Epidemiology of Diabetes and Its Complications

Ia, O'Brien; Rj, Corrall

doi:10.1056/nejm198806163182414

Cited by 26 publications

(4 citation statements)

References 8 publications

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“…Wound healing and tissue regeneration depend on an adequate blood supply to the region. Ischemia due to vascular disease impedes healing by reducing the supply of oxygen, nutrients, and soluble mediators that are involved in the repair process [11]. Purely ischemic diabetic foot ulcers are uncommon, representing only 10% to 15% of ulcers in patients with diabetes.…”

Section: Etiology Of Diabetic Foot Ulcerationmentioning

confidence: 99%

“…Although there are many causes of peripheral neuropathy, diabetes mellitus is by far the most common. Neuropathy, usually distal sensorimotor polyneuropathy, is present in about 42% of diabetic patients after 20 years [11]. The peripheral neuropathy is thought to result from abnormalities in metabolic pathways, of which there are several hypotheses including deficiencies in sorbitol metabolism via the polyol pathway [12, 16].…”

Section: Etiology Of Diabetic Foot Ulcerationmentioning

confidence: 99%

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Contemporary Evaluation and Management of the Diabetic Foot

Sumpio

2012

Scientifica

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Foot problems in patients with diabetes remain a major public health issue and are the commonest reason for hospitalization of patients with diabetes with prevalence as high as 25%. Ulcers are breaks in the dermal barrier with subsequent erosion of underlying subcutaneous tissue that may extend to muscle and bone, and superimposed infection is a frequent and costly complication. The pathophysiology of diabetic foot disease is multifactorial and includes neuropathy, infection, ischemia, and abnormal foot structure and biomechanics. Early recognition of the etiology of these foot lesions is essential for good functional outcome. Managing the diabetic foot is a complex clinical problem requiring a multidisciplinary collaboration of health care workers to achieve limb salvage. Adequate off-loading, frequent debridement, moist wound care, treatment of infection, and revascularization of ischemic limbs are the mainstays of therapy. Even when properly managed, some of the foot ulcers do not heal and are arrested in a state of chronic inflammation. These wounds can frequently benefit from various adjuvants, such as aggressive debridement, growth factors, bioactive skin equivalents, and negative pressure wound therapy. While these, increasingly expensive, therapies have shown promising results in clinical trials, the results have yet to be translated into widespread clinical practice leaving a huge scope for further research in this field.

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Section: Etiology Of Diabetic Foot Ulcerationmentioning

confidence: 99%

Section: Etiology Of Diabetic Foot Ulcerationmentioning

confidence: 99%

Contemporary Evaluation and Management of the Diabetic Foot

Sumpio

2012

Scientifica

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“…Diabetes mellitus (DM) is a chronic disease caused by acquired deficiency in production of insulin by the pancreas, or by the ineffectiveness of the insulin produced (Riaz, 2009). This deficiency results in increased concentrations of glucose in the blood, which in turn leads to retinopathy, nephropathy, neuropathy, coronary heart disease, cerebrovascular disease, and peripheral vascular diseases (Gregg et al, 2016;O'Brien and Corrall, 1988). The main purpose of diabetes treatment is to prevent or delay the complications by improving blood sugar control (Kooti et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Comparative pharmacokinetics of four major compounds after oral administration of Mori Cortex total flavonoid extract in normal and diabetic rats

Xiong

Li²,

Chu³

et al. 2023

Front. Pharmacol.

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Introduction: Mori Cortex has been used in traditional Chinese Medicine as an antidiabetic agent. The aim of this study was to establish a UPLC-MS/MS method for simultaneous determination of morin, morusin, umbelliferone and mulberroside A in rat plasma and investigate the pharmacokinetics differences between normal and diabetic rats following oral administration of Mori Cortex total flavonoid extract.Methods: Samples were pre-treated by protein precipitation and genkwanin was used as internal standard. Chromatographic separation was performed using a Hypersil GOLD C18 column (50 mm × 2.1 mm, 3 μm). The mobile phase consisted of acetonitrile and water (containing 0.1% formic acid) in gradient mode at a flow rate of 0.5 ml/min. The transitions of m/z 300.9→107.1, m/z 419.3→297.1, m/z 160.9→77.0, m/z 567.1→243.2 and m/z 283.1→268.2 were selected for morin, morusin, umbelliferone, mulberroside A and internal standard, respectively.Results: The intra- and inter-day precision for analytes were less than 12.5% and the accuracy ranged from −8.1% to 3.5%. The extraction recovery was >88.5% and no obvious matrix effect was observed. The AUC(0-t) and Cmax of morin were 501.3 ± 115.5 ng/mL*h and 127.8 ± 56.0 ng/mL in normal rats and 717.3 ± 117.4 ng/ml*h and 218.6 ± 33.5 ng/ml in diabetic rats. Meanwhile, the AUC(0-t) and Cmax of morusin were 116.4 ± 38.2 ng/ml*h and 16.8 ± 10.1 ng/mL in normal rats and 325.0 ± 87.6 ng/mL*h and 39.2 ± 5.9 ng/ml in diabetic rats. For umbelliferone and mulberroside A, the AUC(0-t) and Cmax also increased significantly in diabetic rats (p < 0.05).Discussion: The validated method was successfully applied to the pharmacokinetic study in normal and diabetic rats.

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“…The classical therapeutic strategy for patients with T1D is the administration of insulin injections to maintain normal levels of blood glucose. However, this approach is unable to provide real-time blood-glucose modulation and is ineffective for maintaining stable blood-glucose levels, which frequently leads to clinical complications [8]. Maintaining stable glucose levels is important to prevent the development of secondary complications that can result from T1D.…”

Section: Introductionmentioning

confidence: 99%

Alpha-Lipoic Acid Inhibits Spontaneous Diabetes and Autoimmune Recurrence in Non-Obese Diabetic Mice by Enhancing Differentiation of Regulatory T Cells and Showed Potential for Use in Cell Therapies for the Treatment of Type 1 Diabetes

Huang

Kuo

Chen

et al. 2022

IJMS

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Type 1 diabetes (T1D) is caused by the destruction of β cells in pancreatic islets by autoimmune T cells. Islet transplantation has been established as an effective treatment for T1D. However, the survival of islet grafts is often disrupted by recurrent autoimmunity. Alpha-lipoic acid (ALA) has been reported to have immunomodulatory effects and, therefore, may have therapeutic potential in the treatment of T1D. In this study, we investigated the therapeutic potential of ALA in autoimmunity inhibition. We treated non-obese diabetic (NOD) mice with spontaneous diabetes and islet-transplantation mice with ALA. The onset of diabetes was decreased and survival of the islet grafts was extended. The populations of Th1 cells decreased, and regulatory T cells (Tregs) increased in ALA-treated mice. The in vitro Treg differentiation was significantly increased by treatment with ALA. The adoptive transfer of ALA-differentiated Tregs into NOD recipients improved the outcome of the islet grafts. Our results showed that in vivo ALA treatment suppressed spontaneous diabetes and autoimmune recurrence in NOD mice by inhibiting the Th1 immune response and inducing the differentiation of Tregs. Our study also demonstrated the therapeutic potential of ALA in Treg-based cell therapies and islet transplantation used in the treatment of T1D.

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Epidemiology of Diabetes and Its Complications

Cited by 26 publications

References 8 publications

Contemporary Evaluation and Management of the Diabetic Foot

Contemporary Evaluation and Management of the Diabetic Foot

Comparative pharmacokinetics of four major compounds after oral administration of Mori Cortex total flavonoid extract in normal and diabetic rats

Alpha-Lipoic Acid Inhibits Spontaneous Diabetes and Autoimmune Recurrence in Non-Obese Diabetic Mice by Enhancing Differentiation of Regulatory T Cells and Showed Potential for Use in Cell Therapies for the Treatment of Type 1 Diabetes

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