Patients newly diagnosed with diabetes mellitus (diabetes), who require insulin must acquire diabetes "survival" skills prior to discharge home. COVID-19 revealed considerable limitations of traditional in-person, time-intensive delivery of diabetes education and survival skills training (diabetes survival skills training). Furthermore, diabetes survival skills training has not been designed to meet the specific learning needs of patients with diabetes and their caregivers, particularly if delivered by telehealth. The objective of the study was to identify and understand the needs of users (patients newly prescribed insulin and their caregivers) to inform the design of a diabetes survival skills training, specifically for telehealth delivery, through the application of user-centered design and adult learning and education principles.

Users included patients newly prescribed insulin, their caregivers, and laypersons without diabetes. In semi-structured interviews, users were asked about experienced or perceived challenges in learning diabetes survival skills. Interviews were audio-recorded and transcribed. Investigators performed iterative rounds of coding of interview transcripts utilizing a constant comparative method to identify themes describing the dominant challenges users experienced. Themes were then mapped to adult learning and education principles to identify novel educational design solutions that can be applied to telehealth-based learning.

We interviewed 18 users: patients (N = 6, 33 %), caregivers (N = 4, 22 %), and laypersons (N = 8, 44 %). Users consistently described challenges in understanding diabetes survival skills while hospitalized; in preparing needed supplies to execute diabetes survival skills; and in executing diabetes survival skills at home. The challenges mapped to three educational strategies: (1) spiral learning; (2) repetitive goal directed practice and feedback, which have the potential to translate into design solutions supporting remote/virtual learning; and (3) form fits function organizer, which supports safe organization and use of supplies to execute diabetes survival skills independently.

Learning complex tasks, such as diabetes survival skills, requires time, repetition, and continued support. The combination of a user-centered design approach to uncover learning needs as well as identification of relevant adult learning and education principles could inform the design of more user-centered, feasible, effective, and sustainable diabetes survival skills training for telehealth delivery.

Diabetes Mellitus develops when the body becomes unable to fuel its cells with glucose, which results in the accumulation of sugar excess in the bloodstream. Because it has diverse pathophysiological impacts on the body, diabetes mellitus represents a significant issue of concern in an attempt to find suitable treatment modalities and medications for afflicted diabetic patients. Glucagon-like peptide 1 (GLP-1) plays a pivotal role in the incretin effect, emerging as a prospective treatment for diabetes mellitus and a promising means of regenerating pancreatic cells, whether directly or through its receptor agonists. It has been shown that GLP-1 efficiently increases insulin production, lowers blood sugar levels in patients with type 2 diabetes mellitus, and decreases appetite, craving, and hunger, therefore amplifying the sensation of fullness and satiety. Moreover, since they are all dependent on GLP-1 effect, intricate signaling pathways share some similarities during specific phases, although the pathways continue to exhibit significant divergence engendered by specific reactions and effects in each organ, which encompasses the rationale behind observed differences. This triggers an expanding range of GLP-1 R agonists, creating new unforeseen research and therapeutic application prospects. This review aims to explain the incretin effect, discuss how GLP-1 regulates blood glucose levels, and how it affects different body organs, as well as how it transmits signals, before introducing selenium's role in the incretin impact.

Hyperglycemia is a common finding in patients presenting to the emergency department (ED). Recommendations addressing uncomplicated hyperglycemia in the ED are limited, and the management of those without a prior diagnosis of diabetes presents a challenge.

This narrative review will discuss the ED evaluation and management of hyperglycemic adult patients without a history of diabetes who do not have evidence of a hyperglycemic crisis, such as diabetic ketoacidosis or hyperosmolar hyperglycemic state.

Many adults who present to the ED have risk factors for diabetes and meet American Diabetes Association (ADA) criteria for diabetes screening. A new diagnosis of type 2 diabetes can be established in the ED by the ADA criteria in patients with a random plasma glucose ≥ 200 mg/dL (11.1 mmol/L) and symptoms of hyperglycemia. The diagnosis should be considered in patients with an elevation in random blood glucose > 140 mg/dL (7.8 mmol/L). Treatment may begin in the ED and varies depending on the presenting severity of hyperglycemia. Treatment options include metformin, long-acting insulin, or deferring for close outpatient management.

Emergency clinician knowledge of the evaluation and management of new-onset hyperglycemia and diabetes is important to prevent long-term complications.

Type 1 diabetes (T1D) is a life-threatening condition for which islet transplantation offers a way to extend longevity and vastly improve quality of life, but the degree and duration of success can vary greatly due to the patient's protective immunity against foreign material. The field is in need of cellular engineering modalities to promote a localized, tolerogenic environment to protect transplanted islet tissue. Artificial antigen-presenting cells (aAPCs) can be designed exogenously to mimic immune cells, such as dendritic cells, and administered to patients, allowing greater control over T cell differentiation. As regulatory T cell (Treg) modulation can reduce the activity of cytotoxic T-effector populations, this strategy can be used to promote immune acceptance of both biomaterials and cellular transplants, such as islets. A new class of poly(lactic-co-glycolic acid) (PLGA) and PLGA/PBAE-blend aAPCs containing transforming growth factor beta and conjugated with anti-CD3 and anti-CD28 antibodies, called tolerogenic aAPCs (TolAPCs), are specifically designed to generate a tolerogenic response by inducing Tregs. We characterized TolAPCs' physical and chemical properties via advanced particle imaging and sizing modalities and investigated their impact on the local and systemic immune system across BALB/c and C57BL/6 mouse strains as well as healthy male and female mice via histologic, gene expression, and immunofluorescence staining methods. Strain-specific differences were observed, whereas sex made no difference in the TolAPC response. TolAPCs stimulated the expansion of FOXP3+ Tregs and provided islet cell protection, maintaining improved glucose-stimulated insulin secretion in vitro when co-cultured with cytotoxic CD8+ T cells. We also explored the ability of this TolAPC platform to promote tolerance in a streptozotocin-induced murine T1D C57BL/6 mouse model. We achieved partial islet protection over the first few days following co-injection with PLGA/PBAE TolAPCs; however, grafts failed soon thereafter. Analysis of the local injection site demonstrated that other immune cell types, including APCs and cytotoxic natural killer cells, increased in the islet injection site. While we aimed to promote a localized tolerogenic microenvironment in vivo using biodegradable TolAPCs to induce Tregs and extend islet transplant durability, further TolAPC improvements will be required to both elongate efficacy and control additional immune cell responders.

One distinguishing feature of the persimmon, that differentiates it from other fruits, is its high proanthocyanidins content, known as persimmon tannin (PT). Despite the poor absorption of PT in the small intestine, results from animal studies demonstrate that PT has many health benefits. Our goal in this review is to summarize the literature that elucidates the relationship between PT structure and activity. In addition, we also summarize the potential mechanisms underlying the health benefits that result from PT consumption; this includes the hypolipidemic, hypoglycemic, antioxidant, anti-inflammatory, antiradiation, antibacterial and antiviral, detoxification effects on snake venom, and the absorption of heavy metals and dyes. Studies show that PT is a structurally distinct proanthocyanidins that exhibits a high degree of polymerization. It is galloylation-rich and possesses unique A-type interflavan linkages in addition to the more common B-type interflavan bonds. Thus, PT is converted into oligomeric proanthocyanidins by depolymerization strategies, including the nucleophilic substitution reaction, acid hydrolysis, and hydrogenolysis. In addition, multiple health benefits exerted by PT mainly involve the inactivation of lipogenic and intracellular inflammatory signaling pathways, activation of the fatty acid oxidation signaling pathway, regulation of gut microbiota, and highly absorptive properties.

Diabetes mellitus is a long-term chronic disease characterized by abnormal high level blood glucose (BG). An artificial closed-loop system that mimics pancreatic β-cells and releases insulin on demand has potential to improve the therapeutic efficiency of diabetes. Herein, a lectin Concanavalin A modified oxidized starch nanogel was designed to regulate glucose dynamically according to different glucose concentrations. The nanogels were formed by double cross-linking the Concanavalin A and glucose units on oxidized starch via specific binding and amide bonds to achieve the high drug loading and glucose responsiveness. The results showed that oxidized starch nanogels prolonged the half-life of antidiabetic peptide drug exenatide and released it in response to high BG concentrations. It could absorb BG at a high level and maintain glucose homeostasis. Besides, the oxidized starch nanogels performed well in recovering regular BG level from hyperglycemia state and maintaining in euglycemia state that fitted in a biological rhythm. In addition, the nanogels showed high biocompatibility in vivo and could improve plasma half-life and therapeutic efficacy of exenatide. Overall, the nanogels protected peptide drugs from degradation in plasma as a glucose-responsive platform showing a high potential for peptide drugs delivery and antidiabetic therapy.

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemia state (HHS) are two life-threatening metabolic complications of diabetes that significantly increase mortality and morbidity. Despite major advances, reaching a uniform consensus regarding the diagnostic criteria and treatment of both conditions has been challenging. A significant overlap between these two extremes of the hyperglycemic crisis spectrum poses an additional hurdle. It has well been noted that a complete biochemical and clinical patient evaluation with timely diagnosis and treatment is vital for symptom resolution. Worldwide, there is a lack of large-scale studies that help define how hyperglycemic crises should be managed. This article will provide a comprehensive review of the pathophysiology, diagnosis, and management of DKA-HHS overlap.

The regulation of carbohydrate metabolizing enzymes is an effective way of reducing blood glucose levels and improving glycogen synthesis during the management of type 2 diabetes. The present investigation was conducted to explain the detailed mechanism with which a Seagrass, Halophila beccarii extract (HBE) enhances the glucose uptake in the 3T3-L1 adipocyte cell culture system in invitro. HBE stimulates the glucose uptake by the translocation of glucose transporter 4 (GLUT4) on to plasma cell membrane through induction of insulin receptor substrate 1 (IRS-1)/protein kinase B (Akt) signaling pathways. To assess the effect of HBE on T2DM, we used invivo experimental diabetes rat models induced with streptozotocin (STZ) to perform oral GTT and ITT. Furthermore, we assessed the enzymatic profile of Glycolysis, Pentose phosphate pathway, and gluconeogenesis from liver tissue homogenate. After long-term exposure with HBE, our results confirmed, that HBE improves the glucose uptake in 3T3-L1 cell lines by up-regulation of glucose transporter type 4 (GLUT4) through uptake of glucose by the adipocytes. The resulting data indicated that HBE had a great potentiality in preventing diabetes and maintaining glucose homeostasis through improving glucose uptake. The present data also showed that HBE with its insulin mimetic activity activates glycogen synthesis and enhances glucose utilization by regulating the carbohydrate metabolic enzymes. The similarity between HBE and insulin indicates that the HBE follows the mechanisms same as the insulin signaling pathway to show the antidiabetic activity.

Insulin resistance (IR) plays a key role in the pathogenesis and clinical outcome of patients with multiple diseases and diabetes. In this study, we examined the antidiabetic effects of a terpenoid-rich extract from Dillenia indica L. bark (TRDI) in palmitic acid-induced insulin resistance (PA-IR) in C2C12 myotube and a streptozotocin (STZ)-induced diabetic mice model and explored the possible underlying mechanism. TRDI showed potential DPPH- and ABTS-radical scavenging effects with a half-maximal inhibitory concentration (IC50) value of 9.76 ± 0.50 µg/mL and 17.47 ± 1.31 µg/mL, respectively. Furthermore, TRDI strongly mitigated α-glucosidase activity with an IC50 value of 3.03 ± 1.01 µg/mL, which was 92-fold higher than the positive control, acarbose (IC50 = 279.49 ± µg/mL). TRDI stimulated the insulin receptor substrarte-1 (INS-1), downregulated phosphoinositide-dependent kinase-1 (PDK1) and protein kinase B (Akt) in both normal and PA-IR C2C12 cells as well as in STZ-induced diabetic mice, enhanced glucose transporter 4 (GLUT4) translocation to the plasma membrane (PM), and increased glucose absorption. Furthermore, TRDI administration significantly reduced PA-induced reactive oxygen species (ROS) formation in C2C12 cells and increased the protein level of numerous antioxidant enzymes such as superoxide dismutase 1 (SOD1), catalase (CAT), glutathione peroxidase-1 (GPx-1) and thioredoxin reductase (TrxR) both in vitro and in vivo. Furthermore, TRDI facilitated nuclear factor erythroid 2 related factor 2 (Nrf2) nuclear translocation and increased HO-1 expression in PA-IR C2C12 cells and STZ-induced diabetic mice. However, for the inhibition of Nrf2, TRDI failed to resist the effects of IR. Thus, this study provides new evidence to support the use of TRDI for diabetes treatment.

The aim of this study is to investigate the antidiabetic effect of lariciresinol (LSR) in C2C12 myotubes and streptozotocin (STZ)-induced diabetic mice.

To investigate antidiabetic potential of LSR, α-glucosidase inhibitory assay, molecular docking, glucose uptake assay, western blot assay on antidiabetic biomarkers are performed. STZ-induced diabetic model is used for in vivo study by calculating oral glucose tolerance test, histochemical examination, and glycogen assay. LSR inhibits α-glucosidase activity with an IC₅₀ value of 6.97 ± 0.37 µM and acts as a competitive inhibitor with an inhibitory constant (Ki) value of 0.046 µM. In C2C12 cells, LSR activates insulin signaling leading to glucose transporter 4 (GLUT4) translocation and augmented glucose uptake. Furthermore, in Streptozotocin (STZ)-treated diabetic mice, 3 weeks of oral LSR administration (10 mg kg^-1 ) considerably decrease blood glucose levels, while increasing insulin levels in an oral glucose tolerance test, improve pancreatic islet size, increase GLUT4 expression, and significantly enhance insulin signaling in skeletal muscle. LSR treatment also activates glycogen synthase kinase 3β (GSK-3β) resulting in improved glycogen content.

The findings indicate a potential usefulness for oral LSR in the management and prevention of diabetes by enhancing glucose homeostasis.

Clinicians in the Emergency Center (EC) and Urgent Care (UC) can play a vital role in preventing hospital admissions and improving outcomes of patients with newly diagnosed diabetes or pre-existing diabetes who present with hyperglycemia and the need to initiate insulin.

This article describes a unique EC/UC discharge insulin starter kit protocol with clinician instructions via an Electronic Medical Record (EMR) order set that includes: starting doses for insulin, a prescription for glucose monitoring supplies, and an emergent referral to diabetes education at International Diabetes Center. Patients receive insulin during the EC/UC visit and are provided an insulin pen to take home. Nurses from the EC or UC review and provide educational material on how to use an insulin pen, treating hypoglycemia and healthy eating. The Certified Diabetes Care and Education Specialist (CDCES) sees patients within 24-72 hours after the referral is placed.

Within our single healthcare system's EC and UC (multiple sites), the kit has enabled clinicians to metabolically stabilize patients and decrease the need for hospitalization without experiencing hypoglycemia. In the recent three years of use, of 42 patients given the insulin starter kit, there were only 2 patients with repeat EC/UC visits within the first six months (1 hyperglycemia and 1 hypoglycemia).

An insulin starter kit and EMR-based order set initiated in the EC/UC setting is a tool that can be used to improve the quality of care for people with newly diagnosed or pre-existing diabetes experiencing significant hyperglycemia.

The transition of diabetes care from home to hospital, within the hospital, and upon discharge is fraught with gaps that can adversely affect patient safety and length of stay. We aimed to highlight the variability in care during these transitions and point out areas where research is needed.

A PubMed search was performed with a combination of search terms that pertained to diabetes, hyperglycemia, hospitalization, locations in the hospital, discharge to home or a nursing facility, and diabetes medications. Studies with at least 50 patients that were written in the English language were included.

With the exception of transitioning from intravenous insulin infusion to subcutaneous insulin and perhaps admission to the regular floors, few studies pointedly focused on transitions of care, leading us to extrapolate recommendations based on data from disparate areas of care in the hospital. There is evidence at every stage of care, starting from the entry into the hospital and ending with discharge home or to a facility, that patients benefit from having protocols in place guiding overall care.

Pockets of care exist in hospitals where methods of effective diabetes management have been studied and implemented. However, there is no sustained continuum of care. Protocols and care teams that follow patients from one physical location to the other may result in improved clinical outcomes during and following a hospital stay.

Agriophyllum squarrosum (L.) Moq. is a traditional Mongol medicine generally used to treat diabetes.

To investigate the protective effects and potential mechanisms of Agriophyllum oligosaccharides (AOS) on liver injury in type 2 diabetic db/db mice.

The db/db mice were divided into the model group (Model), metformin group (MET), high-dose AOS group (HAOS), and low-dose AOS group (LAOS). Nondiabetic littermate control db/m mice were used as the normal control group (Control). Mice in AOS groups were treated with AOS (380 or 750 mg/kg) daily, for 8 weeks. At 8 weeks, blood samples were collected to detect lipid and enzyme parameters concerning hepatic function, including alanine aminotransferase (ALT), aspartate aminotransferase (AST), total protein (TP), albumin (ALB), globulin (GLB), triglyceride (TG), total cholesterol (TC), and high-density lipoprotein cholesterol (HDL-C). Random blood glucose (RBG) test, oral glucose tolerance test (OGTT), and oral maltose tolerance test (OMTT) were also conducted. Microscopy was used to observe morphological changes in the liver of AOS-treated groups. Real-time PCR was used to detect the mRNA expression, including insulin receptor substrate 2 (IRS-2), phosphatidylinositol 3 kinase (PI3K), protein kinase B (AKT), peroxisome proliferator-activated receptor (PPAR)-γ, insulin receptor (INS-R), and Glut4. Furthermore, western blotting was performed to identify proteins, including phosphorylation of IRS-2 (p-IRS-2), PI3K, p-AKT, PPAR-γ, INS-R, and Glut4. Hepatic protein expression of p-IRS-2, PI3K, p-AKT, PPAR-γ, INS-R, and Glut4 was observed using immunohistochemical staining.

AOS treatment significantly decreased RBG, OGTT, and OMTT in mice, as well as serum ALT and AST activities. AOS groups demonstrated significantly higher expressions of p-IRS-2, PI3K, PPAR-γ, p-AKT, INS-R, and Glut4 protein and IRS-2, PI3K, AKT, PPAR-γ, INS-R, and Glut4 mRNA in the liver tissue of db/db mice; the degeneration and necrosis of hepatocytes and formation of collagen fibres markedly reduced, improving the structural disorder in the liver.

The results suggest that AOS could protect the liver in type 2 diabetes, in part by activating insulin in the INS-R/IRS2/PI3K/AKT/Glut4/PPAR-γ signal pathway, facilitating hepatocyte proliferation, and further reducing the blood glucose levels.

Diabetic ketoalkalosis (DKAlk) was first described in 1967 as a rare complication of diabetic ketoacidosis with normal or elevated pH/bicarbonate and elevated anion gap (AG) from high β-hydroxybutyrate (BHB).

We report a case series of patients with DKAlk to show how venous blood gas (VBG) electrolytes alone may misdiagnose these patients.

This was a case series of DKAlk patients with concomitant VBG and basic metabolic panel (BMP) electrolytes who met the following criteria for DKAlk: BMP hyperglycemia (glucose >250 mg/dL), elevated AG (>15 mEq/L), elevated BHB (>1.2 mmol/L), and high Delta (Δ) gap (>6 mEq/L [bicarbonate gap (BG): measured bicarbonate - 24] - [AG - 12]). Data are reported as median with interquartile range (IQR) (25%, 75%) and group comparisons utilized Mann-Whitney U test (two-tailed, α = 0.05).

We found 10 patients with DKAlk in 2 months. Patients ranged in age from 13 to 77 years, 50% were male, and all were African American. Most patients (8 of 10) were vomiting with hyperglycemia (350 to >600 mg/dL). DKAlk BMP AG ranged from 18 to 34 mmol/L and BHB from 1.74 to 9.09 mmol/L. For bicarbonate, we found no significant difference between VBG (24 mmol/L) and BMP (22 mmol/L) (p = 0.796). VBG chloride (98 mmol/L) was significantly higher than BMP chloride (88 mmol/L) (p < 0.005). This falsely elevated VBG chloride resulted in undervaluing of all VBG AGs, missing almost all of the patients with DKAlk.

We found that DKAlk is more common than previously reported. We recommend screening with BMP electrolytes and BHB levels for hyperglycemic ED patients who are vomiting or suspected of hypovolemia.

This study assesses the ability of anthraquinone derivative, 2-methyl-1,3,6-trihydroxy-9,10-anthraquinone (MTAQ) to decrease postprandial hyperglycemia or enhance glucose uptake and to elucidate the underlying molecular mechanism. We investigated α-glucosidase inhibition, glucose uptake, and translocation of glucose transporter 4 (GLUT4) in C2C12 myotubes. The data indicate that MTAQ strongly inhibited α-glucosidase activity in a concentration-dependent manner, with an IC50 value of 6.49 ± 1.31 μM, and functioned as a reversible competitive inhibitor, with a dissociation constant of 41.88 μM. Moreover, MTAQ significantly augmented basal and insulin-stimulated glucose uptake as well as translocation of GLUT4 to the plasma membrane. It also stimulated the phosphorylation of insulin receptor β isoform, insulin receptor substrate-1,3-phosphoinositide-dependent protein kinase 1, and protein kinase B (AKT). A pretreatment with an AKT inhibitor, LY294002, attenuated the ability of MTAQ to activate an insulin-like signaling pathway and to enhance basal and insulin-stimulated glucose uptake and stimulate GLUT4 translocation to the plasma membrane. These findings reveal the fact that MTAQ may have potential for the development of new antidiabetic drugs to manage blood glucose levels.

Glucose absorption from the gut and glucose uptake into muscles are vital for the regulation of glucose homeostasis. In the current study, we determined if gossypol (GSP) reduces postprandial hyperglycemia or enhances glucose uptake; we also investigated the molecular mechanisms underlying those processes in vitro and in vivo. GSP strongly and concentration dependently inhibited α-glucosidase by functioning as a competitive inhibitor with IC50 value of 0.67 ± 0.44. GSP activated the insulin receptor substrate 1 (IRS-1)/protein kinase B (Akt) signaling pathways and enhanced glucose uptake through the translocation of glucose transporter 4 (GLUT4) into plasma membrane in C2C12 myotubes. Pretreatment with a specific inhibitor attenuated the in vitro effects of GSP. We used a streptozotocin-induced diabetic mouse model to assess the antidiabetic potential of GSP. Consistent with the in vitro study, a higher dose of GSP (2.5 mg/kg-1) dramatically decreased the postprandial blood glucose levels associated with the upregulated expressions of GLUT4 and the IRS-1/Akt-mediated signaling cascade in skeletal muscle. GSP treatment also significantly boosted antioxidant enzyme expression and mitigated gluconeogenesis in the liver. Collectively, these data imply that GSP has the potential in managing and preventing diabetes by ameliorating glucose uptake and improving glucose homeostasis.

Hyperglycemia is commonly encountered in the ED; the importance of glucose reduction in patients well enough to be discharged is unknown.

We conducted a prospective, randomized trial of ED patients with hyperglycemia with a glucose value 400-600 mg/dL who were discharged from the ED, excluding those with type 1 diabetes mellitus. Patients were randomly assigned to a discharge glucose goal, <350 mg/dL (moderate control) or < 600 mg/dL (loose control). The primary outcome was ED length of stay.

Among 110 enrolled patients, 57 were assigned to moderate and 53 to loose glycemic control. Median (IQR) length of stay was 211 min (177-288 min) for the moderate group and 216 min (151-269 min) for the loose group (difference, 17 min [95% CI -15 to 49 min]). ED length of stay for those with an actual discharge glucose <350 mg/dL was 29 min longer (95% CI -1 to 59 min). Repeat ED visits for hyperglycemia (7% vs 6%), hospitalization for hyperglycemia (0% vs 2%), and hospitalization for any reason (4% vs 8%) did not differ significantly between groups.

In the intention-to-treat analysis, ED length of stay and 7-day outcomes were not significantly different whether moderate or loose glycemic control was pursued. However, the length of stay for those with discharge glucose <350 mg/dL was approximately 29 min longer. ED glycemic control did not appear to be associated negative short-term outcomes. Glucose reduction in well-appearing ED patients may consume time and resources without conferring short- or long-term benefits.

Clinicaltrials.govNCT02478190.