Dopamine increased with vitamin D supplementation (in rats)

The Vitamin D Content of a High-Fat Diet Modulates Brain Reward Neurochemistry

The FASEB Journal, vol. 30 no. 1 Supplement lb202 , April 2016

Ruslan Kubant1, Diptendu Chatterjee1, Emanuela Pannia1 and G. Harvey Anderson1,2

1Nutritional Sciences, University of Toronto, Toronto, ON, Canada

2Physiology, University of Toronto, Toronto, ON, Canada

Rats on high fat diet (60% of calories) Age 3 weeks to 17 weeks Compare 7,000 IU vs 1000 IU of Vitamin D per kilogram of feed

	Increase
Dopamine	48%
* 3,4-Dihydroxyphenylacetic acid	330%
Vitamin D blood level	300%

See Dopamine on web * DOPAMINE Psychology Today * “Dopamine is a neurotransmitter that helps control the brain's reward and pleasure centers. Dopamine also helps regulate movement and emotional responses, and it enables us not only to see rewards, but to take action to move toward them. Dopamine deficiency results in Parkinson's Disease , and people with low dopamine activity may be more prone to addiction.” * Google Summaries – April 2016 * “Dopamine is used for: Treating shock and low blood pressure due to heart attack, trauma, infections, surgery, and other causes. It is also used to help improve heart function when it is unable to pump enough blood.” * “Dopamine is a brain chemical involved in many different functions including movement, motivation, reward — and addiction. Nearly all drugs of abuse directly or indirectly increase dopamine in the pleasure and motivation pathways and in so doing, alter the normal communication between neurons.” See also VitaminDWiki * Dopamine quickly increased by Calcitriol (fully activated vitamin D) – might be a way to treat ADHD – Oct 2024 * Hypothesis: Drug addiction in humans can be prevented and treated by vitamin D -May 2014 * Search VitaminDWiki for DOPAMINE 1,120 items as of Nov 2024 * Parkinson’s, Restless Legs, Sleep

Background Obesity is associated with increased consumption and preference for palatable foods as well as reduced blood levels of 25[OH]D3, which has been linked to altered dopaminergic and serotonergic signalling in the brain. The effect of vitamin D on high fat diet induced changes in brain reward systems is unknown.

Objective To determine if vitamin D plays a role in modulating hedonic regulation of food intake in the brain in response to chronic consumption of a high fat diet.

Methods and Design Male Wistar rats at 21 days of age were fed ad libitum for 14 weeks a high-fat diet (60 kcal% fat) containing either: 1) the recommended amount (1,000 IU/kg diet) of vitamin D3 (HF-RD) or 2) high vitamin D3 (HF-HD, 7-fold increase of the recommended amount). Rats fed a normal-fat diet with the recommended amount of vitamin D3 (NF-RD, 16 kcal% from fat) served as control. Body weight, food intake, serum 25[OH]D3, and concentrations of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA) were measured in the nucleus accumbens (NAc) and β-endorphin in the ventral tegmental area (VTA). DA and 5-HT turnover rates were calculated by the ratio of their primary metabolites DOPAC to DA and 5-HIAA to 5-HT respectively, and used as an index of dopamine/serotonin transmission.

Results The HF-RD group consumed more calories and gained more weight than the NF-RD group as well as exhibited increased DA (48%, P<0.05), DOPAC (330%, P<0.05), dopamine turnover (195%, P<0.05), 5-HT (85%, P<0.05), 5-HIAA (51%, P<0.05), and lower serotonin turnover (16%, P<0.05) in NAc. VTA levels of β-endorphin were lower (46%, P<0.05) in the HF-RD group compared to the NF-RD. Supplementation of a HF diet with high vitamin D3 for 14 weeks resulted in a 3-fold increase (P<0.05) in serum 25[OH]D3 and reduction (≈30%, P<0.05) in DOPAC levels and dopamine turnover compared to the HF-RD group, but had no statistically significant effect on food intake, body weight, 5-HT, 5-HIAA, serotonin turnover rate or β-endorphin levels in the brain.

Conclusion The vitamin D content of a high-fat diet modulates brain reward neurochemistry and may be a factor in neurotransmitter-mediated regulation of the reward-seeking behaviors.

Support or Funding Information

Canadian Institute of Health Research, Institute of Nutrition, Metabolism and Diabetes (CIHR-INMD), Reference MOP-130286.

This abstract is from the Experimental Biology 2016 Meeting.

There is no full text article associated with this abstract published in The FASEB Journal.