Author Interviews, Genetic Research, JCEM, Weight Research / 31.07.2014
Brain Reward System Underactive In Some Overweight People
MedicalResearch.com Interview with:
Dr. Agatha van der Klaauw, PhD
Wellcome Trust Postdoctoral Clinical Fellow
Wellcome Trust-MRC Institute of Metabolic Science
University of Cambridge Metabolic Research Laboratories
Addenbrooke's Hospital
Cambridge, United Kingdom
Medical Research: What are the main findings of the study?
Dr. van der Klaauw: Obesity occurs when we eat more calories than we burn which is often easy to do as many foods are highly palatable and high in calories. Highly palatable foods such as chocolate trigger signals in the brain that give a feeling of pleasure and reward (sometimes called cravings) which can contribute to overeating. These signals are processed in the reward centres in the brain, where sets of neurons release chemicals such as dopamine. However, very little is known about whether the reward centres of the brain work differently in some people who are overweight.
In this study, we were interested in studying overweight people who had a problem with the melanocortin 4 receptor (MC4R) gene. About 1% of obese people have a problem in this gene which contributes to weight gain from a young age. We compared three groups of people: people who were overweight due to a problem in the MC4R gene, people who were overweight but the gene was normal and some people who were normal weight. We performed functional Magnetic Resonance Imaging (fMRI) scans to look at how the reward centres in the brain were activated by pictures of appetizing food such as chocolate cake compared to bland food such as rice or broccoli and non-food items such as staplers.
We found that in normal weight people, the reward centres are activated (light up) when they are shown pictures of cake or chocolate and the same was seen in overweight people with a problem in the MC4R gene. But we found that the reward centres were underactive in overweight volunteers (in whom the gene was normal).
alResearch.com Interview with:
David C. Johnson, MD, MPH
Department of Urology
University of North Carolina School of Medicine
Medical Research: What are the main findings of the study?
Dr. Johnson: The first main finding from this study is that the likelihood of benign pathology after surgical removal of a renal mass suspected to be malignant based on pre-operative is inversely proportionate to size. This concept is well-established, however we systematically reviewed the literature for surgical series that published rates of benign pathology stratified by size and combined these rates to determine a single pooled estimate of benign pathology of pre-operatively suspicious renal masses for each size strata. Using benign pathology rates from US studies only, we found that 40.4% of masses < 1 cm, 20.9% of masses 1-2 cm, 19.6% of masses 2-3 cm, 17.2% of masses 3-4 cm, 9.2% of masses 4-7 cm, and 6.4% of masses >7 cm are benign.
The more novel finding from this study was the quantification of a previously unmeasured burden of over treatment in kidney cancer. By combining the above mentioned rates of benign pathology with epidemiological data, we estimated that the overall burden of benign renal masses surgically removed in the US to approach 6,000 per year in 2009. This represented an 82% increase over the course of a decade. Most importantly, we found an overwhelmingly disproportionate rise in the surgical treatment of renal masses in the smallest size categories – those which were most likely to be benign. We found a 233%, 189% and 128% increase in surgically removed benign renal lesions < 1 cm, 1-2 cm, and 2-3 cm, respectively from 2000 – 2009 in the US.
edicalResearch.com Interview with
Steven M. Hill, Ph.D.
Professor, Structural & Cellular Biology
Edmond & Lily Safra Chair for Breast Cancer Research
Co-Director, Molecular Signaling Program, Louisiana Cancer Research Consortium
Director, Tulane Circadian Biology Center
Medical Research: What are the main findings of the study?
Dr. Hill: The main findings of our study are that exposure to even dim light at night can drive human breast tumors to a hyper metabolic state, activating key tumor cell signaling pathways involved in tumor cell survival and proliferation, leading to increased tumor growth, all resulting in a tumor which is completely resistant to therapy. Our work shows that this effect is due to the repression of nighttime melatonin by dim light at night. When nighttime melatonin is replace the tumors become sensitive to tamoxifen resulting in cell death and tumor regression.
