Lipids: A Suitable Therapeutic Target in Diabetic Neuropathy?

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Term Occurence Count Dictionary
rosuvastatin 2 endocrinologydiseasesdrugs
simvastatin 1 endocrinologydiseasesdrugs
Insulin 4 endocrinologydiseasesdrugs
diabetic neuropathy 5 endocrinologydiseases
fenofibrate 6 endocrinologydiseasesdrugs
metabolic syndrome 3 endocrinologydiseases
obesity 1 endocrinologydiseases
diabetes mellitus 2 endocrinologydiseases
ezetimibe 3 endocrinologydiseasesdrugs
hyperglycemia 5 endocrinologydiseases
niacin 1 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
Insulin 11808 neuropathy [[26]].4. Mechanisms Linking Lipids to Diabetic Neuropathy4.1. Peripheral Nerves Are Affected by Insulin ResistanceEven though glucose uptake in the nervous system is largely insulin-independent, there is
Insulin 11975 is largely insulin-independent, there is evidence of insulin signaling in peripheral nerves [[27]]. Insulin signaling in peripheral neurons proceeds in a way analog to that in other cells, with successive phosphorylation
Insulin 13958 peripheral neuropathy (Odds Ratio: 1.2 per unit, 95% CI: 1.1–1.4) [[35]].4.2. Free Fatty Acids Mediate Insulin Resistance and Dysfunction in Peripheral NervesHigh plasma levels of free fatty acids (FFA) are a hallmark
Insulin 31397 nicotinamide-adenine dinucleotide phosphate oxidase, PL: phospholipid, and SFFA: saturated free fatty acids. Insulin resistance or a high-fat diet increase the cellular supply of FFA, leading to decreased expression of
ezetimibe 1536 and secondary analyses of clinical trials have found benefits of cholesterol reducing (statins and ezetimibe ), triglyceride-reducing (fibrates), or lipid antioxidant (thioctic acid) therapies over the progression
ezetimibe 26421 [[85]].There is also evidence of DPN improvement with cholesterol-lowering therapies such as statins or ezetimibe in clinical studies. In the Fremantle Diabetes Study, patients with DM2 treated with statins evidenced
ezetimibe 26660 incidence of DPN [[77]]. A recent study demonstrated that patients with DM2 treated with simvastatin + ezetimibe or rosuvastatin had lower lipid peroxidation (LPO) markers versus placebo and a significant reduction
fenofibrate 22672 neuropathy measures like mechanical sensitivity and NCV [[75]]. In a trial comparing treatment with fenofibrate versus niacin for 6 weeks in patients with primary hypercholesterolemia or mixed dyslipidemia, fenofibrate
fenofibrate 22779 fenofibrate versus niacin for 6 weeks in patients with primary hypercholesterolemia or mixed dyslipidemia, fenofibrate effectively lowered atypical sphingolipids (0.13 microM before, 0.09 microM after treatment, p ≤ 0.001)
fenofibrate 23614 DM2 followed for 5 years using either statins or fibrates as lipid-lowering therapy, treatment with fenofibrate was associated with a significant decrease in the appearance of neuropathy (measured by the Michigan
fenofibrate 23907 Fenofibrate and Event-Lowering in Diabetes (FIELD) study of 9795 patients with DM2 who were randomized to fenofibrate or placebo, the fenofibrate group had a significantly lower rate of nontraumatic amputations (HR 0.62,
fenofibrate 23935 Diabetes (FIELD) study of 9795 patients with DM2 who were randomized to fenofibrate or placebo, the fenofibrate group had a significantly lower rate of nontraumatic amputations (HR 0.62, p = 0.011) [[78]]. Mechanistic
fenofibrate 24097 nontraumatic amputations (HR 0.62, p = 0.011) [[78]]. Mechanistic studies in obese db/db mice have found that fenofibrate markedly activates the above-mentioned PPARalpha-AMPK-PGC1 pathway in the sciatic nerve, while improving
niacin 22691 like mechanical sensitivity and NCV [[75]]. In a trial comparing treatment with fenofibrate versus niacin for 6 weeks in patients with primary hypercholesterolemia or mixed dyslipidemia, fenofibrate effectively
rosuvastatin 26010 of their NCV of the saphenous and sciatic nerves after 2 weeks of treatment with 0.3–20 mg/kg of rosuvastatin and a normalization of thermal hyperalgesia with the 20 mg/kg dose. These results indicated improvement
rosuvastatin 26673 [[77]]. A recent study demonstrated that patients with DM2 treated with simvastatin + ezetimibe or rosuvastatin had lower lipid peroxidation (LPO) markers versus placebo and a significant reduction in the Neuropathy
simvastatin 26646 reduction in the incidence of DPN [[77]]. A recent study demonstrated that patients with DM2 treated with simvastatin + ezetimibe or rosuvastatin had lower lipid peroxidation (LPO) markers versus placebo and a significant
Select Disease Character Offset Disease Term Instance
diabetes mellitus 2308 morbidity, mortality, and quality of life. There are five types of neurological syndromes related to diabetes mellitus : distal symmetric polyneuropathy (most frequent), autonomic neuropathy, small-fiber neuropathy (earliest),
diabetes mellitus 28010 effects [[88]].6. Summary/ConclusionDPN is a frequent, serious, and debilitating chronic complication of diabetes mellitus . Despite its relevance, very little is known about the details of its molecular pathogenesis and consequently
diabetic neuropathy 2026 complication of both type 1 (DM1) and type 2 (DM2) diabetes. In patients with DM2, the prevalence of diabetic neuropathy has been estimated at 20–40% in different populations [[1]–[3]]. Diabetic neuropathy is a progressive,
diabetic neuropathy 8634 kappa-B) and other proinflammatory transcription factors.The hexosamine pathway may also contribute to diabetic neuropathy . When cells have a high glucose influx, some of the fructose-6 phosphate in the glycolytic pathway is
diabetic neuropathy 12437 insulin at doses insufficient to change plasma glucose was able to prevent and reverse features of diabetic neuropathy (motor conduction velocities and axonal atrophy) in the sural nerves of streptozotocin-induced diabetic
diabetic neuropathy 19577 AMPK signaling has improved neuropathic manifestations like thermal hypoalgesia in a rodent model of diabetic neuropathy [[63]]. Administration of troglitazone (a PPAR-gamma agonist) to diabetic obese rats improved NCV [[64]].4.4.
diabetic neuropathy 30837 strategy against DPN.Figure 1Pathogenic mechanisms linking abnormal lipid metabolism to progression of diabetic neuropathy . HFD: high-fat diet, FA: fatty acids, PGC-1alpha: PPAR-gamma coactivator 1-alpha, NRF-1: nuclear respiratory
hyperglycemia 6466 risk with newer oral antidiabetic therapies but did not report on neuropathy endpoints [[14], [15]].So hyperglycemia does not seem to be the sole factor explaining the appearance and progression of DPN, and the effect
hyperglycemia 6834 been implicated in the development and progression of DPN. The high oxidative stress characteristic of hyperglycemia exerts injury to nerve cells through lipid peroxidation, direct damage to DNA with pathological activation
hyperglycemia 7103 antioxidants, and induction of proinflammatory transcription factors [[16]]. Another pathway leading from hyperglycemia to DPN entails the activation of the intracellular enzyme aldose reductase, which transforms glucose
hyperglycemia 12943 impact of insulin on the nerve action potential under normal or high glucose conditions have found that hyperglycemia prolongs the action potential, an effect that is abolished by insulin [[31]]. However, under normoglycemic
hyperglycemia 29682 lipids and DPN.In summary, DPN is a complex and multifactorial entity in which various factors besides hyperglycemia play an important role. There is a host of indirect evidence showing that deranged lipid metabolism
metabolic syndrome 10115 propose that alterations of lipid metabolism (which are very frequent in patients with DM2 and/or the metabolic syndrome ) participate in several key pathways of DPN pathogenesis and that normalization of lipid metabolism
metabolic syndrome 13537 action in other tissues (adipose and liver) are also present in nerve tissue. Human patients with the metabolic syndrome are characterized by insulin resistance and a chronic low-degree inflammation status [[33], [34]]. In
metabolic syndrome 21658 DM2 [[72]].Observational studies have demonstrated that DOSL levels are increased in patients with metabolic syndrome and/or DM2. A study comparing the sphingolipid profile of patients with DM1, DM2, and controls found
obesity 24621 Experimentally, an increased production of omega-3 in a diabetic mice model confers resistance to diet induced obesity and diabetes [[81]]. Supplementation with fish oil containing DHA completely prevented the development

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