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N in ways that could cause insulin/IGF resistance in the brain, their specific effects were not identical. The main effect of NDEA, with or without HFD feeding, was to reduce mRNA levels of insulin receptor, IGF-2 receptor, and IRS-2, which would have impaired signaling at the receptor level, and downstream through IRS-2, one of main docking proteins responsible for transmitting survival, growth,
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Tylcholine receptor binding in the cerebellum and brainstem [103]. In previous studies using a mouse model of dietinduced obesity [45,46], we showed that chronic HFD feeding causes brain insulin resistance [46]. Similarly, herein we demonstrated that the HFD-fed rats had reduced levels of brain IRS-1 mRNA, which would have been sufficient to cause brain insulin resistance due to impaired transmiss
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Tylcholine receptor binding in the cerebellum and brainstem [103]. In previous studies using a mouse model of dietinduced obesity [45,46], we showed that chronic HFD feeding causes brain insulin resistance [46]. Similarly, herein we demonstrated that the HFD-fed rats had reduced levels of brain IRS-1 mRNA, which would have been sufficient to cause brain insulin resistance due to impaired transmiss
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E formation of DNA and protein adducts [105-107] that can serve as persistent sources of oxidative stress, and cause further DNA damage and protein dysfunction. Recently, we demonstrated a role for ceramidemediated neurodegeneration in a model of diet-induced obesity with T2DM [45], and showed that in vitro ceramide exposure causes neurodegeneration with impairments in neuronal viability, energy m
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Tylcholine receptor binding in the cerebellum and brainstem [103]. In previous studies using a mouse model of dietinduced obesity [45,46], we showed that chronic HFD feeding causes brain insulin resistance [46]. Similarly, herein we demonstrated that the HFD-fed rats had reduced levels of brain IRS-1 mRNA, which would have been sufficient to cause brain insulin resistance due to impaired transmiss
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Ould reduce cases of lenses' falling off.Some patients, (7.1 ) made optometric consultations on account of their lost spectacles with consequential visual discomfort. In a population-based study of spectacles use in southern India, as many as 19.6 of people using spectacles had lost the pairs and could not afford to buy another pairs [21]. The patients should be counselled on how to take good car
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F HNE were similar in the HFD+VEH and HFD+NDEA groups, and both were significantly higher than in the LFD+VEH and LFD +NDEA groups (P
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Ation with impairments in insulin/IGF signaling mechanisms, and deficits in cholinergic and neuronal cytoskeletal gene and protein expression in brain, whereas chronic HFD feeding alone produces more restrictive deficits in insulin/IGF signaling mechanisms with reduced ChAT expression and increased oxidative stress. The combined exposures caused overlapping structural and molecular abnormalities t