THE NEURODEGENERATION PROCESS IN THE STRIATUM OF MICE EXPOSED TO OBESOGENIC DIETS
(2020) MOBN03 20192Degree Projects in Molecular Biology
- Abstract
- Obesity and diabetes are known to impact brain function and alter metabolism. Studies in rodents show that consumption of high fat and high sugar diets lead to brain dysfunction affecting memory and cognition, and increases risk of cerebro-vascular and neurodegenerative disorders. Striatum, which is involved in reward-based behaviour and motor control, undergoes changes on exposure to such diets leading to movement defects, loss of impulse control, increased susceptibility to neurotoxins like MPTP and 6-OHDA. This effect is brought about by insulin resistance and loss of dopaminergic neurons thereby reducing dopamine signalling. In this study, striatal degeneration was investigated by measuring levels of synaptic proteins by immunoblotting... (More)
- Obesity and diabetes are known to impact brain function and alter metabolism. Studies in rodents show that consumption of high fat and high sugar diets lead to brain dysfunction affecting memory and cognition, and increases risk of cerebro-vascular and neurodegenerative disorders. Striatum, which is involved in reward-based behaviour and motor control, undergoes changes on exposure to such diets leading to movement defects, loss of impulse control, increased susceptibility to neurotoxins like MPTP and 6-OHDA. This effect is brought about by insulin resistance and loss of dopaminergic neurons thereby reducing dopamine signalling. In this study, striatal degeneration was investigated by measuring levels of synaptic proteins by immunoblotting and evaluating the phenotype of glial cells in mice exposed to fat-rich diets (10%, 45% and 60% of total energy intake) for 6 months. Relative to control fed the 10%-fat diet, mice fed 60% fat showed a decrease in levels of synaptic proteins Synaptosome-associated protein (SNAP25) and Syntaxin-1 whereas 45% fat diet reduced levels of Synaptophysin. The data from this study does not point to significant changes in dopamine signalling, astrogliosis or neuroinflammation. In sum, the trend observed in terms of reduction in levels of synaptic proteins that are crucial for maintaining efficient synaptic plasticity is likely to cause to neuronal networks involving the striatum, which controls, motor function and emotional behaviours. (Less)
- Popular Abstract
- THE NEURODEGENERATION PROCESS IN THE STRIATUM OF MICE EXPOSED TO OBESOGENIC DIETS
Obesity and diabetes are known to impact brain function and alter metabolism. Studies in rodents show that consumption of high fat and high sugar diets lead to brain dysfunction affecting memory and cognition, and increases risk of cerebro-vascular and neurodegenerative disorders. Striatum, which is involved in reward-based behaviour and motor control, undergoes changes on exposure to such diets leading to movement defects, loss of impulse control, increased susceptibility to neurotoxins. This effect is brought about by insulin resistance and loss of dopaminergic neurons thereby reducing dopamine signalling.
Obesity arises due to the imbalance in... (More) - THE NEURODEGENERATION PROCESS IN THE STRIATUM OF MICE EXPOSED TO OBESOGENIC DIETS
Obesity and diabetes are known to impact brain function and alter metabolism. Studies in rodents show that consumption of high fat and high sugar diets lead to brain dysfunction affecting memory and cognition, and increases risk of cerebro-vascular and neurodegenerative disorders. Striatum, which is involved in reward-based behaviour and motor control, undergoes changes on exposure to such diets leading to movement defects, loss of impulse control, increased susceptibility to neurotoxins. This effect is brought about by insulin resistance and loss of dopaminergic neurons thereby reducing dopamine signalling.
Obesity arises due to the imbalance in energy intake and expenditure which in turn increases the risk of developing Type 2 Diabetes (T2D). Food intake controlled by homeostatic system through hypothalamic neurons is regulated by satiety signals and hormones such as insulin and leptin whereas physiological stimuli like taste, hunger, palatable food intake controls the reward system. The deregulation of these systems is linked to obesity further promoting a preference for high calorie diet, which results in a cycle of over-eating causing long-term obesity and development of T2D. In addition, these systems also play a role in emotional behaviour and their deregulation results in mood disorders such as anxiety and depression.
The rewarding value of food consumption is encoded by dopamine (DA) signalling in striatum. Upon consumption of palatable food and certain drugs. The synaptic levels of dopamine are regulated by DA transporters which reduce under the effect of high calorie diets resulting in an imbalance in DA levels. This imbalance results in reduction of impulse control leading to altered food seeking and binge-like eating behaviour. DA signalling also controls motor function which is affected in Parkinson’s disease (PD) due to damage in dopamine releasing neurons.
High fat diet (HFD) feeding is used extensively as a model to understand the underlying causes for obesity and its associated metabolic alterations. Mice model exposed to HFD feeding with varying percentage of lard-based fat which is rich in saturated fats were reported to show a phenotype of obesity. In this study, striatal degeneration was investigated by measuring levels of synaptic proteins by immunoblotting and evaluating the phenotype of glial cells in mice exposed to fat-rich diets (10%, 45% and 60% of total energy intake) for 6 months.
Relative to control fed the 10%-fat diet, mice fed 60% fat showed a decrease in levels of synaptic proteins Synaptosome-associated protein (SNAP25) and Syntaxin-1 whereas 45% fat diet reduced levels of Synaptophysin. The data from this study does not point to significant changes in dopamine signalling, astrogliosis or neuroinflammation. In sum, the trend observed in terms of reduction in levels of synaptic proteins that are crucial for maintaining efficient synaptic plasticity is likely to cause damage to neuronal networks involving the striatum, which controls motor function and emotional behaviours. The impact of these changes in the function of the striatum remain to be studied in detail.
Master’s Degree Project in Molecular Biology 60 credits 2020
Department of Biology, Lund University
Advisor: João Duarte
Principal investigator
Diabetes and Brain function lab, Department of Experimental Medicine
Lund University (Less)
Please use this url to cite or link to this publication:
http://lup.lub.lu.se/student-papers/record/9028286
- author
- Talukdar, Ankita
- supervisor
-
- Joao Duarte LU
- organization
- course
- MOBN03 20192
- year
- 2020
- type
- H2 - Master's Degree (Two Years)
- subject
- language
- English
- id
- 9028286
- date added to LUP
- 2020-09-08 14:04:25
- date last changed
- 2020-09-08 14:04:25
@misc{9028286,
abstract = {{Obesity and diabetes are known to impact brain function and alter metabolism. Studies in rodents show that consumption of high fat and high sugar diets lead to brain dysfunction affecting memory and cognition, and increases risk of cerebro-vascular and neurodegenerative disorders. Striatum, which is involved in reward-based behaviour and motor control, undergoes changes on exposure to such diets leading to movement defects, loss of impulse control, increased susceptibility to neurotoxins like MPTP and 6-OHDA. This effect is brought about by insulin resistance and loss of dopaminergic neurons thereby reducing dopamine signalling. In this study, striatal degeneration was investigated by measuring levels of synaptic proteins by immunoblotting and evaluating the phenotype of glial cells in mice exposed to fat-rich diets (10%, 45% and 60% of total energy intake) for 6 months. Relative to control fed the 10%-fat diet, mice fed 60% fat showed a decrease in levels of synaptic proteins Synaptosome-associated protein (SNAP25) and Syntaxin-1 whereas 45% fat diet reduced levels of Synaptophysin. The data from this study does not point to significant changes in dopamine signalling, astrogliosis or neuroinflammation. In sum, the trend observed in terms of reduction in levels of synaptic proteins that are crucial for maintaining efficient synaptic plasticity is likely to cause to neuronal networks involving the striatum, which controls, motor function and emotional behaviours.}},
author = {{Talukdar, Ankita}},
language = {{eng}},
note = {{Student Paper}},
title = {{THE NEURODEGENERATION PROCESS IN THE STRIATUM OF MICE EXPOSED TO OBESOGENIC DIETS}},
year = {{2020}},
}