Diabetes/metabolism research and reviews
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Diabetes Metab. Res. Rev. · Nov 2008
Time course of pain sensation in rat models of insulin resistance, type 2 diabetes, and exogenous hyperinsulinaemia.
Small sensory fibre dysfunction has been recently recognized as a component of impaired glucose tolerance and insulin resistance (IR) syndrome. However, few studies have investigated whether small sensory fibre dysfunction develops in normoglycaemic or pre-diabetic animal models of IR and/or hyperinsulinaemia. In addition, scant information is available on the metabolic features of IR in relation to small sensory fibre dysfunction due to the progressive failure of beta cells to compensate for IR during the development of frank diabetes. ⋯ In addition to insulin treatment, IR with or without compensatory hyperinsulinaemia is associated with nociceptive dysfunction of different phenotypes, independent of glycaemic levels.
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Diabetes Metab. Res. Rev. · Oct 2008
Plasma glycooxidation protein products in type 2 diabetic patients with nephropathy.
In diabetes mellitus, hyperglycaemia accelerates non-enzymatic glycation and oxidative stress leading to damage of macromolecules, among others proteins. This manifests in the increased levels of advanced glycation end products (AGE) and advanced oxidation protein products (AOPP). ⋯ The connection between plasma levels of both glycooxidation protein products-AGE and AOPP with nephropathy severity, measured by the degree of albuminuria, in T2DM patients was observed. We can suggest that the AOPP better reflect the progression of kidney damage than AGE in examined diabetic patients.
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Diabetes Metab. Res. Rev. · May 2008
ReviewPainful diabetic neuropathy: treatment and future aspects.
Around one of three diabetic patients is affected by distal symmetric polyneuropathy (DSP) which represents a major health problem, as it may present with partly excruciating neuropathic pain and is responsible for substantial morbidity and increased mortality. Treatment is based on four cornerstones: (1) multifactorial intervention aimed at (near)-normoglycaemia and reduction in cardiovascular risk factors, (2) treatment based on pathogenetic mechanisms, (3) symptomatic treatment, and (4) avoidance of risk factors and complications. Among the pathogenetic treatments only alpha-lipoic acid and epalrestat are available for treatment in several countries. ⋯ More recently, significant pain relief has been reported in clinical trials of painful diabetic neuropathy using agents such as the dual selective serotonin noradrenaline reuptake inhibitor (SNRI), duloxetine and the anticonvulsant pregabalin, a specific modulator of the alpha(2)delta subunit of the voltage-dependent calcium channels. A promising new anticonvulsant is lacosamide. In future, drug combinations might also include those aimed at symptomatic pain relief and quality of life on one hand and improvement or slowing the progression of the underlying neuropathic process on the other hand.
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Diabetes Metab. Res. Rev. · May 2008
ReviewThe value of debridement and Vacuum-Assisted Closure (V.A.C.) Therapy in diabetic foot ulcers.
Treatment of diabetic foot ulcers includes a number of different regimes such as glycaemic control, re-vascularization, surgical, local wound treatment, offloading and other non-surgical treatments. Although considered the standard of care, the scientific evidence behind the various debridements used is scarce. This presentation will focus on debridement and V.A.C. Therapy, two treatments widely used in patients with diabetes and foot ulcers. ⋯ Although debridement of the ulcer is considered a prerequisite for healing of diabetic foot ulcers, the grade of evidence is quite low. This may be due to a lack of studies rather than lack of effect. Negative pressure wound therapy seems to be safe and effective in the treatment of some diabetic foot ulcers, although there is still only one well-performed trial that evaluates the effect.