Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Short Communication
  • Published:

Obese individuals with more components of the metabolic syndrome and/or prediabetes demonstrate decreased activation of reward-related brain centers in response to food cues in both the fed and fasting states: a preliminary fMRI study

International Journal of Obesity volume 41, pages 471–474 (2017)Cite this article

Subjects

Abstract

It remains unknown whether obese individuals with more components of the metabolic syndrome and/or prediabetes demonstrate altered activation of brain centers in response to food cues. We examined obese individuals with prediabetes (n=26) vs obese individuals without prediabetes (n=11) using fMRI. We also performed regression analyses on the basis of the number of MetS components per subject. Obese individuals with prediabetes have decreased activation of the reward-related putamen in the fasting state and decreased activation of the salience- and reward-related insula after eating. Obese individuals with more components of MetS demonstrate decreased activation of the putamen while fasting. All these activations remain significant when corrected for BMI, waist circumference (WC), HbA1c and gender. Decreased activation in the reward-related central nervous system areas among the obese is more pronounced in subjects with prediabetes and MetS. Prospective studies are needed to quantify their contributions to the development of prediabetes/MetS and to study whether they may predispose to the exacerbation of obesity and the development of comorbidities over time.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Figure 1

Similar content being viewed by others

References

  1. Ko BJ, Park KH, Mantzoros CS . Diet patterns, adipokines, and metabolism: where are we and what is next? Metabolism 2014; 63: 168–177.

    Article  CAS  Google Scholar 

  2. Mathew H, Farr OM, Mantzoros CS . Metabolic health and weight: Understanding metabolically unhealthy normal weight or metabolically healthy obese patients. Metabolism 2016; 65: 73–80.

    Article  CAS  Google Scholar 

  3. Pursey KM, Stanwell P, Callister RJ, Brain K, Collins CE, Burrows TL . Neural responses to visual food cues according to weight status: a systematic review of functional magnetic resonance imaging studies. Front Nutr 2014; 1: 7.

    Article  Google Scholar 

  4. Farr OM, Li CS, Mantzoros CS . Central nervous system regulation of eating: Insights from human brain imaging. Metabolism 2016; 65: 699–713.

    Article  CAS  Google Scholar 

  5. Association AD. Professional Practice Committee for the Standards of Medical Care in Diabetes-2016. Diabetes Care 2016; 39: S107–S108.

    Article  Google Scholar 

  6. Farr OM, Fiorenza C, Papageorgiou P, Brinkoetter M, Ziemke F, Koo BB et al. Leptin therapy alters appetite and neural responses to food stimuli in brain areas of leptin-sensitive subjects without altering brain structure. J Clin Endocrinol Metab 2014; 99: E2529–E2538.

    Article  CAS  Google Scholar 

  7. Farr OM, Sofopoulos M, Tsoukas MA, Dincer F, Thakkar B, Sahin-Efe A et al. GLP-1 receptors exist in the parietal cortex, hypothalamus and medulla of human brains and the GLP-1 analogue liraglutide alters brain activity related to highly desirable food cues in individuals with diabetes: a crossover, randomised, placebo-controlled trial. Diabetologia 2016; 59: 954–965.

    Article  CAS  Google Scholar 

  8. Farr OM, Tsoukas MA, Triantafyllou G, Dincer F, Filippaios A, Ko BJ et al. Short-term administration of the GLP-1 analog liraglutide decreases circulating leptin and increases GIP levels and these changes are associated with alterations in CNS responses to food cues: A randomized, placebo-controlled, crossover study. Metabolism 2016; 65: 945–953.

    Article  CAS  Google Scholar 

  9. Farr OM, Upadhyay J, Gavrieli A, Camp M, Spyrou N, Kaye H et al. Lorcaserin administration decreases activation of brain centers in response to food cues and these emotion- and salience-related changes correlate with weight loss effects: a four week long randomized, placebo-controlled, double-blinded clinical trial. Diabetes 2016; 65: 2943–2953.

    Article  CAS  Google Scholar 

  10. Ten Kulve JS, Veltman DJ, van Bloemendaal L, Barkhof F, Deacon CF, Holst JJ et al. Endogenous GLP-1 mediates postprandial reductions in activation in central reward and satiety areas in patients with type 2 diabetes. Diabetologia 2015; 58: 2688–2698.

    Article  CAS  Google Scholar 

  11. van Bloemendaal L, RG IJ, Ten Kulve JS, Barkhof F, Konrad RJ, Drent ML et al. GLP-1 receptor activation modulates appetite- and reward-related brain areas in humans. Diabetes 2014; 63: 4186–4196.

    Article  CAS  Google Scholar 

  12. Burger KS, Stice E . Greater striatopallidal adaptive coding during cue-reward learning and food reward habituation predict future weight gain. NeuroImage 2014; 99: 122–128.

    Article  Google Scholar 

  13. DiLeone RJ, Taylor JR, Picciotto MR . The drive to eat: comparisons and distinctions between mechanisms of food reward and drug addiction. Nat Neurosci 2012; 15: 1330–1335.

    Article  CAS  Google Scholar 

  14. Wang GJ, Volkow ND, Fowler JS . The role of dopamine in motivation for food in humans: implications for obesity. Expert Opin Ther Targets 2002; 6: 601–609.

    Article  CAS  Google Scholar 

  15. Frankort A, Roefs A, Siep N, Roebroeck A, Havermans R, Jansen A . Neural predictors of chocolate intake following chocolate exposure. Appetite 2015; 87: 98–107.

    Article  Google Scholar 

  16. Stice E, Burger KS, Yokum S . Reward region responsivity predicts future weight gain and moderating effects of the TaqIA allele. J Neurosci 2015; 35: 10316–10324.

    Article  CAS  Google Scholar 

  17. Yoshimi K, Kumada S, Weitemier A, Jo T, Inoue M . Reward-induced phasic dopamine release in the monkey ventral striatum and putamen. PloS One 2015; 10: e0130443.

    Article  Google Scholar 

  18. Dunn JP, Kessler RM, Feurer ID, Volkow ND, Patterson BW, Ansari MS et al. Relationship of dopamine type 2 receptor binding potential with fasting neuroendocrine hormones and insulin sensitivity in human obesity. Diabetes Care 2012; 35: 1105–1111.

    Article  CAS  Google Scholar 

  19. Thanos PK, Michaelides M, Piyis YK, Wang GJ, Volkow ND . Food restriction markedly increases dopamine D2 receptor (D2R) in a rat model of obesity as assessed with in-vivo muPET imaging ([11C] raclopride) and in-vitro ([3H] spiperone) autoradiography. Synapse 2008; 62: 50–61.

    Article  CAS  Google Scholar 

  20. Volkow ND, Wang GJ, Telang F, Fowler JS, Thanos PK, Logan J et al. Low dopamine striatal D2 receptors are associated with prefrontal metabolism in obese subjects: possible contributing factors. Neuroimage 2008; 42: 1537–1543.

    Article  Google Scholar 

Download references

Acknowledgements

These projects were supported by Harvard Clinical and Translational Science Center Grant UL1 RR025758 from the National Center for Research Resources and NIDDK DK081913. Olivia M Farr is supported by training grant 5T32HD052961. This study was in part funded by Eisai, who supported the study through an Investigator-Initiated Study grant. Eisai approved the design of the study, but had no role in study design; conduct of the study; collection, management, analysis, and interpretation of the data; or the preparation, review, or approval of the manuscript. OMF and CSM collected the data and wrote the manuscript. OMF analyzed the data. Dr Olivia Farr is the guarantor of this work and, as such, had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Author information

Authors and Affiliations

  1. Division of Endocrinology, Department of Medicine, Beth-Israel Deaconess Medical Center/Harvard Medical School, Boston, MA, USA

    O M Farr & C S Mantzoros

Authors
  1. O M Farr
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. C S Mantzoros
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to C S Mantzoros.

Ethics declarations

Competing interests

The authors declare no conflict of interest.

Additional information

Supplementary Information accompanies this paper on International Journal of Obesity website

Supplementary information

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Farr, O., Mantzoros, C. Obese individuals with more components of the metabolic syndrome and/or prediabetes demonstrate decreased activation of reward-related brain centers in response to food cues in both the fed and fasting states: a preliminary fMRI study. Int J Obes 41, 471–474 (2017). https://doi.org/10.1038/ijo.2016.231

Download citation

  • Received:

  • Revised:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/ijo.2016.231

Search

Advanced search

Quick links