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Obesity/hyperleptinemic phenotype impairs structural and functional plasticity in the rat hippocampus
Claudia A Grillo1, Gerardo G Piroli, Lorain Junor
1Department of Pharmacology, Physiology and Neuroscience, University of South Carolina School of Medicine, 6439 Garners Ferry Road, Columbia, SC 29208, USA.
Physiology & Behavior
|March 1, 2011
Summary
Obesity impacts the brain, potentially harming the hippocampus. This study shows that disrupting insulin signaling in rats leads to obesity and impaired hippocampal function, suggesting leptin resistance contributes to these neurological deficits.
Area of Science:
- Neuroscience
- Metabolic Syndrome Research
- Obesity Studies
Background:
- Over 60% of US adults are overweight or obese, with growing evidence of central nervous system (CNS) complications.
- While hypothalamic effects of obesity are well-studied, the hippocampus is increasingly recognized as affected.
- Leptin, a hormone from fat cells, is implicated in CNS abnormalities, with potential leptin resistance in the hippocampus.
Purpose of the Study:
- To investigate the role of leptin in obesity-related hippocampal neuroplasticity deficits.
- To examine hippocampal structural and functional plasticity in a rat model with downregulated hypothalamic insulin receptors (hypo-IRAS).
Main Methods:
- Lentivirus-mediated downregulation of hypothalamic insulin receptors (hypo-IRAS) in rats.
- Assessment of body weight, adiposity, plasma leptin, and triglyceride levels.
- Evaluation of hippocampal morphological plasticity and performance in hippocampal-dependent behavioral tasks.
- Measurement of leptin-mediated signaling in the hippocampus.
Main Results:
- Hypo-IRAS rats developed increased body weight, adiposity, hyperleptinemia, and hypertriglyceridemia, mimicking metabolic syndrome features.
- Adversely affected hippocampal morphological plasticity was observed in hypo-IRAS rats.
- Impaired performance in hippocampal-dependent tasks and decreased leptin signaling were noted in hypo-IRAS rats.
Conclusions:
- Downregulating hypothalamic insulin receptors induces an obesity phenotype with associated hippocampal dysfunction.
- Hyperleptinemia and hypertriglyceridemia may mediate neurological consequences of impaired hippocampal synaptic plasticity in obesity.
- Leptin resistance may contribute to hippocampal deficits in obesity models.
