Document Type : Original Article
Authors
1
Medical physiology department, Faculty of Medicine for Girls, Al-Azhar University, Cairo, Egypt
2
Histology department, Faculty of Medicine for Girls, Al-Azhar University, Cairo, Egypt
3
Department of Medical Biochemistry, Faculty of Medicine, Al-Azhar University, Cairo, Egypt.
4
Medical physiology department, Damietta Faculty of Medicine, Al-Azhar University, Damietta, Egypt
5
Anatomy and Embryology department, Faculty of Medicine for Girls, Al-Azhar University, Cairo, Egypt
6
Department of Medical Physiology, Faculty of Medicine, Al-Azhar University, Cairo, Egypt
7
Department of Medical Pharmacology, Faculty of Medicine, Al-Azhar University, Cairo, Egypt.
8
Biochemistry department, faculty of medicine for girls, Al-Azhar University, Cairo, Egypt
9
Pharmacology department, Faculty of medicine for girls, Al- Azhar University, Cairo, Egypt
10
Medical Physiology Department, Faculty of Medicine, Al-Azhar University, Cairo, Egypt
Abstract
The prevalence of metabolic syndrome (MetS) makes type 2 diabetes mellitus and its consequences more common in communities. Dysfunctions of the nervous system has negative implications on the lives of affected individuals and their families. This study aimed to elucidate the possible role of MetS and treatment with in insulin like growth factor 1 (IGF-1) on some biochemical and immunohistochemical parameters related to neuronal functions in adult male albino rats. For this purpose, fifty adult male albino rats were recruited and divided into five groups. (1) control group, (2) MetS group (induced by high fat diet for eight weeks), (3) MetS group treated with IGF-1 for six weeks started two weeks before induction of MetS, (4) MetS group treated with IGF-1 for six weeks started with induction of MetS, (5) MetS group treated with IGF-1 for six weeks started two weeks after starting induction of MetS. Fasting blood glucose (FBG), insulin, lipid profile, glucagon like peptide 1 (GLP1), tumor necrosis factor-α (TNF-α) and adiponectin levels were measured in the serum whereas malonaldehyde, glutathione peroxidase (GPx), brain derived neurotrophic factor (BDNF), synapsin 1 and sortilin were measured in brain tissue homogenate. Histo pathological and immunohistochemical studies for B cell lymphoma 2 (BCL2) and glial fibrillary acidic protein (GFAP) were also done. The results showed that induction of MetS caused hyperglycemia, hyperinsulinemia, dyslipidemia, elevation of the oxidant marker MDA and the proinflamatory TNF-α whereas the anti-oxidant GPx and the anti-infalimatory adiponectin were elevated. BDNF and the anti-apoptotic BCL2 were reduced whereas synapsin 1, sortilin and the astrocytes proliferation marker GFAP were increased. Treatment with IGF-1 was associated with improvement in all these parameters. It could be concluded that MetS is associated with reduction in neuronal protective factors and enhancement of factors which impair neuronal functions and structures. These effects may underlie the pathogenesis of cognitive dysfunction associating MetS. By antagonizing such effects of MetS, IGF-1 may be helpful in managing MetS and associated cognitive dysfunction.
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