Dopamine transporter and D2 receptor binding densities in mice prone or resistant to chronic high fat diet-induced

Xu-Feng Huang1, Katerina Zavitsanou, Xin Huang

  • 1Department of Biomedical Science, University of Wollongong, NSW 2522, Australia.

Behavioural Brain Research
|September 27, 2006
PubMed

Insights

Obesity alters brain dopamine transporter (DAT) and D2 receptor densities. Obese-resistant mice showed lower DAT, while obese mice had reduced D2 receptors in specific brain regions.

Area of Science:

  • Neuroscience
  • Metabolic Research
  • Dietary Impact on Brain Chemistry

Background:

  • Obesity is linked to neurochemical alterations.
  • Dopamine transporter (DAT) and D2 receptors play roles in reward pathways and appetite regulation.
  • Diet-induced obesity models are crucial for understanding these changes.

Purpose of the Study:

  • To investigate the density of DAT and D2 receptors in different brain regions of mice subjected to chronic high-fat diets.
  • To compare neurochemical profiles between obese (cDIO), obese-resistant (cDR), and control (LF) mice.

Main Methods:

  • Utilized positron emission tomography (PET) or autoradiography to quantify DAT and D2 receptor densities.
  • Compared receptor densities across three groups: chronic high-fat diet-induced obese (cDIO), obese-resistant (cDR), and low-fat-fed (LF) control mice.
  • Focused analysis on key brain regions including the nucleus accumbens, striatum, hypothalamus, and caudate putamen.

Main Results:

  • Significantly decreased DAT densities were observed in obese-resistant (cDR) mice compared to both obese (cDIO) and control (LF) mice.
  • These DAT reductions were prominent in the nucleus accumbens, striatal, and hypothalamic regions.
  • D2 receptor density was significantly lower in the rostral caudate putamen of obese (cDIO) mice when compared to obese-resistant (cDR) and control (LF) mice.

Conclusions:

  • Chronic high-fat feeding differentially impacts dopamine system components in obese versus obese-resistant phenotypes.
  • Reduced DAT availability in obese-resistant mice may indicate compensatory mechanisms or distinct neurobiological pathways.
  • Altered D2 receptor density in obese mice suggests disruptions in reward signaling pathways contributing to the obese state.