Regulation Of Glucose Levels Research Articles

Molecular module for glucose production influences sex pheromone synthesis in Bactrocera dorsalis

Some insects have evolved beneficial relationships with intestinal microbes for sex pheromone production to communicate with conspecifics effectively. However, it is not clear whether the sex pheromone synthesis activity of intestinal microbes can be controlled by the host, and the molecular mechanisms need to be further unraveled. In this study, we find that rectal gland Bacillus species of male Bactrocera dorsalis specifically produce sex pheromones in the evening, which is significantly associated with glucose levels. Invitro Bacillus culture assays show that glucose levels significantly influence the amount of sex pheromone produced. Comparative rectal gland transcriptome analysis reveals that the expressions of the alpha-galactosidase gene (GLA), a Bactrocera dorsalis transcription factor (BDTF), and a pigment-dispersing factor (PDF) are responsible for producing glucose. Our findings reveal that the PDF-BDTF-GLA module influences the intestinal-microbe-produced sex pheromone by regulating glucose levels and advance our understanding of interactions between insects and their intestinal microbes.

Injectable Multifunctional Hyaluronan based Hydrogel Suppressing the Excessive Glucose and Reactive Oxygen Species in Diabetic Wound Treatment

In diabetic wounds, the overlapping presence of excessive glucose and reactive oxygen species (ROS) forming a vicious cycle that severely impedes the wound healing process. Despite advancements in wound care, current treatments often limit in addressing these two critical factors simultaneously. To address these challenges, this study introduces a multifunctional hydrogel system capable of dual regulation of excessive glucose and ROS levels in a hyperglycemic environment, while also provide a platform with favorable properties that support wound healing. First, by modifying hyaluronic acid (HA) chains with vinyl sulfone and thiol functional groups, the resulting hydrogel exhibited tunable gelation time, elastic modulus, and degradation rates, making it adaptable for diabetic wound management. Notably, this hydrogel allows for precise glucose and ROS regulation by encapsulating glucose oxidase (GOx), horseradish peroxidase (HRP), and tannic acid (TA) within the HA hydrogel matrix. It was verified that the hydrogels could reduce the glucose levels to desired concentration by varying the encapsulated GOx content. Simultaneously, the combined ROS-scavenging effect of HRP and TA effectively addressed the excessive ROS problem. Specifically, H2O2 generated from the GOx-glucose reaction was consumed in the HRP-mediated polymerization of TA, and free radicals (OH•, DPPH) were scavenged up to 70% by TA. Due to the glucose and ROS regulation properties, this hydrogel system was able to promote the proliferation and migration of human dermal fibroblast in a hyperglycemic environment. Overall, this study offers a simple and effective approach to regulate the excessive levels of glucose and ROS in a hyperglycemic condition, which has potential in creating a multifunctional platform for diabetic wound treatment.

CARBOHYDRATE METABOLISM IN BLOOD DONORS

Objective: This study investigates the effects of blood donation on carbohydrate metabolism and examines dietary strategies to support donor health. Blood donation is vital for healthcare but can temporarily disrupt glucose levels, potentially causing symptoms like fatigue and dizziness, particularly in donors susceptible to blood sugar fluctuations. Method: The research integrates a review of WHO guidelines, an analysis of recent studies on carbohydrate metabolism in blood donors, and the development of specific nutritional recommendations to support recovery. The WHO guidelines offer foundational insights into safe donation practices, while scientific research provides data on glucose regulation and recovery needs. Results: Findings reveal that complex carbohydrates before donation stabilize glucose levels, while fast-absorbing carbohydrates after donation rapidly restore energy, reducing symptoms associated with blood sugar dips. Regular donation may also benefit individuals with high carbohydrate intake by regulating glucose levels and reducing disease risks. Novelty: This study uniquely combines WHO recommendations with recent scientific insights to provide a practical, evidence-based dietary framework specifically tailored for blood donors, addressing both donor safety and physiological recovery. This approach emphasizes the importance of carbohydrate type and timing, offering a nuanced perspective for dietary management in donation contexts, and underscores the need for future research on personalized nutrition strategies for optimal donor health.

Deep quantification of substrate turnover defines protease subsite cooperativity

Substrate specificity determines protease functions in physiology and in clinical and biotechnological applications, yet quantitative cleavage information is often unavailable, biased, or limited to a small number of events. Here, we develop qPISA (quantitative Protease specificity Inference from Substrate Analysis) to study Dipeptidyl Peptidase Four (DPP4), a key regulator of blood glucose levels. We use mass spectrometry to quantify >40,000 peptides from a complex, commercially available peptide mixture. By analyzing changes in substrate levels quantitatively instead of focusing on qualitative product identification through a binary classifier, we can reveal cooperative interactions within DPP4’s active pocket and derive a sequence motif that predicts activity quantitatively. qPISA distinguishes DPP4 from the related C. elegans DPF-3 (a DPP8/9-orthologue), and we relate the differences to the structural features of the two enzymes. We demonstrate that qPISA can direct protein engineering efforts like the stabilization of GLP-1, a key DPP4 substrate used in the treatment of diabetes and obesity. Thus, qPISA offers a versatile approach for profiling protease and especially exopeptidase specificity, facilitating insight into enzyme mechanisms and biotechnological and clinical applications.

Engineered tools to study endocrine dysfunction of pancreas.

Pancreas, a vital organ with intricate endocrine and exocrine functions, is central to the regulation of the body's glucose levels and digestive processes. Disruptions in its endocrine functions, primarily regulated by islets of Langerhans, can lead to debilitating diseases such as diabetes mellitus. Murine models of pancreatic dysfunction have contributed significantly to the understanding of insulitis, islet-relevant immunological responses, and the optimization of cell therapies. However, genetic differences between mice and humans have severely limited their clinical translational relevance. Recent advancements in tissue engineering and microfabrication have ushered in a new era of in vitro models that offer a promising solution. This paper reviews the state-of-the-art engineered tools designed to study endocrine dysfunction of the pancreas. Islet on a chip devices that allow precise control of various culture conditions and noninvasive readouts of functional outcomes have led to the generation of physiomimetic niches for primary and stem cell derived islets. Live pancreatic slices are a new experimental tool that could more comprehensively recapitulate the complex cellular interplay between the endocrine and exocrine parts of the pancreas. Although a powerful tool, live pancreatic slices require more complex control over their culture parameters such as local oxygenation and continuous removal of digestive enzymes and cellular waste products for maintaining experimental functionality over long term. The combination of islet-immune and slice on chip strategies can guide the path toward the next generation of pancreatic tissue modeling for better understanding and treatment of endocrine pancreatic dysfunctions.

Stimulation of kappa opioid receptors in the nucleus accumbens promotes feeding behavior in mice: Acute restoration of feeding during anorexia induced by 5-fluorouracil

Though μ and δ opioid receptors are reported to regulate energy homeostasis, any role for κ opioid receptors in these processes remains unclear. The present study investigated the role of κ opioid receptors in regulation of feeding behavior and plasma glucose levels using nalfurafine, a κ opioid receptor agonist used clinically. Systemic injection of nalfurafine increased food intake under non-fasted conditions, but not after food deprivation, and this effect was inhibited by the κ opioid receptor antagonist norbinaltorphimine. In contrast, nalfurafine did not affect plasma glucose levels. I.c.v. injection of nalfurafine increased food intake, whereas systemic injection of nalfurafine methiodide, which does not penetrate the blood brain barrier, was without effect. In addition, nalfurafine tended to increase preproorexin mRNA in the hypothalamus. However, neither the orexin OX1 receptor antagonist YNT-1310 nor the non-selective orexin receptor antagonist suvorexant inhibited the increase in food intake induced by nalfurafine. While nalfurafine injected into the lateral hypothalamus did not affect food intake, nalfurafine injected into the nucleus accumbens increased food intake, which was inhibited by norbinaltorphimine. Finally, we examined the effect of nalfurafine on anorexia induced by the anti-cancer agent 5-fluorouracil. Reduced food intake at 2 days following 5-fluorouracil administration was alleviated across the first 3 h following daily injection of nalfurafine, though daily food intake was not influenced. These results indicate that nalfurafine promotes feeding behavior through stimulation of κ opioid receptors in the nucleus accumbens and may be a candidate for reducing anorexia due to anti-cancer agents.

Estimation of Meal-Time Insulin Based on Glycemic Load versus Carbohydrate Counting among Patients with Type 1 Diabetes Using Insulin Pump

Abstract Background Dietary carbohydrates have a major effect on postprandial glycemic response. Therefore, the current guidelines recommend the usage of insulin/carbohydrate ratio for calculation of prandial insulin dose based on the carbohydrate count in a given meal. However, some studies pointed to the importance of the quality of carbohydrates, as reflected by their glycemic index, in addition to their quantity on the regulation of postprandial glucose level. Objectives To identify a safe, feasible and effective method for calculation of prandial insulin dose based on the glycemic load of a meal. This could minimize postprandial glycemic variability in type 1 diabetic patients. Patients and Methods Our study included 15 type 1 diabetic participants; their ages ranged from 8 to 15 years. The participants were given a breakfast with the same amount of fat, protein and carbohydrates, which was prepared similarly in all studied patients. Sequence, quality and amounts of meals consumed during the first week of the study were replicated during the second week. Calculation of prandial insulin doses using one regimen for 1 week and a crossover to the other regimen for an additional week was done. A detailed medical history was collected, including the age of onset of diabetes, disease duration, and symptoms of diabetic complications. Results Blood glucose postprandial excursions was significantly lower during the glycemic load counting (GLC) than the carbohydrate counting (CC) period from baseline to 120 min (-10.20 ± 8.18 vs 8.47 ± 6.65 mg/dl, respectively, p = < 0.001), baseline to 180 min (-11.80 ± 8.16 vs 5.13 ± 7.01 mg/dl, respectively, p = < 0.001) and baseline to 240 min (-9.60 ± 6.07 vs -0.53 ± 7.31 mg/dl, respectively, p = 0.007). However, there was no postprandial glucose difference between the two periods from baseline to 60 min (-2.87 ± 8.09 vs 2.53 ± 7.76 mg/dl, respectively, p = 0.083). Conclusion The data from this study showed that glycemic load counting for prandial insulin doses is a feasible and effective method in short term glucose control.

Cu–N–C single-atom nanozyme as an ultrasensitive sensing platform for α-glucosidase detection

Alpha-glucosidase (α-Glu) is a hydrolase that promotes the rise of glucose in the blood during the digestion process, and it plays a crucial role in regulating glucose levels within a normal range. Herein, we developed an ultrasensitive colorimetric platform by preparing a Cu–N–C single-atom nanozyme (Cu–N–C SAzyme) with a potent oxidase-like effect on accurately detection of α-Glu and efficient screening of its potential inhibitors. This artificial nanoenzyme was able to catalyze the oxidation of colorless 3,3′,5,5′-tetramethylbenzidine (TMB) to blue oxide (oxTMB) without the assistance of H2O2. In addition, with the participation of α-Glu, l-ascorbic acid-2-O-α-d-glucopyranose (AAG) can be catalyzed to produce ascorbic acid (AA), which significantly reduces the oxidation, resulting in a noticeable fading of the blue color. Therefore, we designed a straightforward colorimetric test for α-Glu activity, achieving detection limits as low as 0.09 U/L and a linear response from 0.25 to 8 U/L. Most importantly, this platform has been effectively applied to measure α-Glu in real samples.

Low-intensity pulsed ultrasound ameliorates insulin resistance in type 2 diabetes mice via promoting glucagon-like peptide-1 release

Abstract Glucagon-like peptide-1 (GLP-1) is a hormone secreted by intestinal L-cells. It regulates glucose levels by boosting insulin secretion, inhibiting glucagon release, and preventing β-cell death. GLP-1 is increasingly used in managing type 2 diabetes mellitus (T2DM). This study assessed the effectiveness of low-intensity pulsed ultrasound (LIPUS), a non-pharmacological intervention, in enhancing insulin resistance in diabetic mice by stimulating GLP-1 release. T2DM was induced in C57BL/6J mice through a high-fat diet and streptozotocin injection. Mice were divided into Control, T2D-sham and T2D-LIPUS groups. The T2D-LIPUS group received LIPUS treatment with a frequency of 1MHz, intensity of 120mW/cm2, and duty cycle of 20%for 20 minutes/day, 5 days/week for 4 weeks. Glucose tolerance and insulin resistance were measured through tests. Pancreatic histology and GLP-1 expression in serum were evaluated. Results showed that T2DM increased insulin resistance, but LIPUS treatment alleviated it. GLP-1 levels significantly increased in the T2D-LIPUS group compared to the T2D-sham group, approaching the control group’s level. LIPUS also reduced apoptosis of islet β cells. These findings suggest that LIPUS stimulation of the intestine can enhance islet β-cell activity through GLP-1 regulation of the gut-pancreas axis, mitigating insulin resistance in T2DM.

Authentication of the shelf-life of NPH injectable insulins samples using NIR and MS spectral fingerprints

Insulin is essential for regulating glucose levels, and its hormonal deficiency leads to diabetes. Treatment involves the use of different types of insulin tailored to individual needs. Properly stored and transported Neutral Protamine Hagedorn (NPH) insulin remains effective and stable, highlighting the importance of quality control to ensure its efficacy and patient safety. This study aims to develop an analytical method to evaluate the shelf-life of NPH injectable insulin samples while preserving packaging integrity. The approach consisted of analyzing intact insulin samples, with and without expired shelf-life dates, using near-infrared spectroscopy (NIR) obtained from two instruments: a benchtop and a portable device. These measurements were coupled with chemometric methods, specifically single-class classification algorithms. The classifiers considered were Data Driven-Soft Independent Modeling of Class Analogy (DD-SIMCA) and One-Class Partial Least Squares (OC-PLS). For benchtop NIR, the DD-SIMCA method, with Savitzky-Golay smoothing preprocessing (41-point window) and baseline offset (BO), achieved excellent results, reaching 100% sensitivity, specificity, and efficiency in both training and test sets. As for portable NIR, the most effective methods were DD-SIMCA and OC-PLS, using datasets preprocessed with Savitzky-Golay smoothing with first derivative, second-order polynomial (SGD-1st-2nd), and 9-point windows combined with Standard Normal Variate (SNV), and Savitzky-Golay smoothing filters (SGS) using second-order polynomial and 7-point windows combined with baseline offset (BO) and Multiplicative Scattering Correction (MSC). The results were corroborated by mass spectrometry, correlating the structural changes of degraded insulin with NIR data. The proposed methodology is a promising tool for non-destructive, rapid, and cost-effective authentication of the preservation state of NPH insulin, aligning with green chemistry principles and allowing for in-situ evaluation, thereby preserving medication integrity.

Nuclear Receptor Corepressors NCOR1 and SMRT Regulate Metabolism via Intestinal Regulation of Carbohydrate Transport.

Nuclear receptor action is mediated in part by the nuclear receptor corepressor 1 (NCOR1) and the silencing mediator of retinoic acid and thyroid hormone receptor (SMRT). NCOR1 and SMRT regulate metabolic pathways that govern body mass, insulin sensitivity, and energy expenditure, representing an understudied area in the realm of metabolic health and disease. Previously, we found that NCOR1 and SMRT are essential for maintaining metabolic homeostasis and their knockout (KO) leads to rapid weight loss and hypoglycemia, which is not survivable. Because of a potential defect in glucose absorption, we sought to determine the role of NCOR1 and SMRT specifically in intestinal epithelial cells (IECs). We used a postnatal strategy to disrupt NCOR1 and SMRT throughout IECs in adult mice. These mice were characterized metabolically and underwent metabolic phenotyping, body composition analysis, and glucose tolerance testing. Jejunal IECs were isolated and profiled by bulk RNA sequencing. We found that the postnatal KO of NCOR1 and SMRT from IECs leads to rapid weight loss and hypoglycemia with a significant reduction in survival. This was accompanied by alterations in glucose metabolism and activation of fatty acid oxidation in IECs. Metabolic phenotyping confirmed a reduction in body mass driven by a loss of body fat without altered food intake. This appeared to be mediated by a reduction of key intestinal carbohydrate transporters, including SGLT1, GLUT2, and GLUT5. Intestinal NCOR1 and SMRT act in tandem to regulate glucose levels and body weight. This in part may be mediated by regulation of intestinal carbohydrate transporters.

A multifunctional injectable, self-healing, and adhesive hydrogel-based wound dressing stimulated diabetic wound healing with combined reactive oxygen species scavenging, hyperglycemia reducing, and bacteria-killing abilities

The proficient handling of diabetic wounds, a rising issue coinciding with the global escalation of diabetes cases, poses significant clinical difficulties. A range of biofunctional dressings have been engineered and produced to expedite the healing process of diabetic wounds. This study proposes a multifunctional hydrogel dressing for diabetic wound healing, which is composed of Polyvinyl Alcohol (PVA) and N1-(4-boronobenzyl)-N3-(4-boronophenyl)-N1, N1, N3, N3-teramethylpropane-1, 3-diaminium (TSPBA), and a dual-drug loaded Gelatin methacryloyl (GM) microgel. The GM microgel is loaded with sodium fusidate (SF) and nanoliposomes (LP) that contain metformin hydrochloride (MH). Notably, adhesive and self-healing properties the hydrogel enhance their therapeutic potential and ease of application. In vitro assessments indicate that SF-infused hydrogel can eliminate more than 98% of bacteria within 24 h and maintain a sustained release over 15 days. Additionally, MH incorporated within the hydrogel has demonstrated effective glucose level regulation for a duration exceeding 15 days. The hydrogel demonstrates a sustained ability to neutralize ROS throughout the entire healing process, predominantly by electron donation and sequestration. This multifunctional hydrogel dressing, which integrated biological functions of efficient bactericidal activity against both MSSA and MRSA strains, blood glucose modulation, and control of active oxygen levels, has successfully promoted the healing of diabetic wounds in rats in 14 days. The hydrogel dressing exhibited significant effectiveness in facilitating the healing process of diabetic wounds, highlighting its considerable promise for clinical translation.Graphical

Metabolism and diabetes in Ramadan fasting: Exploring health trends and relationships through systematic literature network analysis.

Ramadan fasting is widely acknowledged for its positive impacts on health, yet it also presents inherent risks, prompting a need for comprehensive exploration into its metabolic implications and its effects on diabetes. This study introduces a novel methodology called systematic literature network analysis (SLNA), which merges bibliometric analysis with systematic literature review (SLR). The aim of this study was to examine the global research landscape concerning Ramadan fasting, metabolism, and diabetes. Through the systematic search strategy, 206 relevant documents were analyzed. Through co-occurrence analysis mapping, the study uncovered four distinct cluster groups, revealing intricate relationships and evolving trends within the field. Moreover, the trajectory of research publications on Ramadan fasting from 2001 to 2023 was tracked, highlighting a growing interest in this domain. The bibliometric analysis emphasized a consensus regarding the beneficial effects of Ramadan fasting on individual health, particularly in improving lipid profiles, managing body weight, regulating glucose levels, and nutrient intake. However, significant variations in research focus were observed across predominantly Muslim countries, with notable exceptions like Indonesia and Brunei Darussalam absent among the top contributors. Furthermore, the analysis shed light on the balanced selection of research subjects by authors, indicating a nuanced approach to exploring the multifaceted aspects of Ramadan fasting, metabolism, and diabetes. These findings offer significant perspectives for researchers aiming to contextualize their studies within the wider conversation on this subject, thereby aiding in a more profound comprehension of the intricate relationship between fasting, metabolic functions, and the management of diabetes.

Pancreatic stellate cells support human pancreatic β-cell viability in vitro and enhance survival of immunoisolated human islets exposed to cytokines

Pancreatic islet transplantation is proposed as a cure for type 1 diabetes mellitus (T1D). Despite its success in optimal regulation of glucose levels, limitations in longevity of islet grafts still require innovative solutions. Inflammatory stress post-transplantation and loss of extracellular matrix attribute to the limited β-cell survival. Pancreatic stellate cells (PSCs), identified as pancreatic-specific stromal cells, have the potential to play a crucial role in preserving islet survival. Our study aimed to determine the effects of PSCs co-cultured with human CM β-cells and human islets under inflammatory stress induced by a cytokine cocktail of IFN-γ, TNF-α and IL-1β. Transwell culture inserts were utilized to assess the paracrine impact of PSCs on β-cells, alongside co-cultures enabling direct interaction between PSCs and human islets. We found that co-culturing PSCs with human CM β-cells and human cadaveric islets had rescuing effects on cytokine-induced stress. Effects were different under normoglycemic and hyperglycemic conditions. PSCs were associated with upregulation of β-cell mitochondrial activity and suppression of inflammatory gene expression. The rescuing effects exist both in indirect and direct co-culture methods. Furthermore, we tested whether PSCs have rescuing effects on human islets in conventional alginate-based microcapsules and in composite microcapsules composed of alginate-pectin collagen type IV, laminin sequence RGD, Nec-1, and amino acid. PSCs partially prevented cytokine-induced stress in both systems, but beneficial effects were stronger in composite capsules. Our findings show novel effects of PSCs on islet health. Islets and PSCs coculturing or co-transplantation might mitigate the inflammation stress and improve islet transplantation outcomes.

Anthocyanins and Type 2 Diabetes: An Update of Human Study and Clinical Trial.

Anthocyanins are phenolic compounds occurring in fruits and vegetables. Evidence from pre-clinical studies indicates their role in glucose level regulation, gut microbiota improvement, and inflammation reduction under diabetic conditions. Therefore, incorporating these research advancements into clinical practice would significantly improve the prevention and management of type 2 diabetes. This narrative review provides a concise overview of 18 findings from recent clinical research published over the last 5 years that investigate the therapeutic effects of dietary anthocyanins on diabetes. Anthocyanin supplementation has been shown to have a regulatory effect on fasting blood glucose levels, glycated hemoglobin, and other diabetes-related indicators. Furthermore, increased anthocyanin dosages had more favorable implications for diabetes treatment. This review provides evidence that an anthocyanin-rich diet can improve diabetes outcomes, especially in at-risk groups. Future research should focus on optimal intervention duration, consider multiple clinical biomarkers, and analyze anthocyanin effects among well-controlled versus poorly controlled groups of patients with diabetes.

A nutrient responsive lipase mediates gut-brain communication to regulate insulin secretion in Drosophila

Pancreatic β cells secrete insulin in response to glucose elevation to maintain glucose homeostasis. A complex network of inter-organ communication operates to modulate insulin secretion and regulate glucose levels after a meal. Lipids obtained from diet or generated intracellularly are known to amplify glucose-stimulated insulin secretion, however, the underlying mechanisms are not completely understood. Here, we show that a Drosophila secretory lipase, Vaha (CG8093), is synthesized in the midgut and moves to the brain where it concentrates in the insulin-producing cells in a process requiring Lipid Transfer Particle, a lipoprotein originating in the fat body. In response to dietary fat, Vaha stimulates insulin-like peptide release (ILP), and Vaha deficiency results in reduced circulatory ILP and diabetic features including hyperglycemia and hyperlipidemia. Our findings suggest Vaha functions as a diacylglycerol lipase physiologically, by being a molecular link between dietary fat and lipid amplified insulin secretion in a gut-brain axis.

From Gut to Glucose: A Comprehensive Review on Functional Foods and Dietary Interventions for Diabetes Management.

In the realm of diabetes research, considerable attention has been directed toward elucidating the intricate interplay between the gastrointestinal tract and glucose regulation. The gastrointestinal tract, once exclusively considered for its role in digestion and nutrient assimilation, is presently acknowledged as a multifaceted ecosystem with regulatory supremacy over metabolic homeostasis and glucose metabolism. Recent studies indicate that alterations in the composition and functionality of the gut microbiota could potentially influence the regulation of glucose levels and glucose homeostasis in the body. Dysbiosis, characterized by perturbations in the equilibrium of gut microbial constituents, has been irrevocably linked to an augmented risk of diabetes mellitus (DM). Moreover, research has revealed the potential influence of the gut microbiota on important factors, like inflammation and insulin sensitivity, which are key contributors to the onset and progression of diabetes. The key protagonists implicated in the regulation of glucose encompass the gut bacteria, gut barrier integrity, and the gut-brain axis. A viable approach to enhance glycemic control while concurrently mitigating the burden of comorbidities associated with diabetes resides in the strategic manipulation of the gut environment through adapted dietary practices. This review aimed to provide a deep understanding of the complex relationship between gut health, glucose metabolism, and diabetes treatment. This study has presented an exhaustive overview of dietary therapies and functional foods that have undergone extensive research to explore their potential advantages in the management of diabetes. It looks into the role of gut health in glucose regulation, discusses the impact of different dietary elements on the course of diabetes, and evaluates how well functional foods can help with glycemic control. Furthermore, it investigates the mechanistic aspects of these therapies, including their influence on insulin sensitivity, β-cell activity, and inflammation. It deliberates on the limitations and potential prospects associated with integrating functional foods into personalized approaches to diabetes care.

Morin-Based Nanoparticles for Regulation of Blood Glucose.

Morin, a naturally occurring bioactive compound shows great potential as an antioxidant, anti-inflammatory agent, and regulator of blood glucose levels. However, its low water solubility, poor lipid solubility, limited bioavailability, and rapid clearance in vivo hinder its application in blood glucose regulation. To address these limitations, we report an enzymatically synthesized nanosized morin particle (MNs) encapsulated in sodium alginate microgels (M@SA). This approach significantly enhances morin's delivery efficiency and therapeutic efficacy in blood glucose regulation. Utilizing horseradish peroxidase, we synthesized MNs averaging 305.7 ± 88.7 nm in size. These MNs were then encapsulated via electrohydrodynamic microdroplet spraying to form M@SA microgels. In vivo studies revealed that M@SA microgels demonstrated prolonged intestinal retention and superior efficacy compared with unmodified morin and MNs alone. Moreover, MNs notably improved glucose uptake in HepG2 cells. Furthermore, M@SA microgels effectively regulated blood glucose, lipid profiles, and oxidative stress in diabetic mice while mitigating liver, kidney, and pancreatic damage and enhancing anti-inflammatory responses. Our findings propose a promising strategy for the oral administration of natural compounds for blood glucose regulation, with implications for broader therapeutic applications.

Frequency of missed doses and its effects on the regulation of glucose levels in patients with type 2 diabetes: A retrospective analysis.

This study aimed to investigate the association between medication adherence to oral hypoglycemic agents (OHAs) and HbA1c levels in patients with type 2 diabetes mellitus (T2DM) for more than 48 weeks, as well as the factors affecting long-term adherence to OHAs. This retrospective study included 83 patients who had been receiving OHAs for T2DM for ≥48 weeks. Medication adherence values (MAVs) were calculated using the following formula: (total prescription days - prescription days of OHAs brought at admission)/(days from the initiation of OHAs to hospitalization). We assessed the association between HbA1c and MAVs using the Jonckheere-Terpstra test. Furthermore, we examined the association between patient- and medication-related factors and MAVs affecting HbA1c levels. Based on the results, MAVs were categorized as MAV ≤0.86 and MAV >0.86, and factors affecting MAVs were analyzed. Logistic regression analysis revealed that the total number of medications, the number of nonhypoglycemic agents, and a family history of diabetes were independent determinants of MAV ≤0.86 (P < .05). Multiple regression analyses indicated that the number of dosages per day and the timing of OHA administration at lunch were independent determinants of lower MAVs (P < .05). Our findings suggest that poor medication adherence is associated with elevated HbA1c levels in T2DM patients. Independent factors contributing to poor adherence include a lower number of prescribed medications, fewer nonhypoglycemic agents, no family history, a higher daily dosage frequency, and the administration of OHAs at lunch.

Unraveling Light-Activated Insulin Action in Regulating Blood Glucose: New Photoactivatable Insight as a Novel Modality in Diabetes Management.

Diabetes, particularly type 2 diabetes (T2D), is the main component of metabolic syndrome. It is highly prevalent and has drastically increased with sedentary lifestyles, notably behaviors linked to ease of access and minimal physical activity. Central to this condition is insulin, which plays a pivotal role in regulating glucose levels in the body by aiding glucose uptake and storage in cells, and what happens to diabetes? In diabetes, there is a disruption and malfunction in insulin regulation. Despite numerous efforts, effectively addressing diabetes remains a challenge. This article explores the potential of photoactivatable drugs in diabetes treatment, with a focus on light-activated insulin. We discuss its advantages and significant implications. This article is expected to enrich the existing literature substantially, offering a comprehensive analysis of potential strategies for improving diabetes management. With its minimal physical intrusion, light-activated insulin promises to improve patient comfort and treatment adherence. It offers precise regulation and localized impact, potentially mitigating the risks associated with conventional diabetes treatments. Additionally, light-activated insulin is capable of explicitly targeting RNA and epigenetic factors. This innovative approach may pave the way for more personalized and effective diabetes treatments, addressing not only the symptoms but also the underlying biological causes of the disease. The advancement of light-activated insulin could revolutionize diabetes management. This study represents a pioneering introduction to this novel modality for diabetes management.