Pathogenesis and neuroimaging of cerebral large and small vessel disease in type 2 diabetes: A possible link between cerebral and retinal microvascular abnormalities

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Term Occurence Count Dictionary
diabetes mellitus 2 endocrinologydiseases
diabetic retinopathy 6 endocrinologydiseases
hyperglycemia 12 endocrinologydiseases
hyperinsulinemia 1 endocrinologydiseases
type 2 diabetes mellitus 1 endocrinologydiseases
Insulin 2 endocrinologydiseasesdrugs

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Insulin 11571 cascade activated through hyperglycemia‐induced polyol pathway hyperactivity, as seen in Figure 1. Insulin resistance is also thought to be a risk factor for cerebral infarction, and it has been reported that
Insulin 11833 half of non‐diabetic individuals who had experienced transient ischemic attack or ischemic stroke45. Insulin resistance is not only related to impaired glucose tolerance, it is also considered to promote atherosclerosis
Select Disease Character Offset Disease Term Instance
diabetes mellitus 26972 (standard error). †White matter lesions (WML) volumes are analyzed as log‐transformed values. DM, diabetes mellitus ; DWML, deep white matter lesion; NA, not applicable; NS, not significant; PVH, periventricular hyperintensity;
diabetes mellitus 27187 hyperintensity; PWML, periventricular white matter lesion; SBI; silent brain infarction; T2DM; type 2 diabetes mellitus ; WMH, white matter hyperintensity.John Wiley & Sons, LtdCMBs are also a manifestation of cerebral SVD
diabetic retinopathy 4565 polyol pathway hyperactivity is considered to be one possible mechanism underlying the development of diabetic retinopathy 13. As retinal microvascular abnormalities are associated with magnetic resonance imaging (MRI) markers
diabetic retinopathy 33514 linked to ischemic cerebral SVD.In fact, there are several studies suggesting an association between diabetic retinopathy and lacunar stroke120, 121, 122 or cognitive impairment123, 124 in patients with diabetes. As a potential
diabetic retinopathy 35138 wall in the retinal tissue initiates the abnormality of morphological detection in the early stage of diabetic retinopathy 126, 127. The interaction between pericytes and the endothelial cells plays a crucial role in maintaining
diabetic retinopathy 35485 hyperglycemia might contribute to breakdown of the blood–retina barrier, and the subsequent development of diabetic retinopathy . Although an exact mechanism for the disruption of the blood–retina barrier in patients with diabetes
diabetic retinopathy 36654 diabetes patients.Figure 6Cerebro–retinal interaction in diabetes. A 76‐year‐old woman with simple diabetic retinopathy . (a) Magnetic resonance imaging expressions of cerebral small vessel disease including silent brain
diabetic retinopathy 36888 (red arrow), white matter lesion (white arrow) and microbleed (arrow head). (b) Retinal photograph of diabetic retinopathy signs showing microaneurysm and retinal hemorrhages (arrow), and hard exudates (arrow head).Conclusion
hyperglycemia 4157 and inflammatory processes have been implicated10, 11. In addition, a previous study has shown that hyperglycemia ‐induced polyol pathway hyperactivity might play an important part in the development of diabetes atherosclerosis12.
hyperglycemia 7999 infarction.The risk factors for the development of atherosclerosis in patients with diabetes are chronic hyperglycemia , dyslipidemia, hypertension and hyperinsulinemia. These risk factors and their related abnormalities,
hyperglycemia 8791 including microvascular disease and atherosclerosis, has been proposed on the basis of findings for hyperglycemia ‐induced metabolic abnormalities, such as oxidative stress, changes in protein kinase C, glycation
hyperglycemia 9563 through the polyol pathway accounts for less than 3% of glucose consumption in cells. However, during hyperglycemia , total consumption of glucose through this pathway represents up to 30%137, resulting in the enhancement
hyperglycemia 9744 30%137, resulting in the enhancement of glucose utilization through metabolic cascade shown. Thus, hyperglycemia ‐induced polyol pathway hyperactivity might contribute to developing not only microvascular disease,
hyperglycemia 10258 molecule.Previous studies by our group28, 29, 30, 31, 32 and others33, 34, 35, 36, 37, 38, 39 have suggested that hyperglycemia ‐induced polyol pathway hyperactivity might, in part, play an important role in the development of
hyperglycemia 10460 development of diabetes atherosclerosis. Recently, Tang et al.40 have observed that the combination of hyperglycemia during collagen activation leads to a positive feedback cycle of release of platelet thromboxane and
hyperglycemia 10853 human AR mice aortas by Vedantham et al.41 surmised that glucose flux through the polyol pathway in hyperglycemia mediates atherosclerosis in part by influencing nicotinamide phosphoribosyl transferase‐mediated nicotinamide
hyperglycemia 11497 microangiopathy12, 27, 42, 43, 44, and might partly develop from the metabolic cascade activated through hyperglycemia ‐induced polyol pathway hyperactivity, as seen in Figure 1.Insulin resistance is also thought to be
hyperglycemia 32290 research.Interaction between Cerebral and Retinal Microvascular Abnormalities in DiabetesAssociation of hyperglycemia and polyol pathway hyperactivity with diabetes atherosclerosisCerebral and retinal small vessels have
hyperglycemia 35376 structural and functional integrity of the retinal vascular walls. The failure of this integrity induced by hyperglycemia might contribute to breakdown of the blood–retina barrier, and the subsequent development of diabetic
hyperglycemia 35669 blood–retina barrier in patients with diabetes has not been established, one of the possibilities is that hyperglycemia ‐induced polyol pathway hyperactivity might partially play an important role13, 42, 44, 128, 129, 130,
hyperinsulinemia 8045 atherosclerosis in patients with diabetes are chronic hyperglycemia, dyslipidemia, hypertension and hyperinsulinemia . These risk factors and their related abnormalities, such as decreased bioavailability of vascular nitric
type 2 diabetes mellitus 27180 periventricular hyperintensity; PWML, periventricular white matter lesion; SBI; silent brain infarction; T2DM; type 2 diabetes mellitus ; WMH, white matter hyperintensity.John Wiley & Sons, LtdCMBs are also a manifestation of cerebral SVD

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