The Effect of Obesity on the Availabilities of Dopamine and Serotonin Transporters

Abstract

The authors investigated relations between obesity, age, and sex and the availabilities of striatal dopamine transporter (DAT) and extrastriatal serotonin transporter (SERT) by 123I-FP-CIT single-photon emission computed tomography. The study population consisted of 192 healthy controls with screening 123I-FP-CIT scans. Specific bindings of 123I-FP-CIT to DAT and SERT were calculated using regions of interest. Specific binding ratios (SBRs) of DAT and SERT except pons (r = 0.2217, p = 0.0026), were not correlated with body mass index (BMI). SBRs of midbrains correlated negatively with the BMIs of obese subjects (r = −0.3126, p = 0.0496), and positively with the those of non-obese subjects (r = 0.2327, p = 0.0053). SBRs of caudate nucleus (r = −0.3175, p < 0.0001), striatum (r = −0.226, p = 0.0022), and thalamus (r = −0.1978, p = 0.0074) reduced with age, and SERT availability was higher in males. However, DAT availability was similar in males and females. In conclusion, obesity has an effect on midbrain SERT availability. In addition, BMI was correlated with pontine SERT availability but not with striatal DAT availability. SERT availability was higher in males, but DAT availability showed no gender predilection.

Striatal dopamine transporter changes after glucose loading in humans

“…12 With the exception of one study, 33 most baseline studies have shown no significant association between DAT availability and BMI. [13][14][15] Consistent with previous studies, DAT availability in the placebo-loaded participants (baseline) did not show any significant correlation with BMI in this study. However, eating behavior is a complicated and incompletely understood process, resulting from a combination of visual stimulation, olfactory stimulation, expectation, gastric distension and glucose levels.…”

“…Although synaptic dopamine concentrations are regulated by the DAT, it is insensitive to the synaptic dopamine concentration, unlike DR, and it is affected neither by the depletion of dopamine via the tyrosine hydroxylase inhibitor nor by the release of dopamine by the DR antagonist . With the exception of one study, most baseline studies have shown no significant association between DAT availability and BMI . Consistent with previous studies, DAT availability in the placebo‐loaded participants (baseline) did not show any significant correlation with BMI in this study.…”

“…11,12 Although the DAT is a major target of various pharmacologically active drugs, its role in obesity has not been established. The majority of previous studies reported no significant correlation between DAT availability and body mass index (BMI), [13][14][15] and the DAT was not thought to be involved in the neurobiology underlying obesity in humans. 13 However, according to animal studies, insulin increases the levels and activity of DAT mRNA and, thereby, enhances the clearance of dopamine from the synapse.…”

Metabolic, Molecular, and Behavioral Effects of Western Diet in Serotonin Transporter-Deficient Mice: Rescue by Heterozygosity?

“…Individuals with metabolic syndrome and obesity display decreased SERT expression in the brain and periphery (Giannaccini et al, 2013;Nam et al, 2018). Excessive intake of a hypercaloric diet, enriched with saturated fat and sugars, was shown to suppress the binding of hypothalamic SERT in obese subjects and in insulin-resistant subjects that is independent of body weight gain (Koopman et al, 2013;Versteeg et al, 2017).…”

Lost in Translation? On the Need for Convergence in Animal and Human Studies on the Role of Dopamine in Diet-Induced Obesity

“…Although playing a central role in motivation and cognition, dopamine is not the only neurotransmitter involved. In fact, dopamine interacts closely with other systems such as the opioid, serotonin and noradrenergic system [57,71,189,190]. A relationship to obesity has been demonstrated for all of them.…”