As this year’s Congress President, together with World Obesity Federation President Dr. Walmir Coutinho, it will be our pleasure to welcome delegates from around the world to what I am certain will be a most exciting and memorable event in one of the world’s most beautiful and livable cities.
The program committee, under the excellent leadership of Dr. Paul Trayhurn, has assembled a broad and stimulating program featuring the latest in obesity research ranging from basic science to prevention and management.
I can also attest to the fact that the committed staff both at the World Obesity Federation and the Canadian Obesity Network have put in countless hours to ensure that delegates have a smooth and stimulating conference.
The scientific program is divided into six tracks:
Track 1: From genes to cells
- For example: genetics, metagenomics, epigenetics, regulation of mRNA and non–coding RNA, inflammation, lipids, mitochondria and cellular organelles, stem cells, signal transduction, white, brite and brown adipocytes
Track 2: From cells to integrative biology
- For example: neurobiology, appetite and feeding, energy balance, thermogenesis, inflammation and immunity, adipokines, hormones, circadian rhythms, crosstalk, nutrient sensing, signal transduction, tissue plasticity, fetal programming, metabolism, gut microbiome
Track 3: Determinants, assessments and consequences
- For example: assessment and measurement issues, nutrition, physical activity, modifiable risk behaviours, sleep, DoHAD, gut microbiome, Healthy obese, gender differences, biomarkers, body composition, fat distribution, diabetes, cancer, NAFLD, OSA, cardiovascular disease, osteoarthritis, mental health, stigma
Track 4: Clinical management
- For example: diet, exercise, behaviour therapies, psychology, sleep, VLEDs, pharmacotherapy, multidisciplinary therapy, bariatric surgery, new devices, e-technology, biomarkers, cost effectiveness, health services delivery, equity, personalised medicine
Track 5: Populations and population health
- For example: equity, pre natal and early nutrition, epidemiology, inequalities, marketing, workplace, school, role of industry, social determinants, population assessments, regional and ethnic differences, built environment, food environment, economics
Track 6: Actions, interventions and policies
- For example: health promotion, primary prevention, interventions in different settings, health systems and services, e-technology, marketing, economics (pricing, taxation, distribution, subsidy), environmental issues, government actions, stakeholder and industry issues, ethical issues
I look forward to welcoming my friends and colleagues from around the world to what will be a very busy couple of days.
For more information on the International Congress on Obesity click here
For more information on the World Obesity Federation click here
For more information on the Canadian Obesity Network click here
Liraglutide, a GLP-1 analogue now available for the treatment of obesity (as Saxenda) in North America, works by reducing appetite and increasing satiety, thus making it easier to lose weight and keep it off (with continuing treatment).
Now, a study by Olivia Farr and colleagues, in a paper published in Diabetologia not only present data showing the presence of GLP-1 receptors in human cortex, hypothalamus and medulla, but also provide functional evidence for altered brain response to food cues.
After documenting the presence of GLP-1 receptor in human brains using immunohistochemistry, the researchers conducted a randomised controlled placebo-controlled, double-blind, crossover trial in 18 individuals with type 2 diabetes who were treated with placebo and liraglutide for a total of 17 days each (0.6 mg for 7 days, 1.2 mg for 7 days, and 1.8 mg for 3 days).
Using functional MRI neuroimaging studies, the researchers found that liraglutide remarkably decreased activation of the parietal cortex in response to highly desirable (vs less desirable) food images.
They also observed decreased activation in the insula and putamen, areas involved in the reward system.
Furthermore, using neurocognitive testing, the researchers showed that increased ratings of hunger and appetite correlated with increased brain activation in response to highly desirable food cues while on liraglutide.
In contrast, ratings of nausea (a well-known side effect of liraglutide) correlated with decreased brain activation.
As the authors note,
“Our data point to a central mechanism contributing to, or underlying, the effects of liraglutide on metabolism and weight loss.”
These findings no doubt match the reports from my own patients of experiencing less interest in highly palatable foods and finding it much easier to pass up on foods that they would have otherwise found hard to resist.
Clearly, as we learn more about brain function in eating behaviour, we are thankfully moving towards treatments that are clearly proving to be far more effective than just telling patients to “simply eat less” (which I have often likened to telling people with depression to “simply cheer up”).
Disclaimer: I have received honoraria for speaking and consulting from Novo Nordisk, the maker of liraglutide
Shortly after a meal, there is a spike in the cerebrospinal fluid concentration of nutrients with direct access to various nutrient-sensitive sites in the brain.
Now a paper by Olof Lagerlöf and colleagues, published in SCIENCE, shows that in mice, the glycosylation enzyme O-GlcNAc transferase (OGT), present in a wide range of neurons involved in energy regulation and feeding behaviours, may play an important role in the satiety response.
Genetic and molecular manipulation of this enzyme in adult mice resulted in marked effects on feeding and weight gain.
Reducing the activity of the enzyme resulted in animals eating much larger meals (but not more often) with substantial gain in fat (but not lean) mass.
In contrast, increasing the activity of this enzyme resulted in reduced food intake during eating episodes.
Not only does it make sense that a molecule known to play a role as a nutrient-sensor would play a role in the central regulation of food intake, but the authors are optimistic that this enzyme may be a target for finding new anti-obesity medications.
Countless studies now show that there are important metabolic differences between people living with obesity and those living with normal weight.
Of particular interest are studies showing difference in hormonal and neuronal response to eating.
Now, a study by Nancy Puzziferri and colleagues from the University of Texas, published in OBESITY, show that the brain response to eating may differ substantially between people with normal weight and those living with obesity.
The study was conducted in 15 women with severe obesity and 15 age-matched lean women (18-65 years old).
When fasting, brain perfusion measured by arterial spin labeling was similar between obese and normal-weight volunteers and both groups showed significantly increased activity in the neo- and limbic cortices and midbrain activity in functional magnetic resonance imaging (fMRI).
However, after a standard meal, the lean group showed significantly decreased activation in these areas, whereas the group with severe obesity showed no such decreases.
In line with these findings, after eating, subjective appeal ratings of food decreased in lean but not in the obese women.
As the researchers note, these findings are in line with previous brain imaging studies.
“…after eating, participants with severe obesity maintain activation in the midbrain, one of the most potent reward centers. Thus, once satiated after eating, participants with severe obesity continue to perceive food as appealing and their brains continue to be activated by visual food cues as though they were hungry.”
These finding would explain why individuals with obesity are perhaps at a far greater risk to continue eating (especially highly-palatable foods such as dessert) even when satiated.
What these type of studies do not tell us whether these differences are primary (i.e. could have led to the weight gain in the first place) or secondary (i.e. the consequence of weight gain).
Be that as it may, the findings do show that there are significant differences in how the brain responds to eating between people with obesity and those with normal weight.
Clearly, the next step would be to see if this lack of response can be restored through weight loss (e.g. bariatric surgery) or through anti-obesity medication.
At least the findings perhaps explain why simply telling people with an activated limbic system to “push away from the table” may not be all that effective.
At one time in my research career, I was enamoured by the potential role of the renin-angiotensin system in the biology of adipose tissue – in fact, my lab was one of the first to characterize this system in human tissue.
Since then, my interests have moved on to a other things but I still keep an eye open for research on this system as it relates to body weight.
Thus, the recent work by Martina Winkler and colleagues from the University of Lübeck and the Max-Delbrück-Centre for Molecular Medicine in Berlin (where I used to work), published in the British Journal of Pharmacology caught my attention.
The researchers studied rats with a brain-specific angiotensinogen deficiency compared to controls using various dietary regimens.
Compared to SD rats, the brain-angioteninogen-deficient rats had lower weights during chow feeding, did not become obese during a high-caloric diet, had normal baseline leptin plasma concentrations independent of the feeding regimen, showed a reduced energy intake, had a higher, strain-dependent energy expenditure which is additionally enhanced during high-caloric feeding, had enhanced mRNA levels of pro-opiomelanocortin, and showed improved glucose control.
While the Angiotensin type 1 receptor blocker telmisartan reduced weight gain and energy intake in control rats, it had less effect in the brain-angiotensin-deficient rats
Thus, the researchers conclude that the brain renin-angiotensin system may play an important role in body weight regulation, feeding behavior, and metabolic disorders – at least in rats.
How relevant these findings are for humans remains doubtful.
For one, the widespread clinical use of inhibitors of the renin-angiotensin-system (ACE inhibitors, AT1 receptor blockers) are not generally associated with clinically significant weight loss. However, this may be because most of these agents do not reach high enough concentrations in human brain tissue. But it may also well be that this system is less important for body weigh regulation in humans than in rodents.