Abstract
BackgroundDiabetic encephalopathy is a chronic complications of diabetes mellitus that affects the central nervous system. We evaluated the effect of ω3 and ω6 polyunsaturated fatty acids (PUFAs) supplementation plus the antioxidant agent nordihydroguaiaretic acid (NDGA) on the etiopathology of diabetic encephalopathy in eSS rats, a spontaneous model of type 2 diabetes.MethodsOne hundred twenty spontaneous diabetic eSS male rats and 38 non-diabetic Wistar, used as healthy control, received monthly by intraperitoneal route, ω3 or ω6 PUFA (6.25 mg/kg) alone or plus NDGA (1.19 mg/kg) for 12 months. Diabetic rats had a worse performance in behavioural Hole-Board test. Histopathological analysis confirmed lesions in diabetic rats brain tissues. We also detected low expression of synaptophysin, a protein linked to release of neurotransmitters, by immunohistochemically techniques in eSS rats brain. Biochemical and histopathological studies of brain were performed at 12th month. Biochemical analysis showed altered parameters related to metabolism. High levels of markers of oxidative stress and inflammation were detected in plasma and brain tissues. Data were analysed by ANOVA test and paired t test was used by comparison of measurements of the same parameter at different times.ResultsThe data obtained in this work showed that behavioural, biochemical and morphological alterations observed in eSS rats are compatible with previously reported indices in diabetic encephalopathy and are associated with increased glucolipotoxicity, chronic low-grade inflammation and oxidative stress burden. Experimental treatments assayed modulated the values of studied parameters.ConclusionsThe treatments tested with ω3 or ω3 plus NDGA showed improvement in the values of the studied parameters in eSS diabetic rats. These observations may form the basis to help in prevent and manage the diabetic encephalopathy.
Highlights
Diabetic encephalopathy (DE) is a chronic complication of diabetes mellitus that affects the central nervous system (CNS) and is characterized by cognitive impairment and motor dysfunctions that can cause postural balance impairment
We evaluated the effects of intraperitoneal administration of polyunsaturated fatty acids (PUFAs) ω6 and ω3 alone or in combination with nordihydroguaiaretic acid (NDGA), a potent natural antioxidant compound isolated from native plant Larrea sp. [9], on the etiopathology of glucolipotoxicity observed in DE and focused on hippocampal tissues in a spontaneous rat Type 2 diabetes mellitus (DM2) model
Activity of desaturases that are needed for fatty acid synthesis are known to be affected in DM2 animals and humans [24] that could explain differences in the levels of various PUFAs noted in the plasma among control, diabetic Stillman-Salgado rats (eSS) and Wistar groups and improvements induced by low doses of ω3 PUFAs administration alone or in combination with NDGA
Summary
Diabetic encephalopathy (DE) is a chronic complication of diabetes mellitus that affects the central nervous system (CNS) and is characterized by cognitive impairment and motor dysfunctions that can cause postural balance impairment. The concept of glucolipotoxicity refers to the combined, deleterious effects of elevated glucose, triglycerides (TG), higher energy intake and free fatty acid levels (FFA) on pancreatic beta-cell function and survival. Excessive levels of circulating FFA and glucose leads to decreased insulin secretion, impaired insulin gene expression, and in turn beta-cell death by apoptosis [4, 5]. Diabetic encephalopathy is a chronic complications of diabetes mellitus that affects the central nervous system. We evaluated the effect of ω3 and ω6 polyunsaturated fatty acids (PUFAs) supplementation plus the antioxidant agent nordihydroguaiaretic acid (NDGA) on the etiopathology of diabetic encephalopathy in eSS rats, a spontaneous model of type 2 diabetes
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