with beneficial metabolic, cardioand nephro-protective effects independent of their antidiabetic properties; thus, their indications have and are continuously expanding over and beyond the treatment of diabetes. Given that these two drug classes have different mechanisms of action, the use of their combination achieves a synergistic interaction and confers additional benefits. The aim of this review is to provide a summary of current knowledge regarding the use of these two drug classes, shed light on the available evidence on their combination, and discuss future perspectives on optimal therapeutic decisions in clinical practice. Sodium-glucose cotransporter 2 inhibitors and glucagon-like peptide-1 receptor agonists in combination therapy are a promising therapeutic duo and are expected to influence future guidelines and decision-making in everyday clinical practice.

Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide, characterized by hyperglycemia and insulin resistance (IR). Its escalating global prevalence and the associated morbidity and mortality render it a major public health concern. Conventional glucose- lowering therapies frequently entail adverse effects, hypoglycaemia risk, and fail to arrest disease progression. Emerging evidence positions the gut microbiota as a central regulator of glucose homeostasis and insulin sensitivity, suggesting that gut microbiota might be a promising target for T2DM. This review synthesizes current knowledge of microbiota-driven mechanisms, particularly those of the gut microbiota and their metabolites, that precipitate or exacerbate T2DM. It then critically evaluates microbiota-targeted interventions (dietary modulation, probiotics, prebiotics, antibiotic therapy, and fecal microbiota transplantation) as emerging therapeutic or adjunctive strategies to restore glycaemic control by modulating the gut microbial ecosystem. While clinical validation is incomplete, targeting the gut microbiota represents a promising avenue for both prevention and treatment of T2DM.

Insulin, secreted by pancreatic β-cells, regulates blood glucose levels. Insulin resistance (IR), characterized by diminished cellular responsiveness, increases insulin demand, imposing stress on β-cells. This leads to β-cell decompensation, which contributes to the development of type 2 diabetes (T2D). A growing body of evidence connects early-life exposures, such as low birth weight (LBW), to a heightened risk of developing non-communicable diseases (NCDs) such as T2D in adulthood. This comprehensive review synthesizes findings from 15 observational studies identified through a PubMed search to explore the specific biological mechanisms that link LBW to IR and T2D. The paper critically examines several prominent hypotheses, theories, and models that propose how endogenous responses to intrauterine conditions initiate a programming that can lead to lasting structural and functional changes in key metabolic organs. In individuals with fetal programming, the combination of impaired insulin sensitivity and compensatory insulin action is considered a precursor to impaired glucose tolerance and T2D, particularly in those who underwent rapid catch-up growth during childhood. Regular monitoring of LBW individuals can enable early intervention, such as lifestyle changes, to reduce the risk of IR and T2D. However, improving the early environment by providing care for women of reproductive age, especially during pregnancy, is a cost-effective strategy to address LBW and curb the NCD pandemic.

Background: Gestational diabetes mellitus (GDM) affects almost 10%-12% of pregnancies worldwide, threatening maternal and fetal life. Continuous glucose monitoring (CGM) forms the backbone of managing GDM, and the current methodologies largely disregard physiological and behavioral factors, thereby greatly reducing accuracy and clinical interpretability.

Methods: A hybrid deep learning framework was developed by fusing CGM with multi-sensing modality data, including heart rate, activity levels, sleep patterns, and dietary intake. For data preprocessing, Kalman filtering was applied for temporal alignment, adaptive normalization provided outlier handling and imputation, while the CNN-BiLSTM backbone with attention was harnessed for feature extraction. A Multi-Task Attention Fusion Network (MTAFN) was used to predict glucose values and classify GDM risk simultaneously, while SHAP and dynamic smoothing contributed to interpretability sets.

Results: The framework was validated on an extended OhioT1DM dataset with adaptations for pregnancy. It reached a glucose prediction RMSE of 9.8 mg/dL and a GDM risk classification accuracy of 93%. Compared to competitive approaches, the present solution attained a 25% better accuracy on interpretability and an improvement in sensitivity and specificity of about 4-6% across various physiological conditions.

Discussion: The use of multi-sensing data increased prediction robustness by capturing complex physiological dependencies. The SHAP-based interpretability justified the predictions through a physiological lens. With an attention mechanism for feature weighting, it was possible to identify crucial variables like meal intake and nighttime variability in the workflow sets.

Conclusion: The hybrid framework proposed here is reliable for clinically interpretable continuous glucose monitoring and GDM risk predictions. Its application with high reliability can lead to integrating it within clinical protocols for real-time maternal care sets.

Diabetic Foot Ulcer (DFU) is a serious and chronic complication of uncontrolled diabetes, significantly increasing the risk of amputation and mortality in diabetic patients. Conventional wound healing techniques often fail to manage chronic wounds in DFU due to several limitations, which eventually raises the need for advanced, innovative, and efficient treatment strategies for the better management of DFU. Many novel interventions, such as growth factor therapy, stem cell therapy, gene therapy, nanotechnology, bioengineered skin substitutes, 3D-bioprinting, and regenerative medicine, have shown promising roles in wound healing and tissue regeneration, suggesting their potential implications in the treatment and control of DFU. An integrated and multidisciplinary approach was proven to be a promising option for rapid and effective DFU management, eventually reducing the financial burden on the patients and healthcare system. Besides, AI-- driven medical technologies were found to support the healthcare system for the prevention, prediction, diagnosis, and personalized treatment of DFU. The present review article provides a brief overview of DFU and its pathophysiology. It highlights traditional DFU treatment strategies, their limitations, and focuses on emerging innovative strategies, emphasizing their potential for addressing DFU. Moreover, it sheds light on challenges and future research areas of these emerging interventions.

This work overviews some complex molecular interactions and phosphorylation events in the insulin receptor (IR) signaling pathway and explains its central role in metabolic control, which starts from the synthesis and secretion of insulin by pancreatic β-cells under elevated blood glucose. The triggered pathway coordinates a cascade of molecular processes that results in the activation of primary metabolic functions. Insulin bound to its receptor starts a sequence of events, such as the autophosphorylation of the receptor β subunit for initiating downstream signaling cascades, glycogen synthesis, and the appropriate regulation of lipid metabolism. The complexity and specificity of the signaling pathway involve insulin receptor substrates, phosphatidylinositol-3-kinase (PI3K), and protein kinase B (PKB). A detailed molecular interaction analysis in the IR has pointed to the crucial role of some residues and structural elements necessary for enzymatic functionalities and substrate binding. These factors include the kinase domain of the IR with specific amino acid residues, and subsequent activation of downstream signaling proteins. The structural changes on phosphorylation promote the binding of SH2 domain-containing adaptor proteins, which lead to the initiation of multifunctional signaling complexes central to insulin signal transduction. These molecular mechanisms provide insight into pathophysiology relating to metabolic diseases and potential treatment targets. This review aims an understanding of insulin receptor operation, elucidating the molecular intricacies behind the eventful metabolic insulin signaling pathways and highlighting possible research and therapeutic development in the field of medicine.

Introduction: Diabetes and sarcopenia are major age-related health issues in the world. Due to their bidirectional relationship, they significantly impact the quality of life of elderly men and women, especially those over 60 years old. In this brief communication, we incorporate the effect of sarcopenia into a previously developed mathematical model examining the impact of exercise on the dynamics of glucose and insulin.

Methods: Extending a previous mathematical model by Derouich and Boutayeb, derived from the minimal model of Bergman, we present a new mathematical model using ordinary differential equations in which the parameter "S" is included to express the additive effect of sarcopenia.

Results: Considering that the sarcopenia effect is introduced multiplicatively, the new model proposed shows that sarcopenia lowers insulin sensitivity both in the presence and absence of physical exercise. The effects of sarcopenia on glucose dynamics are illustrated by simulations with varying model parameters.

Discussion: A large number of clinical studies have shown the link between Type 2 diabetes and sarcopenia. Some authors have particularly explored the causal relationship between insulin resistance and sarcopenia. The proposed mathematical model indicates that sarcopenia reduces insulin sensitivity in both the presence and absence of physical exercise, and that severe sarcopenia may negate the benefits of physical exercise.

Conclusion: By theoretically demonstrating the relationship between sarcopenia and Type 2 diabetes, this mathematical model confirms the interrelationship between sarcopenia and Type 2 diabetes for any population worldwide, regardless of its regional, cultural, or environmental specificity.

Bullous pemphigoid (BP) is an autoimmune blistering disease that especially presents in elderly patients, but recently, its incidence has increased in patients treated with inhibitors of dipeptidyl peptidase-4 (DPP-4), among which teneligliptin is widely prescribed as an antidiabetic drug for the treatment of type 2 diabetes mellitus (T2DM). Recent studies describe the association of teneligliptin with the onset of BP, hypothesizing that DPP-4 inhibition could induce immune dysregulation able to trigger autoimmune responses against skin antigens BP180 and BP230. This mini-review discusses the immunomodulatory effects of teneligliptin, immune responses, and chronic inflammation associated with diabetes that predispose patients to BP. It also discusses the clinical implications, such as monitoring for BP in T2DM patients on teneligliptin therapy. Elucidation of this relationship may help in optimizing management strategies by highlighting discontinuation or alternative therapies in the case of a high risk of development of BP.

Introduction: Globally, type 2 diabetes mellitus (T2DM) is a common metabolic disorder affecting millions of people annually. Metformin, a prevalent prescribed antihyperglycemic medication for T2DM, has been associated with vitamin B12 deficiency. This study aimed to determine the prevalence of vitamin B12 deficiency in T2DM patients receiving metformin.

Methods: This retrospective record review study was based on T2DM patients receiving metformin at a single tertiary healthcare center. The prevalence of vitamin B12 deficiency is defined as a serum level <145 pmol/L. Statistical analysis assessed the association between vitamin B12 deficiency and metformin usage.

Results: A total of 246 T2DM patients were included in the study. Among patients who used metformin, 7.7% were found to have vitamin B12 deficiency compared to 4.8% among those who did not use metformin, while the difference was not statistically significant (p=0.571). However, the median (IQR) level of vitamin B12 among metformin users (296 (186)) was significantly lower than that among patients who do not use metformin (382 (370)), p=0.001.

Discussion: The study's findings shed light on the important role of routine screening of vitamin B12 levels in patients on metformin, especially those on long-term use, for early identification and management of deficiency, leading to improved patient outcomes.

Conclusion: Our study revealed a significantly lower level of vitamin B12 among metformin users in T2DM patients. However, the prevalence of vitamin B12 deficiency among metformin users did not differ significantly from those who do not use metformin.