Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During 2010, 15 articles were published which focused on chronic sensorimotor axonal neuropathy; some will be discussed in this review. Clinical diagnosis from signs and symptoms seems to be excessively variable, often overestimating the incidence of diabetic sensorimotor polyneuropathy. Long-term use of Metformin is associated with malabsorption of vitamin B12. Metformin exposure may be a iatrogenic cause for exacerbation of peripheral neuropathy in patients with type 2 diabetes. The neuroprotective role of vitamin E against cisplatinperipheral neurotoxicity has been suggested by a phase III study. Metallosis after hip arthroplasty with a cobalt-chromium alloy prosthesis can cause progressive sensory disturbance, hearing loss and hypothyroidism. The effects of electrical stimulation on neuromuscular recovery after nerve crush injury in rats do not support a benefit of the tested protocol using electrical stimulation during the period of motor nerve recovery following injury. The rate of motor vehicle accidents in patients with neuropathy, based on surveys from 260 subjects, demonstrated that 40.6% were involved in traffic accidents. Accident frequency and discomfort with driving are higher in neuropathy patients compared to age-matched national statistics. Peripheral neuropathy in primary (AL) amyloidosis may be the cause of stepwise progressive, multiple upper limb mononeuropathies.
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PMID:[Original articles on axonal neuropathy in 2010]. 2210 Mar 24

Psoriasis is a common, chronic inflammatory skin disease that can cause significant discomfort and impairment to quality of life. Recent research indicates that individuals with moderate-to-severe psoriasis are likely at greater risk for chronic cardiometabolic co-morbidities such as cardiovascular disease, type 2 diabetes, obesity and metabolic syndrome. Physical activity can be an effective primary and adjunctive treatment for these maladies in other populations. Unfortunately, only a limited number of studies have examined physical activity in psoriasis, which are limited by poor design and lack of validated physical activity assessment methodologies. A variety of data suggest shared physiologic pathways between physical activity, psoriasis, and psoriasis cardiometabolic co-morbidities. Increased adiposity, inflammation, oxidative stress, adhesion molecules and lipids are physiologically linked to psoriasis, the risk of psoriasis cardiometabolic co-morbidities, and low levels of physical activity. In addition, epigenetic pathways are involved in psoriasis and could be influenced by physical activity. The physical and psychosocial impairments common in psoriasis may make it difficult to participate in regular physical activity, and future studies should aim to determine if physical activity interventions improve functioning and reduce co-morbidities in psoriasis.
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PMID:Psoriasis and physical activity: a review. 2238 2

Since its discovery, insulin has been used as highly specific and effective therapeutic protein to treat type 1 diabetes and later was associated to oral antidiabetic agents in the treatment of type 2 diabetes. Generally, insulin is administered parenterally. Although this route is successful, it still has several limitations, such as discomfort, pain, lipodystrophy at the injection sites and peripheral hyperinsulinemia, which may be the cause of side effects and some complications. Thus, alternative routes of administration have been developed, namely, those based on nanotechnologies. Nanoparticles, made of synthetic or natural materials, have been shown to successfully overcome the inherent barriers for insulin stability, degradation, and uptake across the gastrointestinal tract and other mucosal membranes. This review describes some of the many attempts made to develop alternative and more convenient routes for insulin delivery.
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PMID:Nanotechnology as a promising strategy for alternative routes of insulin delivery. 2244 31

Inactive adults experience a 3% to 8% loss of muscle mass per decade, accompanied by resting metabolic rate reduction and fat accumulation. Ten weeks of resistance training may increase lean weight by 1.4 kg, increase resting metabolic rate by 7%, and reduce fat weight by 1.8 kg. Benefits of resistance training include improved physical performance, movement control, walking speed, functional independence, cognitive abilities, and self-esteem. Resistance training may assist prevention and management of type 2 diabetes by decreasing visceral fat, reducing HbA1c, increasing the density of glucose transporter type 4, and improving insulin sensitivity. Resistance training may enhance cardiovascular health, by reducing resting blood pressure, decreasing low-density lipoprotein cholesterol and triglycerides, and increasing high-density lipoprotein cholesterol. Resistance training may promote bone development, with studies showing 1% to 3% increase in bone mineral density. Resistance training may be effective for reducing low back pain and easing discomfort associated with arthritis and fibromyalgia and has been shown to reverse specific aging factors in skeletal muscle.
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PMID:Resistance training is medicine: effects of strength training on health. 2277 32

The chronicity of chronic disease, and its associated uncertainties and fluctuations in health status, pain and/or discomfort, often leaves those so diagnosed feeling that they have lost control. Treatment can exacerbate this sense of loss of control, as people surrender to the expertise of their biomedical providers and interventions. In principle, self-management aims to return control to the individual, but its promotion is as much motivated by cost-containment as patient autonomy, and is advocated in an environment largely shaped by policy makers and biomedical providers. In this article, we examine how Australians with type 2 diabetes and/or cardiovascular disease supplement medical with complementary and alternative medical (CAM) care. Drawing on in-depth interviews with 69 participants collected in 2009-2010, we illustrate how people rely on medical providers and pharmaceuticals to manage their diabetes, but concurrently consulted with CAM practitioners and used non-biomedical therapies to enhance well-being. In explaining this, participants framed CAM use in the context of reclaiming relative personal and bodily control.
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PMID:Taking control: Complementary and alternative medicine in diabetes and cardiovascular disease management. 2301 92

Wireless microcurrent stimulation (WMCS) is a new method in wound healing that may have advantages compared with conventional electrical stimulation (ES) devices. Although ES has been widely known as an effective method to promote the wound-healing process in patients with type 2 diabetes mellitus, to the authors' knowledge, there are still no data about the ability of WMCS to match the desired effect. In this article, the authors report the results of 2 cases of diabetes-related wounds (1 acute and 1 chronic) that have been treated successfully using WMCS. Neither patient reported discomfort during treatment, and the risk of infection was minimized because there was no direct contact from the device during the treatment course.
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PMID:Use of wireless microcurrent stimulation for the treatment of diabetes-related wounds: 2 case reports. 2326 89

A 70-year-old man came to the Access to Primary Care Clinic at the Interim LSU Public Hospital because he had been told at another hospital that he needed a kidney doctor. The patient had a history of high blood pressure, type 2 diabetes mellitus, long-standing kidney disease, an above the knee amputation on the left, gout, a possible coronary stent procedure five years ago, and recently poor appetite and inability to care for himself. He had a long history of medical noncompliance and was taking no medications when he came to the hospital. He denied all cardiac symptoms, including chest discomfort. He was admitted to hospital because of a blood pressure of 240/110 mmHg, a serum creatinine of 6.0 mg/dL, and an estimated glomerular filtration rate of 11 mL/min - i.e., chronic kidney disease, stage V. His electrocardiogram was read by the computer as normal (Figure 1).
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PMID:ECG of the month. Electrocardiogram in a man with chronic kidney failure. ECG is abnormal and indicative of heart disease. 2336 95

Obesity and type 2 diabetes are increasing in prevalence at an alarming rate in developed and developing nations and over 50% of patients with prolonged stages of disease experience forms of autonomic neuropathy. These patients have symptoms indicating disrupted enteric nervous system function including gastric discomfort, gastroparesis and intestinal dysmotility. Previous assessments have examined enteric neuronal injury within either type 1 diabetic or transgenic type 2 diabetic context. This study aims to assess damage to myenteric neurons within the duodenum of high-fat diet ingesting mice experiencing symptoms of type 2 diabetes, as this disease context is most parallel to the human condition and disrupted duodenal motility underlies negative gastrointestinal symptoms. Mice fed a high-fat diet developed symptoms of obesity and diabetes by 4 weeks. After 8 weeks, the total number of duodenal myenteric neurons and the synaptophysin density index were reduced and transmission electron microscopy showed axonal swelling and loss of neurofilaments and microtubules, suggesting compromised neuronal health. High-fat diet ingestion correlated with a loss of neurons expressing VIP and nNOS but did not affect the expression of ChAT, substance P, calbindin and CGRP. These results correlate high-fat diet ingestion, obesity and type 2 diabetes symptoms with a loss of duodenal neurons, biasing towards those with inhibitory nature. This pathology may underlie dysmotility and other negative GI symptoms experienced by human type 2 diabetic and obese patients.
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PMID:High-fat diet ingestion correlates with neuropathy in the duodenum myenteric plexus of obese mice with symptoms of type 2 diabetes. 2388 4

Diabetes mellitus is not only a clinical syndrome characterizing hyperglycemia, but is also a cause of debilitating problem known as peripheral neuropathy (PN). This review addresses the importance of diagnosing PN in a clinical setting as PN causes pain and discomfort in lower extremities, loss or absence of protective sensations in the lower extremities leading to balance problems, risk of foot ulcerations, and a reduced quality of life in adults with type 2 diabetes. A variety of modalities or methods are available to evaluate both subjective and objective measures of peripheral nerve functions, and have been discussed in detail in this review. It is of utmost importance to understand that evaluating PN as a routine practice in a simple way may also play a vitally important role in preventing foot ulcers or fall-related morbidity and mortality in adults with type 2 diabetes.
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PMID:Diabetic peripheral neuropathy and its evaluation in a clinical scenario: a review. 2462 37

Insulin replacement therapy is a widely adopted treatment for all patients with type 1 diabetes and some with type 2 diabetes. However, injection of insulin has suffered from problems such as tissue irritation, abscesses, discomfort, and inconvenience. The use of orally bioactive insulin mimetics thus represents an ideal treatment alternative. Here we show that a chaetochromin derivative (4548-G05) acts as a new nonpeptidyl insulin mimetic. 4548-G05 selectively activates an insulin receptor (IR) but not insulin-like growth factor receptor-I or other receptor tyrosine kinases. Through binding to the extracellular domain of the IR, 4548-G05 induces activation of the receptor and initiates the downstream Akt and extracellular signal-related kinase pathways to trigger glucose uptake in C2C12 myotubes. Moreover, it displays a potent blood glucose-lowering effect when administrated orally in normal, type 1 diabetic, and type 2 diabetic mice models. Therefore, 4548-G05 may represent a novel pharmacological agent for antidiabetes drug development.
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PMID:Identification of a small molecular insulin receptor agonist with potent antidiabetes activity. 2465 8


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