The mere sight or smell of food can be enough to get our stomachs rumbling and mouths salivating, but a recent study into the mechanism that causes this has discovered that this process could be making it more difficult for overweight people to process sugars and shed the pounds. The study’s author described this as “like a marathon runner: after 42km, he can’t do a fast 100m race.”
This mechanism, called the cephalic phase response, is triggered by inflammation in the brain which causes the pancreas to produce insulin, which helps process the energy in your food and manage blood sugar levels. Unfortunately, researchers found that this inflammatory response in the overweight and the obese was “excessive”, slowing insulin output and making it more difficult to regulate weight.
The University of Basel study measured the output of one inflammatory chemical (IL-1β) within the body of mice, as well as their insulin output, when they were confronted with fake or real food. After protecting a mouse against IL-1β, scientists found that food triggered no corresponding increase in insulin production, while overweight mice would produce it in excess and make little insulin.
The lead author of the study, Professor Marc Donath, explained to MedicalNewsToday why this happens: “Obesity and diabetes lead to chronic inflammation beyond which an acute sensory stimulation no longer has any effect. It’s like a marathon runner: after 42km, he can’t do a fast 100m race.”
This new information is important in the treatment of obesity and type 2 diabetes, as anti-inflammatory foods and supplements could become a useful part of any weight/sugar management plan. Typically an anti-inflammatory diet will be full of anti-oxidising berries and immune-boosting vegetable to reduce levels of inflammation in our tissues and organs.
For Prof. Donath, targeting the specific inflammatory chemical could be a useful application of the research: “IL-1β antagonism is being developed for the treatment of type 2 diabetes and its complications. A better understanding of the mechanism of action of IL-1β on insulin secretion could guide us in the development of clinical studies,”